Тұқымдас антигендерге иммундық жауап

Immune response to nonself antigens from members of the same species
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 (called alloantibodies) 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.

Blood transfusion can result in alloantibodies reacting towards the transfused cells, resulting in a transfusion reaction. Even with standard blood compatibility testing, there is a risk of reaction against human blood group systems other than ABO and Rh.

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 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. 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.

Cytokine microenvironment where CD4+ T lymphocytes recognize alloantigens significantly influences polarization of the immune response. CD4+ T lymphocytes differentiate into Th1 helper cells in the presence of IL 12 (which is usually secreted by mature dendritic cells). Th1 cells produce proinflammatory cytokine IFN γ and destroy the allograft tissue. If there is IL 4, CD4+ T lymphocytes become Th2 cells secreting IL 4 and IL 5. TGF β induces expression of Foxp3 gene in the absence of proinflammatory cytokines and thus differentiation of CD4+ T lymphocytes into regulatory T cells (Treg).

Transplanted tissue is accepted by immunocompetent recipient if it is functional in the absence of immunosuppressive drugs and without histologic signs of rejection. Host can accept another graft from the same donor but reject graft from different donor. Graft acceptance depends on the balance of proinflammatory Th1, Th17 lymphocytes and anti inflammatory regulatory T cells. Immunosuppressive drugs are used to suppress the immune response, but the effect is not specific. Therefore, organism can be affected by the infection much more easily. The goal of the future therapies is to suppress the alloimmune response specifically to prevent these risks. The tolerance could be achieved by elimination of most or all alloreactive T cells and by influencing alloreactive effector regulatory T lymphocytes ratio in favor of regulatory cells which could inhibit alloreactive effector cells.