HSS 3305 Lecture Notes - Lecture 7: Macrocytic Anemia, Glomerular Basement Membrane, Pernicious Anemia
Document Summary
Alteration of patient"s self-antigens causing them to become antigenic, provoking an immune reaction. Formation of cross-reacting antibodies against foreign antigens that also attack patient"s own antigens, ex. Dysregulation of the immune response by regulator t lymphocyte. A genetic component that code for our own unique self-antigens, i. e. macrophage presenting processed antigen to lymphocytes. Frequency in women is higher than men: often a viral infection in a genetically predisposed individual to develop an autoimmune disease. Autoantibody-associated tissue injury results following type ii, iii & iv reactions. not all autoantibodies destroy target tissue. Sometimes, they derange the function of the target but do not destroy it, e. g. thyroid gland. Treatment of autoimmune disease is not very satisfactory. Various methods of treatment have been used to minimize inflammation and tissue damage, to suppress the function of the immune system, and to block the destructive effects of cytokines produced by t lymphocytes and macrophages.