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Īutoantibodies bind to the receptors on target cells, causing dysfunction without causing inflammation or destruction. This is the hallmark of acute rheumatic fever in which antibodies directed against streptococcal antigens structurally mimic cardiac myosin in the human heart, leading to cross-reactivity of these antibodies against bacterial and host antigens and therefore binding to the myosin and damaging the heart tissue. Īntibodies against foreign antigens can also trigger complement activation and inflammation by a mechanism of molecular mimicry. The binding of these antibodies leads to strong activation of the complement system, which recruits leukocytes resulting in inflammation. For example, in Goodpasture syndrome, autoantibodies are directed against collagen in glomerular and alveolar basement membranes. These neutrophils then release enzymes and reactive oxygen species, which damage the tissues. Inflammation Mediated by Complement or Fc Receptor:Īntibodies can activate the complement pathway by binding to self-antigens resulting in the formation of complement components C3a and C5a, which act as chemotactic factors for neutrophils, causing the recruitment of neutrophils to the site and resulting in the activation of neutrophils. This type of cell depletion or destruction without inflammation is seen in autoimmune hemolytic anemia, autoimmune thrombocytopenia, certain blood transfusion reactions, and erythroblastosis fetalis.
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These are primarily natural killer cells that attach to the Fc portion of the antibody and then are activated, releasing perforins and granzymes, causing lysis of the target cell. Īntibody dependant cell-mediated cytotoxicity is a phenomenon by which antibodies bind to the target cell and then the effector cells of the immune system. A single channel is sufficient to induce lysis of anucleated cells like erythrocytes, but nucleated cells require multiple membrane attack complexes to destroy such cells. The membrane attack complex creates a channel to induce the lysis of cells. Īntibodies can also bind to the target cell resulting in complement pathway activation and formation of the membrane attack complex involving complement components C5b6789. This, in turn, activates the macrophages causing them to engulf the cell resulting in depletion of the cell. Īntibodies can also bind to the target cell and activate the complement pathway resulting in the formation of complement component C3b, which also acts as an opsonin and binds to the receptors on the surface of macrophages. Thus by binding to both the target cell and the Fc receptor of the macrophage, it activates the macrophage and causes it to phagocytose the target cell. An opsonin is any molecule that enhances the phagocytosis of any substance. Through their Fc portion, they bind to their respective Fc receptor on the surface of macrophages and thus act as an opsonin.
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The process involves a series of immune-mediated events that might take different forms.Ĭell Depletion or Destruction Without Inflammation:Īntibodies can bind to the target cell's surface, particularly IgG antibodies.