Isoantigen

Alloimmunity (sometimes called isoimmunity) is an immune response to nonself antigens from members of the same species, which are called alloantigens or isoantigens. Two major types of alloantigens are blood group antigens and histocompatibility antigens. In alloimmunity, the body creates antibodies against the alloantigens, attacking transfused blood, allotransplanted tissue, and even the fetus in some cases. Alloimmune (isoimmune) response results in graft rejection, which is manifested as deterioration or complete loss of graft function. In contrast, autoimmunity is an immune response to the self's own antigens. (The allo- prefix means 'other', whereas the auto- prefix means 'self'.) Alloimmunization (isoimmunization) is the process of becoming alloimmune, that is, developing the relevant antibodies for the first time. Alloimmunity (sometimes called isoimmunity) is an immune response to nonself antigens from members of the same species, which are called alloantigens or isoantigens. Two major types of alloantigens are blood group antigens and histocompatibility antigens. In alloimmunity, the body creates antibodies against the alloantigens, attacking transfused blood, allotransplanted tissue, and even the fetus in some cases. Alloimmune (isoimmune) response results in graft rejection, which is manifested as deterioration or complete loss of graft function. In contrast, autoimmunity is an immune response to the self's own antigens. (The allo- prefix means 'other', whereas the auto- prefix means 'self'.) Alloimmunization (isoimmunization) is the process of becoming alloimmune, that is, developing the relevant antibodies for the first time. Alloimmunity is caused by the difference between products of highly polymorphic genes, primarily genes of the major histocompatibility complex, of the donor and graft recipient. These products are recognized by T-lymphocytes and other mononuclear leukocytes which infiltrate the graft and damage it. A failure of cross-matching can allow donor blood of an incompatible blood group to be transfused, resulting in a transfusion reaction. Hemolytic disease of the fetus and newborn is similar to a transfusion reaction in that the mother's antibodies cannot tolerate the fetus's antigens, which happens when the immune tolerance of pregnancy is impaired. In many instances the maternal immune system attacks the fetal blood cells, resulting in fetal anemia. HDN ranges from mild to severe. Severe cases require intrauterine transfusions or early delivery to survive, while mild cases may only require phototherapy at birth. Acute rejection is caused by antigen-specific Th1 and cytotoxic T-lymphocytes. They recognize transplanted tissue because of expression of alloantigens. A transplant is rejected during first several days or weeks after transplantation. Hyperacute and accelerated rejection is antibody-mediated immune response to the allograft. Recipient's blood already contains circulating antibodies before the transplantation – either IgM or antibodies incurred by previous immunization (e.g. by repeated blood transfusion). In case of hyperacute rejection, antibodies activate complement; moreover, the reaction can be enhanced by neutrophils. This type of rejection is very fast, the graft is rejected in a few minutes or hours after the transplantation. Accelerated rejection leads to phagocyte and NK cell activation (not of the complement) through their Fc receptors that bind Fc parts of antibodies. Graft rejection occurs within 3 to 5 days. This type of rejection is a typical response to xenotransplants. Chronic rejection is not yet fully understood, but it is known that it is associated with alloantibody and cytokine production. Endothelium of the blood vessels is being damaged, therefore the graft is not sufficiently supplied with blood and is replaced with fibrous tissue (fibrosis). It takes two months at least to reject the graft in this way. CD4+ and CD8+ T-lymphocytes along with other mononuclear leukocytes (their exact function regarding the topic is not known) participate in the rejection. B-lymphocytes, NK cells and cytokines also play a role in it. Humoral (antibody-mediated) type of rejection is caused by recipient's B-lymphocytes which produce alloantibodies against donor MHC class I and II molecules. These alloantibodies can activate the complement – this leads to target cell lysis. Alternatively, donor cells are coated with alloantibodies that initiate phagocytosis through Fc receptors of mononuclear leukocytes. Mechanism of humoral rejection is relevant for hyperacute, accelerated and chronic rejection.Alloimmunity can be also regulated by neonatal B cells.