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Pathogenesis of immune hemolytic anemias
Last reviewed: 06.07.2025
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Autoimmune hemolytic anemia is considered as a specific state of "dysimmunity" associated with a deficiency of the thymus-derived population of suppressor cells, disruption of cell cooperation during the immune response, and the emergence of a clone of autoaggressive immunocytes (proliferation of an "illegal" clone of immunologically competent cells that have lost the ability to recognize their own antigens). A decrease in the number of T-lymphocytes in the blood is accompanied by an increase in the number of B- and null lymphocytes in the peripheral blood. The absence of the regulatory influence of T-cells causes an increased and uncontrolled B-cell immune response, which is associated with an increase in the level of immunoglobulins in the blood serum of patients. Detection of proliferating immunoglobulins on the surface of target cells indicates the autoaggressive nature of the disease. Other mechanisms of disruption of cellular and humoral factors of immunity are also involved in the implementation of autoimmune aggression, as evidenced by an increase in lymphocytotoxic and a decrease in complementary activity of the blood serum of patients.
Warm anti-erythrocyte antibodies (maximally active at normal body temperature) are in most cases represented by IgG (including various subclasses of IgG1, IgG2, IgG3, IgG4), less often by IgA. Cold antibodies (maximally active in a cold environment - at a temperature of 4-18 °C) are IgM. Biphasic Donath-Landsteiner hemolysins, detected in paroxysmal cold hemoglobinuria, are IgG.
Destruction of red blood cells in autoimmune hemolytic anemia occurs in the spleen or in the spleen and liver simultaneously. In addition, B-lymphocytes of the peripheral blood, especially the spleen, are able to interact with their own red blood cells. These lymphocytes perform a killer function in relation to old red blood cells with an average lifespan, which have absorbed the maximum amount of antibodies.
Three main mechanisms of hemolysis in autoimmune hemolytic anemia have been described: phagocytosis of erythrocytes coated with antibodies and/or complement by monocytes-macrophages; lysis of erythrocytes coated with IgG by monocytes-macrophages; complement-mediated lysis.
For the development of hemolysis of erythrocytes that have absorbed IgG, interaction of spleen macrophages with a cell covered with antibodies is necessary. The rate of cell destruction depends on the number of antibodies on the cell surface. IgM antibodies cause structural damage to erythrocyte membranes, activate the C component of complement; in addition, they cause agglutination of erythrocytes.
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