Diseases produced by helminth parasites occur frequently in underdeveloped countries where they present a serious public health problem. At the same time, in these regions, a lower rate of autoimmune and allergic diseases has been observed. Due to these observations, some researchers have proposed that some helminths, such as Trichinella spiralis or its proteins, have strong anti-inflammatory potential, or have assessed them as modulating agents of the immune response. T. spiralis shifts the host immune response from a Th1 profile, characterized by pro-inflammatory cytokines, to a Th2 profile, characterized by the release of different cytokines with anti-inflammatory properties. This parasite has shown high therapeutic potential in a wide variety of disease models. In one of the most promising, the experimental lupus model in mice, the release of anti-inflammatory cytokines IL-4 and IL-10 and delayed onset of the key clinical features of the experimental lupus model for at least 5 months were observed, when previously parasitized. This is the first study to date that focuses on the use of T. spiralis as an immunomodulator in lupus disease. In conclusion, further study of the immune response generated by the parasite is necessary to advance the development of new therapies for inflammatory diseases.
Part of the book: Parasitic Helminths and Zoonoses
Anti-lipid antibodies are present in some infectious and autoimmune diseases, such as Systemic Lupus Erythematosus (SLE). Particularly, anti-non-bilayer phospholipid arrangement (NPA) antibodies have been detected in patients with SLE, and these antibodies trigger a disease similar to human lupus in mice. NPA are lipid associations different from the lipid bilayer of cellular membranes and, since they are transient, they are not immunogenic. However, if NPA are stabilized by drugs, they induce an immune response with the production of anti-NPA antibodies, which bind to NPA on cell membranes and generate cell lysis. As a result, intracellular antigens are exposed and trigger an immune response that generates more auto-antibodies. In this chapter, we describe the formation and stabilization of NPA, the induction of B cell responses to generate anti-NPA antibodies, and the characteristics that the disease caused by these antibodies in mice shares with human lupus.
Part of the book: Systemic Lupus Erythematosus