Typical properties of some heat treatable aluminum alloys [5].
\\n\\n
More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
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Three areas are covered: theoretical underpinnings and concepts related to national parks, exploring their various modalities and integrated concerns for the environment; an empirical review in lieu of effective management of protected areas as defined by the World Conservation Union IUCN, addressing the efficient use of human and material resources, including national/agency-protected area regulations and legislation, policies, international conventions and designations, management plans, and/or agreements associated with those areas; and evaluation of challenges underlying a country’s intention to gauge the potential of a national park and pinpoint adequate attention on exploiting new strategies for national park management.",isbn:"978-1-78984-230-2",printIsbn:"978-1-78984-229-6",pdfIsbn:"978-1-83968-372-5",doi:"10.5772/intechopen.77900",price:119,priceEur:129,priceUsd:155,slug:"protected-areas-national-parks-and-sustainable-future",numberOfPages:134,isOpenForSubmission:!1,hash:"cbfa2f8e9e9e6d0383298f88b71b4108",bookSignature:"Ahmad Naqiyuddin Bakar and Mohd Nazip Suratman",publishedDate:"January 8th 2020",coverURL:"https://cdn.intechopen.com/books/images_new/8069.jpg",keywords:null,numberOfDownloads:2742,numberOfWosCitations:0,numberOfCrossrefCitations:3,numberOfDimensionsCitations:9,numberOfTotalCitations:12,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"September 24th 2018",dateEndSecondStepPublish:"November 26th 2018",dateEndThirdStepPublish:"January 25th 2019",dateEndFourthStepPublish:"April 15th 2019",dateEndFifthStepPublish:"June 14th 2019",remainingDaysToSecondStep:"2 years",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:"Edited by",kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"216294",title:"Associate Prof.",name:"Ahmad",middleName:"Naqiyuddin",surname:"Bakar",slug:"ahmad-bakar",fullName:"Ahmad Bakar",profilePictureURL:"https://mts.intechopen.com/storage/users/216294/images/system/216294.png",biography:"Ahmad Naqiyuddin Bakar, CMILT (UiTM, IIUM, Exeter, Hull), is an associate professor at the Faculty of Administrative Science and Policy Studies, Universiti Teknologi MARA (UiTM), Malaysia. He is currently rector of the UiTM Johor branch. Prior to this, he was Head of the Research and Publication Unit at the Malaysia Institute of Transport after having previously served as Head of Institutional Research under the Strategic Planning and Information (CSPI) Centre at the Office of the Deputy Vice-Chancellor (Research and Innovation) of UiTM. He is also a senior research fellow at the Centre for Biodiversity and Sustainable Development, UiTM. He holds a Professional Certificate in Science, Technology and Innovation (STI) in Policy Management. 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Aluminum is a metal of great importance because of its excellent corrosion resistance, high electrical and thermal conductivity, good reflectivity and very good recycling characteristics. Aluminum atoms are arranged in a face-centered cubic (FCC) structure with a melting point of 660°C. There are nine different series of aluminum, which will be discussed later in this section, four of which are referred to as heat-treatable aluminum alloys, and these alloys are so-called because of the potential to increase the mechanical properties by precipitation strengthening [1, 2].
\nThe properties of heat treatable Al-alloys can be further enhanced by the inclusion of a reinforcing phase that increases the mechanical properties of the overall composite. Metal matrix composites (MMC) are usually manmade materials that consist of two or more distinct phases; a continuous metallic phase (the matrix) and a secondary reinforcing phase. The secondary phase may take the form of continuous or discontinuous reinforcement as particles or fibers. When this phase is introduced into the matrix the overall impact is an improvement of the mechanical properties of the material [3]. The properties of MMCs are comparatively superior to those of the unreinforced alloys [4, 5].
\nThe properties of discontinuously reinforced aluminum MMCs containing particles or short fibers are modest compared to the continuous fiber reinforced MMCs, however, these materials are less expensive to fabricate and have more flexibility in production making them more cost-effective [6, 7, 8]. The reinforcements used in fabricating the composites are dependent on the desired material properties, ease of processing, and part fabrication.
\nThe stability of the reinforcement/metal matrix interface and the differences in properties such as the coefficient of thermal expansion and thermal conductivity are limiting factors that affect the compatibility of the materials used to make the composite. The quality of the bond is dependent on adequate interaction between the reinforcement and the matrix.
\nOver the last two decade, the application of nano and micro-sized ceramics such as alumina (Al2O3), MgO nanoparticle [9], boron carbide [10] and silicon carbide (SiC) [11] to aluminum metal matrix composites have become popular reinforcing phases, since these hard phases can lead to an increase in flow stress from the matrix by load transfer across a strong interface from the matrix to the reinforcement [12]. An example of the typical microstructure of a particle reinforced aluminum metal matrix composite is presented in Figure 1 and shows an Al2O3 particulate reinforced Al-6061 MMC. The properties of these reinforcements include high strength, high modulus of elasticity and high thermal and electrical resistance. The constraint imposed by the ceramic reinforcements on the plastic deformation of the matrix is large tensile hydrostatic stresses.
\nSEM micrographs of Al-6061 MMC showing Al2O3 particulate reinforcements.
Recently, researchers have explored the use of graphene as a reinforcing phase within an aluminum metal matrix as a method of improving the mechanical properties of the composite [13]. The results of the study showed that the hardness, tensile strength, and ductility of the aluminum-graphene composite were approximately 2–3 times higher than the properties of the unreinforced aluminum alloys. The authors also demonstrated that the enhancements of the mechanical properties of the aluminum-graphene composite were proportional to the concentration of graphene added. Similar findings were published by Kumar et al. [14] and Jauhari et al. [15] who produced Al 6061 MMC reinforced with graphene by ultrasonic liquid processing and microwave sintering respectively.
\nMetal matrix composites (MMCs) find application extensively in the design and construction of engineering components that require a lightweight material with superior mechanical properties such as high tensile strength, high Young’s modulus, good wear resistance [16], and good elevated temperature properties. Al-MMCs are used extensively in industries such as aerospace, automotive, sports goods, and marine.
\nNumerous processes have been investigated for producing aluminum MMC. These include various casting techniques [17] and powder metallurgy approaches [18]. Currently, several additive manufacturing techniques are used to develop rapidly deposit aluminum alloys and composites [19, 20]. From the list available additive manufacturing techniques; selective laser melting (SLM), and wire arc additive manufacturing have shown the greatest promise for producing aluminum alloys and composites [19, 21].
\nAluminum is a nonferrous and relatively low-cost material with a high strength to weight ratio. These characteristics make aluminum alloys and composites very attractive and competitive structural materials in several industries. For applications requiring greater mechanical strength, aluminum is alloyed with metals such as copper, zinc, magnesium, and manganese. The alloying components determine the series assigned to the aluminum alloy. The possible series categories range from 1xxx to 9xxx. Aluminum alloys can be further divided into two categories: heat-treatable and non-heat-treatable alloys. Heat-treatable alloys are those in which strength is developed by precipitation hardening [22].
\nThese alloys are found in the 2xxx (aluminum-copper), 6xxx (aluminum-magnesium-silicon), and 7xxx (aluminum-zinc-magnesium) series [23]. In non-heat-treatable alloys, strength is developed mainly by solid solution strengthening and strain hardening. The non-heat treatable alloys are found in the 1xxx (Al), 3xxx (Al-Mn), 4xxx (Al-Si) and 5xxx (Al-Mg) aluminum series. The Gibbs free energy curves recorded at a 700°C for Al-Mn, Al-Mg, Al-Cu, and Al-Zn are shown in Figure 2 and suggest the formation of various intermetallic compounds having a hexagonal close pack (HCP) crystal structure within the aluminum matrix having a face-centered cubic structure (FCC). The 2xxx series which consists of Al-Cu is a heat-treatable alloy that strengthens due to the precipitation of copper aluminides within the aluminum matrix [23].
\nGibbs free energy curve plotted at a temperature of 700°C for (A) Al-Mg, (B) Al-Cu, (C) Al-Mn, (D) Al-Zn alloys.
Ternary systems of Al-Mg-Si and Al-Mg-Zn which are found in the 6xxx or 7xxx series respectively are other heat treatable aluminum alloys that are used in many applications within the aerospace and automobile industries. The high strength-to-weight ratio and corrosion resistance of heat-treatable aluminum alloys make them a very attractive class of materials. The phase diagrams presented in Figure 3 show the relationship between temperature and composition for the 6xxx series.
\n(A) Isothermal section of the Al-Mg-Si ternary phase diagram at 700°C and (B) pseudo-binary phase diagram of Al-6061.
The research on aluminum alloys and composites has seen substantial development in several new methods of fabricating components using aluminum as the base metal and combining the metal with new forms of reinforcements for various new applications. In a recent study, it was demonstrated that a 3D self-assembly of aluminum nanoparticle can be used for plasmon-enhanced solar desalination and [24]. Table 1 shows a summary of the properties of various heat treatable aluminum alloys. These properties justify the pervasive use of aluminum in automotive, aerospace and explosive mixtures for underwater propulsion. Among the available aluminum alloys, the 2xxx series, 6xxx series, and 7xxx series are used frequently in the aerospace and defense sectors, transportation, automotive, medical appliances, dental implants, sports, mobile phones, etc. [1, 2, 11, 25, 26].
\nAlloy | \nYS (MPa) | \nUTS (MPa) | \nElongation (%) | \nE (GPa) | \n
---|---|---|---|---|
6061 (T6) | \n275 | \n310 | \n20 | \n69 | \n
2014 (T6) | \n476 | \n524 | \n13 | \n73 | \n
2124 (T6) | \n325 | \n470 | \n12 | \n72 | \n
2618 (T6) | \n370 | \n470 | \n9 | \n74 | \n
7075 (T6) | \n505 | \n570 | \n10 | \n72 | \n
8090 (T6) | \n415 | \n485 | \n7 | \n80 | \n
A356 (T6) | \n205 | \n280 | \n6 | \n76 | \n
Typical properties of some heat treatable aluminum alloys [5].
Given the low melting point (660°C) and density (2.7 g/cm3) aluminum is now a key material used in metal additive manufacturing processes such as selective laser melting (SLM), these processes are largely termed layered manufacturing process in which the subject material is deposited in layers and build up to the required dimension [20]. Given the high strength-to-weight ratio and low melting temperature of aluminum, this material is used to fabricate various near-net-shape complex structures by additive manufacturing. Though additive manufacturing has seen extensive development over the last 5 years, there are several areas of the technology that will require significant research investment and investigation [20]. As the technology matures for depositing aluminum alloys will focus on process optimization to remove weaknesses such as oxide film formation on the surface of the metal powder, improve thermodynamic stability of the aluminum oxide and reduce the difficulty of finding low melting point binders to be used with aluminum powders [27, 28, 29].
\nWire arc additive manufacturing (WAAM) using gas metal arc welding (GTAW) has been used successfully to deposit AA5183 aluminum alloy [21]. The technique demonstrated the potential of rapidly depositing large metal structures [30]; however, there is still the need for further development to optimized materials properties, surface texture and internal defects within the components produced.
\nThe development of new aluminum alloys and composites is expected to continue to lower production costs and increasing the strength-weight ratio. These improvements in the properties of MMCs have made these materials important alternatives to traditional materials for high-temperature applications. Increasingly, aluminum MMCs containing SiC are used in engines (engine block and pistons), drive shafts and disc brakes (including rail type). It has been reported in the scientific literature that when MMCs are used to make drive-shafts the increase in stiffness, increases the maximum attainable rotation. The application of aluminum MMCs to the construction of pistons is one of the most significant developments in the automotive industry. In the electronics industry, the new generation of advanced integrated circuits generates more heat than previous types given the increase processing power. Therefore, the dissipation of heat has become a major concern. Thermal fatigue may also occur due to a small mismatch of the coefficient of thermal expansion between the silicon substrate and the heat sink. These problems can be solved by using MMCs with matching coefficients (e.g., Al with boron [10] or graphite fibers and Al with SiC particles [11]).
\nIn addition, Al-based MMCs can be used in situations in which an “adjustable” coefficient of thermal expansion is required. This is possible because the coefficient of thermal expansion is dependent upon the volume fraction of the fibers or particles added. Components produced using Al-MMCs are not only significantly lighter than those produced from aluminum metal alloys, but they provide significant cost savings through net-shape manufacturing [31].
\nThe research shows that the primary challenges affecting aluminum alloys and composite are directly linked to the properties of the material. An example can be seen in additive manufacturing where the growth in the application of aluminum in additive manufacturing has been driven by several important factors which include; low melting point, corrosion resistance, good strength-to-weight ratio. On the other hand, an important hurdle is finding suitable binders with the appropriate melting point to be used with powdered aluminum metals. The technology is also constrained by several other factors such as the need for a better understanding of the material properties, poor reproducibility, the need for additional material, lack of training and education of users and finally the unavailability of standards and certification.
\nMost manufacturers are cautious about using additive manufacturing as a viable manufacturing process due to the lack of repeatability and consistency of the manufactured parts. Manufacturers are also skeptical of the structural integrity of the finished products as compared to conventional manufacturing processes [12]. The primary challenge, however, is that materials produced using these processes contain numerous defects that limit the application.
\nThe verification and validation of the relationships between the process parameters and the finished product have been hampered by the lack of available data, poor understanding of the causes of internal defects, and uncertainty in detecting the critical flaw. These gaps in the existing knowledge limit the wide-scale application of additive manufacturing technology. Research into this area will aim to bridge the gap by quantifying the relationship between the process parameters, surface quality and defects present within the finished products.
\nAluminum alloys and composites (Al-MMCs) are of interest to the automotive and aerospace industries, because of comparably high strength-to-weight ratio, formability, and corrosion resistance. However, despite the unique properties of these materials, the lack of a reliable joining method has limited their use to engineering applications where joining is unnecessary. This can be seen as another major hurdle affecting the proliferation of aluminum alloys as an important material in achieving lightweighting objectives [34, 35].
\nOver the last two decades, numerous joining techniques have been extensive studied to identify a process that can be successfully used for dissimilar joining of aluminum alloys and composites by minimizing undesirable interfacial reactions between the materials being joined. Some of the processes that have been studied include fusion welding [36], brazing [37], friction stir welding [38], solid-state diffusion bonding [39] and transient liquid-phase (TLP) bonding [35, 40]. The key findings have shown that the inclusion of nanoparticles within the joint regions has the capability of significant increases in joint strength while minimizing unwanted interfacial reactions. The procedure has been applied to the diffusion bonding of aluminum alloys to magnesium as showing in see Figure 4 and diffusion bonding of Al-MMCs as shown in Figure 5. Application of the concept to resistance spot welding also proved successful as shown in Figure 6 which demonstrates that Al and Mg can be successfully welded together without the formation of undesirable compounds.
\nEutectic microstructure formed at the joint interface during TLP bonding: (A) eutectic microstructure formed using Cu/Al2O3 interlayer; and (B) EDS spectrum of region-2 [32,33].
(a) SEM micrograph of joint bonded with a 15 μm Ni-Al2O3 coating for 1 min. (b) DS analysis of nano-Al2O3 particle.
SEM micrograph showing: (A) Al/Ni-Al2O3/Mg spot weld; (B) microstructure of point-6; (C) weld nugget/Al interface; and (D) microstructure of point-7 [41, 42].
This introductory chapter presents a brief overview of the state of science and the application of aluminum alloys and composites. Particular attention is paid to the application of new/novel methods of producing aluminum alloys while highlighting the future direction of the technology and some of the key challenges that affect the use of these materials. The book contains seven chapters that have been divided into two sections.
\nThe first section of the text is focused on evaluating the types and properties of advanced aluminum alloys and composites. The chapters in this section provide a comprehensive overview of the processing, processing, formability, chemical composition of advance aluminum alloys and composites and the development of new types of alloys.
\nThe second section of the text contains chapters that are focused on exploring processing, characterization, and testing of aluminum alloys and composites such as wear testing. The advantage of this text is that it provides a detailed review of major advances that have occurred in the development and application of aluminum alloys and composites while outlining a development strategy for these materials.
\nThe human immune system has two major divisions: innate and acquired. We will talk about innate immunity. Innate immunity can be defined as the first line of defense against pathogens, which represents a great machinery to create an adequate and definitive systemic response to prevent infections and maintain homeostasis of the organism. The elements of innate immunity include external physical barriers, humoral and cellular effector mechanisms. This type of immunity recognizes pathogens such as bacteria and viruses. This works thanks to the phagocytosis of the pathogens with the consequent induction of inflammatory reactions. It also has a critical role in the activation and regulation of adaptive immunity. This immunity has the ability to develop an induced response during primoinfection. This response is specific due to the expression of cell surface pattern recognition (PRR) receptors, which are capable of recognizing complex polysaccharides, glycolipids, lipoproteins, and nucleic acids. We know that pathogens contain in their structure various components that act as substances strange (antigens) and this in turn will induce an innate immune response that will subsequently activate the adaptive response. It is imperative to recognize that the important exploration of these innate mechanisms is essential for the understanding of the complex events involved in human innate immunity and is also crucial for the discovery of new antimicrobials, antitumor drugs, and immunomodulators with therapeutic applications [1]. Innate immunity, which is considered a simple immune system, is essential for the onset of acquired immunity and has been found to play an important role in the pathogenesis of the disease age [2]. Among them, it recognizes nucleic acids derived from pathogens. The innate immune pattern recognition (PRR) receptor recognizes self-derived nucleic acids. Innate pattern recognition receptors regulate antigens for the presentation and subsequent responses of B cells and T cells, for example, physiological management of autoantigens, induction of immature dendritic cells to detect tolerant signals to T cells. The activation of toll-like receptors (TLR), NOD type receptors (NLR) or Helicases similar to RIG (RLH) by molecular agents associated with pathogens where the patterns will induce dendritic cell maturation, costimulation.
\nT cell activation and production of antibodies by B cells. Therefore, recognition of innate patterns is now being considered as a central element of immunity modulation. There are at least 80 different autoimmune diseases discovered so far, which in the US alone, affect 20 million people [3]. These pathologies are established systemically or in a specific organ, but require for their expression certain conditions that are the result of multifactorial processes that involve a deregulation of the innate immune system and therefore adaptive that lead the body to erroneous responses with the subsequent attack itself of their own tissues. The innate immune system as discussed above is the first line of immediate defense against invading microorganisms that links to the adaptive response. Specific cells of the innate immune system, which are dendritic cells (DC) (antigen presenting), which are cells with an important and critical role in promoting the responses of B and T cells. This type of immunity is critical to maintain homeostasis and prevent microbial invasion, eliminating a wide variety of pathogens and contributing to the activation of the adaptive immune response.
\nIt is the control point. A dendritic type receptor that bears the title of “access gate” for innate cellular immunity: this basically consists of a type of toll-like receptor. It has been found that it plays a fundamental role as a sensor in the recognition of pathogens in the innate immune system [4].
\nThis pattern recognition receptor acts on bacteria and viruses (PAMP) [5]. The innate immune response in immunological terms controls the infection and prevents its spread. And more recently it is known that to induce this series of reactions against pathogens, in addition to the existence of antigens, another series of molecules in the pathogens is required. These molecules are known as pathogen-associated molecular patterns (PAMPs). PAMPs play and interact with a series of receptors that are mainly present in phagocytic cells (macrophages), and these “gate” receptors have been called recognition patterns to pathogen-associated molecular patterns (PRRs). These receptors contain other subfamilies where we can find toll type receptors (TLRs), NOD type receptors (NLRs), RIG-1 type receptors (RLRs), and lectin C type (CLRs). This molecular pattern related to the associated damage known as DAMP comes to behave as a type of alert that recognizes signals and most importantly this does not involve pathogen detection. The main molecular recognition patterns (PRRs) include TLR and NLR receptors, also known as nucleotide binding oligomerization domains. TLR is the homologous receptor that has already been identified in the Drosophila genetic code, and that to date some TLRs have been found in humans mainly in the cell surface, membrane, and lipids [6]. Types 1, 2, 4, 5, and 6 are those that recognize proteins, nucleic acids located in the endoplasmic reticulum and those that are found in the endosomal membranes. 3, 7, 8, and 9 detect lipopolysaccharides in the outer membrane of gram-negative bacteria (endotoxins). The TLR4 type, which transmits inflammatory signals, is the best known in general and the most studied of the TLR. This receptor responds to MyD88, which becomes a station at the central point of the inflammation signal, and corresponds to the first phase of activation of the transcription factor NF-κB pathway (nuclear factor-kappa B), which a In turn, production begins and a kind of “chain reaction” of inflammatory cytokines to eliminate pathogens [7]. Meanwhile, these TLR receptors are incorporated into PAMPs, which by recognizing nucleic acids act as an inflammatory cytokine. Receptors that mediate innate immune responses, such as toll-like receptors (TLR) and specific C-type lectin receptors (CLR) that recognize associated molecular patterns (PAMP), have been implicated in autoimmune disease mechanisms, both directly through self-recognition ligands and indirectly through the regulation of immune homeostasis [8, 9].
\nIn intracellular infections, in addition to antigens and PAMPs, the participation of another series of molecules that participate in the activation of the immune response is necessary. Recently, some studies have shown that cells can die from a type of immunogenic “apoptosis” and thus expose their nuclear or cytoplasmic molecules to their membrane. These have a way of stimulating the immune response, thanks to their activity. They are also released during the process of necrosis and have been given the name of molecular patterns associated with damage or warning signs, the famous DAMPs. The NLR receptor is present in the cytoplasm. It has the particularity of recognizing not only PAMP but also several DAMP among them [uric acid, cholesterol, sterols crystals, extracellular ATP (adenosine triphosphate), silica] or even recognizing exogenous DAMP such as asbestos, origin of aseptic inflammation, such as gout, arteriosclerosis, and silicosis [10]. It is clear that it is a cause and attracts attention. The abnormalities in the immune system that are the basis and fertilizer for autoimmune diseases are mainly caused by an abnormal acquired immunity [11]. In recent years, in contrast to the concept that autoimmune or auto-inflammatory diseases are mainly due to abnormal innate immunity, it is attracting more attention.
\nDendritic cells, macrophages, and other myeloid cells also play an important role in the innate immune response, both as antigen presenting cells as effector cells that mediate the tissue damage [12, 13, 14]. Therefore, they are fundamental and will be as in conflicts, “the first line of defense” in the face of a bacterial or other stimulus. We will also take them into account in relation to autoimmune diseases, because of their responsiveness and because they are important mediators of innate immunity, an interest has arisen in this potential to contribute to the pathology of these diseases. Proinflammatory cytokines: mainly TNFa (tumor necrosis factor alpha), induce the activation of endothelial cells, resulting in an increase in the expression of different adhesion molecules (CD62E, CD62P, ICAM-1, and VCAM-1). This causes the leukocytes to roll over them, and during this bearing, they are activated by the intracellular signals that are generated through their adhesion molecules and different chemokine receptors, which interact with the ligands found on the surface of the cells endothelial. Subsequently, these activated leukocytes adhere firmly to the endothelium, change their morphology (cell polarization) and carry out their transendothelial migration, and then migrate to the inflammatory focus, guided by the gradient of chemotactic substances that are released. Macrophages are multifunctional antigen presenting cells, with an important role in innate immunity and, therefore, in the inflammation process [15]. Macrophages are found in almost all organs, and recent studies have demonstrated their multifunctionality and heterogeneous capacities established by their numerous subpopulations, adaptation in specific tissue microenvironments and different stages of maturation. For example, during a bacterial infection, classically activated macrophages show inflammatory functions (type 1 or M1 macrophages), while with alternative activation (by Th2 type cytokines, such as IL-4 or IL-13), macrophages acquire anti-inflammatory functions (type 2 macrophages or M2). In addition to depletion or inhibition of macrophage function, reprogramming of M2 has also been explored. Recently, it has been shown that paracoccin, a protein contained in a fungal human pathogen, induces the repolarization of M1 macrophages through interaction with toll as a receptor (TLR) 4, being a new possible immunotherapeutic agent for pathologies related to M2 macrophages. Macrophage-related therapies have been proposed for various autoimmune and inflammatory pathologies. In the case of PPARγ and PPARδ, which are nuclear receptors that control different genes associated with M2 macrophages, and their agonists have been proposed as a therapy directed at macrophages to induce M2 pathways. In addition, the demonstration that TLR9 receptor signaling can reverse the aberrant M2 macrophage phenotype.
\nDendritic cells (DC) are professional antigen presenting cells (APC), often referred to as “orchestra directors of the innate immune response” due to their ability to capture, process, and present antigens to T cells. Depending on the nature of the antigen may exhibit an immunogenic or tolerogenic effect, which will be defined by cytokine secretion. They are often considered tolerogenic, because they have autoantigens in the absence of costimulation and, together with anti-inflammatory stimuli, (TGF-β), can promote the induction of regulatory T cells and/or induce anergy of T cells [16]. After activation by proinflammatory stimuli, they mature and generate an expression of costimulatory molecules and the major histocompatibility complex (HCM) class II, which causes a potent response of specific T cells to the antigens. Therefore, they play a fundamental role in maintaining self-tolerance, and on the other hand, they initiate the response against foreign antigens for their subsequent elimination by effector immune cells. In a state of aberrant hyperreactivity, they could contribute to perpetuating immune responses, backed by evidence of a high frequency of immunogenic infiltration [17]. Due to their ability to modulate the cellular response, they have been considered a powerful target for immune modulation. Strategies such as pharmacological modulation to affect their maturation status and genetic engineering to improve their tolerance or immunogenic properties for the treatment of autoimmune diseases have been studied. In several murine models, they were transduced to express IL-4 and were able to prevent disease in 12-week NOD mice. In a murine model of collagen-induced arthritis (CIA), it was shown that the injection of dendritic cells with tolerogenic activity improves the clinical and the outcome of the disease. Although the treatment was found to be safe and feasible, other studies are needed to evaluate the efficacy of cellular treatment in autoimmunity.
\nThey are a growing family of immune cells that reflect the phenotypes and functions of T cells. Natural killer cells (NK) can be considered innate homologs of cytotoxic CD8 + T cells, while ILC1, ILC2, and ILC3 correspond to innate homologs of T cells CD4 + (TH1), TH2, and TH17. However, in contrast to T cells, they do not express antigen receptors or undergo clonal selection and expansion when stimulated [4]. The ILCs react and respond to the signs of tissue damage and produce a series of cytokines, which direct the immune response and this adapts to contain the lesion. Therefore, these cells can control or unleash the immune response. As with B cells and T cells, these also originate from the common lymphoid lineage but the specific transcription factors of these suppress and modify their development until the generation of the different types of ILC. The precursors of these can migrate from their primary production site in infected and injured tissues, where they complete their maturation, in a process very similar to the differentiation of virgin T cells into TH effectors. The cytokines produced by local cells, as well as some trauma and stress response ligands as well as bacterial and dietary compounds regulate the maturation and activation of ILC in effectors that play an important role in early immune responses to pathogens in particular has been found relationship with symbionts, helminths, and allergens. The cytokines they produce induce innate responses in stromal, epithelial, and myeloid cells that in turn will regulate the activity of dendritic cells and will also play a central role in the transfer of information between ILC and T cells. ILCs by activating DC found in tissues to migrate to the lymph nodes, where they cause specific T-type cellular responses. ILCs also regulate T cells directly through the presentation of peptide antigens through CMH type II. However, ILCs are also involved in autoimmunity, because their cytokine production can exacerbate and exaggerate the inflammatory process.
\nRecent research has revealed new knowledge about the respective roles of these cells in relation to cellular and humoral immunity as well as the extension to adaptive immunity [18]. There is talk of a recent study in which a genetically modified mouse prototype model was developed with an autoimmune disease similar to lupus that does not require to express the adaptive immune system machinery, but is triggered directly by the innate immune response [19]. For many autoimmune diseases, we largely know the roles that key cells (T cells and B cells) play and for example are evident in the success of existing therapies (anti-CD3 and anti-CD20). Then knowing this, each of the functions of myeloid cells, and in general of the innate immune response cells, can “autoimmune” disease occur in the absence of adaptive immunity and these cells act as effectors in disease progression? The answer to this could be yes [20]. The most recent example is the study of mice eaten by moths that have been genetically modified to have deficiencies in hematopoietic cells, and to express an autoimmune disease characterized by alopecia (giving a “peeled or eaten by moths”) and edema in their legs. These were also accompanied by high antibody titers, with renal and pulmonary functions being compromised due to immune complex deposits [21, 22]. However, in another study, mice with deficiency in hematopoietic cell phosphatase were crossed with mice that lack the recombinase-1 activator gene (RAG-1) that caused a subsequent deficiency in the production of T and B cells and found that the disease autoimmune had progressed normally in the absence of an adaptive immune response [22, 23] even though these mice lacked high antibody titers and immune complex deposits, and they exhibited all other symptoms of the disease. Subsequently, although the onset and progression of the disease could not be defined, it was concluded that the autoimmune disease of this type of mice was mediated by an aggressive response of macrophages and other myeloid cells. Now, a study with murine models is also described, with mice with a genetic alteration associated with the deficiency in the enzyme α-mannosidase type II (αM-II) where there is premature aging with the clinical expression and the characteristic symptoms of SLE and Lupus nephritis (high titers of anti-DNA antibodies, glomerulonephritis, and renal compromise due to deposition of immunoglobulins in the kidney) that seems to be driven by a mechanism that also seems to involve the innate immune system [12, 24, 25]. In the case of the murine model, evidence was provided that the abnormal presence of hybrid glycoprotein structures acts as a trigger for the induction of an innate immune response mediated by members of the C-type lectin family that is specific for mannose. Serum mannose-binding lectins (MBL-A and MBL-B) are soluble lectins that mediate innate immunity to pathogenic bacteria and fungi that express glucans (mannose). It is also believed that the macrophage of the mannose receptor cell surface (MMR) participates in innate immune responses, and its expression has been documented in mesangial renal cells [26, 27]. In mice with αM-II deficiency, MBL lectins are deposited in renal glomeruli which, when they express high levels of mannose glucans in mesangial cells, also express higher levels of MMR, which can bind mannose ligands in the serum. Monocyte chemoattractant protein 1 (MCP-1) levels, produced by activated mesangial cells, represent the entry of activated macrophages. By aberrantly expressing mannose-containing glucans in mice with αMII deficiency, they act as triggers for an innate immune response mediated by mannose-specific C-type lectins programmed to recognize mannose glucans as PAMP.
\nThe second point in importance is the role of antibodies in stimulating the innate immune response. How can this be to the production of autoantibodies in autoimmune diseases, such as our old friend, lupus? Systemic lupus erythematosus (SLE) is an autoimmune disease that translates inflammation and exaggerated immune responses and thus with a large generalized associated tissue damage. We are clear that innate immunity plays a great role in its development and sequentially its clinical expression, and it has been shown that defects found in any of the immune recognition pathways will promote autoimmunity. First, dendritic cells and macrophages activated by TLR receptors can regulate the differentiation of self-reactive B cells through the expression of CD40 and the action of IL-6. Second, by nucleic acids. These can activate and in a powerful and disorderly way certain TLR and RLH receptors; therefore, these are normally protected from immune recognition by multiple mechanisms (epigenetic modifications, nuclear compartmentalization, and the rapid elimination of cells that have entered apoptosis and extracellular compartments by a type of DNase and RNAse enzymes). These immune complexes containing chromatin or circulating RNA particles can avoid being “digested” by these enzymes in the extracellular space and facilitate the uptake of the complex in intracellular compartments through Fc receptor-mediated endocytosis (FcR) in dendritic cell-mediated uptake or by B cell receptor (BCR) in B cells. And it has also been confirmed by studies with lupus-prone mice deficient in TLR receptors and their respective signaling molecules. As an exception, mice with TLR-9 deficiency with a predisposition to lupus produce more autoantibodies against it, indicating that TLR-9s have additional functions in the regulation of systemic autoimmunity. Innate pattern recognition (PRR) receptors regulate the production of autoantibodies associated with lupus and self-reactive T cells by modulating the presentation of autoantigens and also contribute directly to the end result that is tissue or organ injury secondary to autoimmunity. In general, it is believed that this “injury” or tissue damage is generated from the deposition of the immune complex, complement activation, and subsequent release of cytokines and chemokines to trigger local inflammation. This concept has been redefined. For example in glomerulonephritis, in the glomerular immune complex, deposits are not always associated with innate and adaptive immune responses. These are traditionally seen as separated from each other, but emerging evidence suggests that they overlap and interact with each other. Recently discovered cell types, particularly innate lymphoid cells and myeloid cell-derived suppressors that are gaining increasing attention. It is a rapidly evolving field with molecular pathways and new types of discovered cells and multiple constantly changing paradigms. In general, it is believed that many autoimmune diseases are triggered by aggressive responses of adaptive immunity by an automatic antigen system, resulting in tissue damage and pathological sequelae.
\nThe third point is undoubtedly the role of infectious agents, which have the potential to trigger an exaggerated immune response, through molecular imitation, polyclonal activation or antigen release. For example, there are certain diseases that respond to certain infectious autoantigen peptides. This is the case of multiple sclerosis, where T cells are activated by Epstein-Barr virus peptides, type A flu, and human papilloma and that react with the myelin autoantigen peptide [28]. In this case, the viral infection could cause the activation of the lymphocytes, and the autoantigen could maintain this activation, even after the eradication of the infectious agent. Microbial infection can also cause polyclonal activation of lymphocytes, and this is the underlying mechanism in increasing the incidence of autoimmunity in murine models exposed to microbial pathogens [29]. Microbes (viruses or bacteria) that destroy cells also cause an inflammatory response and also the release of antigens that have been previously captured and this could also result in autoimmunity. There is another important point. Inflammation, even in the absence of infection, can trigger polyclonal activation and self-activity. This is that through the activation of annergic cells, by inflammatory mediators or the activation of new self-reactive cells in an inflammatory environment for example in the context of ischemia of any tissue, tissue autoreactivity could be caused and because not at a systematic level [3]. Within non-infectious detonators, we have those of the hormonal type that in many autoimmune diseases are more common in women than in men. Drugs can also alter the immune repertoire. One of the most common and studied procainamide induces antinuclear antibodies and sometimes induces a lupus-like syndrome. And even some substances produced by the same cells can act as haptens and make autoantigens immunogenic, for example, CD1 T cells, with receptors (gamma/delta), CD4+, CD25+, and cytokine-producing agents that monitor activity, reduce, and control self-reactive cells, and they can become pathogenic. As some must complete their maturation in the thymus, and others the activation of autoantigens in the periphery, in these processes alterations in the number and function of regulatory cells that can contribute to autoimmunization can be generated.
\nUpon contact with the stimulus, whether microbial or of any substance, the recruitment and activation of macrophages will begin. The macrophages will serve as the primary effector cells that cause tissue damage and loss. And it has been concluded that the vast majority of autoimmune diseases could be explained by an aberrant adaptation as an immune response to the antigens themselves. On the other hand, autoimmunity as a disease contrasts with innate immunity. The first in which the term autoinflammatory was used was the periodic fever syndrome related to the TNF receptor (tumor necrosis factor), whose causative gene is TRAPS 4 and which was directly related to the presence of genetic abnormalities associated with innate immunity autoinflammatory diseases that are generally considered as a group of diseases where we can find an active responsibility for aberrant innate immunity and in which T cells are not detected and include TRAPS, cryopyrine-associated syndrome (secondary to mutations in the NLRP3 gene in children) (CAPS), Familial Mediterranean Fever (FMF), Bechet’s disease, Still’s disease in adults, Crohn’s disease, Gout, Type 2 diabetes, and various metabolic disorders [30]. The mechanism of its many initiation is still unclear, but the symptoms and diseases themselves are caused by the collapse of immune tolerance. Thymus autoreactivity and subsequent and completely abnormal inactivation of receptive and regulatory (Th) T cells suppress the reaction to the foreign antigen. The other part of the aberrant response of the innate immune response is carried out in the recipients of recognition of autoimmune patterns and diseases recognized by nucleic acids (PRR). This recognition is transmembrane due to its location in the cell and is divided into two general and cytoplasmic phases. This receptor is found in the endoplasmic reticulum or endosome and is directly related to autoimmune diseases (SLE = TLR7/9). When comparing the sequence of own nucleic acids and pathogen derivatives by means of the TLR7/9TLR9 receptors, it is noted that it contains unmethylated CpG sequences, and these are derived from pathogens that in turn recognize a type of single stranded DNA. TLR7 on the other hand recognizes single stranded RNA derived from viruses and other types, as well as messenger RNA (mRNA). From this, TLR7/9 is self-sufficient, and this receptor can strictly distinguish between conventional nucleic acids and pathogen derivatives. Stimulates an immune response in response to auto-nucleic acid. In other words, viruses and infected cells are captured by endosomes, and these nucleic acids are recognized by TLR7/9. In the case of SLE, the TLR7/9 receptor, due to the genetic modification secondary to the aberrant response to the own nucleic acids that were released and transferred to the endosome and therefore increases the genetic expression of the type I IFN and is known as the “IFN signature.” This signature of IFN is directly related to SLE, rheumatoid arthritis (RA), and systemic sclerosis (SSc) and its effects, suggesting the importance of type I IFN in autoimmune disease [31]. It also activates and stimulates plasma cells that in turn produce large amounts of type I IFN.
\nThe TLR7/9 receptor also mediates the response of plasmacytoid cells and is considered an IFN type I producing cell, which through the TLR7/9 Fc receptor activates the signal to induce the production of non-protein IFN type I histone in the core (HMGB1), to subsequently activate DAMP. The balance between TLR7 and TLR9 is also considered important for inflammation and immune response. The other transmembrane PRR receptors TLR3 and TLR8 also recognize double stranded and single stranded RNA. On the other hand, the cytoplasmic PRR receptor, type RIG-I, and MDA-5 normally identifies a specific structure of single stranded RNA. By recognizing double-stranded RNA, the specific proteins of these DAI, IFI16, and DDX41 receptors induce the production of IFN and inflamasome and, in turn, the production of IL-1β and IL-18.
\n“The authors declare no conflict of interest.”
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