Myelodysplastic syndrome (MDS) is a hematopoietic stem cell disorder affecting individuals over the age of 60 years. It is characterized by ineffective hematopoiesis and extensive apoptosis of hematopoietic cells. MDS patients are at a high risk of transforming in to acute myeloid leukemia. The main cause of apoptosis and escape from immune surveillance in MDS is immune dysregulation caused by a number of factors such as aberrant cytokine production and influence of various immune cells. In the past decade various pro-inflammatory cytokines and a number of immune cells such as Natural Killer cells, regulatory T cells, cytotoxic T cells, mesenchymal stem cells, myeloid derived suppressor cells and dendritic cells have been implicated in immune dysregulation leading to MDS pathogenesis. In this review we focus on the current data available on the role of these immune factors.
Part of the book: Recent Developments in Myelodysplastic Syndromes
Alloimmunization also known as isoimmunization, during pregnancy is the production of IgG antibodies by the mother against the paternally inherited antigens (IPA) in the foetus/newborn. The alloimmunization during pregnancy leads to various alloimmune disorders, such as, haemolytic disease of the foetus and newborn (HDFN), neonatal alloimmune neutropenia (NAN) and foetal and neonatal alloimmune thrombocytopenia (FNAIT) due to the production of maternal alloantibodies against the red blood cell antigen, neutrophils and platelets cell antigens, respectively. Recent studies suggest that maternal anti-HLA class I alloantibodies may also be the cause of FNAIT in addition to antibodies against platelet antigens. On the contrary, studies have also suggested that HLA-C, a classical HLA class I molecule, and HLA-G, a nonclassical HLA molecule, play an important role in placentation and modulation of the maternal immune system during pregnancy, respectively, and thereby leading to acceptance of the semi allogeneic fetus. So far most of the studies have discussed alloimmunization in pregnancy relating to Rh antigen. Thus, in this chapter an attempt has been made to discuss alloimmunization in pregnancy caused because of maternal alloantibody against HLA antigen and its role in immune modulation during pregnancy.
Part of the book: Complications of Pregnancy
Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is a potential curative treatment for both congenital and hematological malignancies. Immune reconstitution after allogeneic hematopoietic stem cell transplantation is implicated in successful transplant outcomes such as overall survival and relapse-free survival. The reconstitution of immune cell subsets after HSCT occurs in different phases at different time points encompassing pre-engraftment, engraftment, and post-engraftment. The recovery of innate cellular immunity with the appearance of monocytes, dendritic cells, and natural killer cells in peripheral blood correlates with initiation of cellular engraftment. The cellular adaptive immunity is characterized by both thymic-independent expansion of T cells infused with graft and thymus-dependent expansion of naïve T cells derived from donor stem cells. The humoral immunity consists of B-cell reconstitution, which consists primarily of transitional and naïve subsets with the recovery of memory B cells that occur much later. In this review, we highlight the factors affecting immune reconstitution, the reconstitution of innate and adaptive immunity, techniques to assess immune reconstitution, and ways to enhance it.
Part of the book: Cells of the Immune System