Cell-mediated damage, autoimmune

R6. Reichlin, M., Cellular dysfunction induced by penetration of autoantibodies into living cells Cellular damage and dysfunction mediated by antibodies to dsDNA and ribosomal P proteins. J. Autoimmun. 11, 557-561 (1998). 

E. Abnormal Immune Responses Abnormal immune responses include hypersensitivity, autoimmunity, and inununodeficiency states. Immediate hypersensitivity is usually antibody-mediated and includes anaphylaxis and hemolytic disease of the newborn delayed hyptersensitiv-ity, associated with extensive tissue damage, is cell-mediated. Autoinununity arises from self-reactive lymphocytes that react to one s own molecules, or self-antigens. Examples of autoimmune diseases that are amenable to dmg treatment include rheumatoid arthritis and systemic lupus erythematosus. Immunodeficiency states may be genetically acquired (eg, Di George s syndrome) or result from extrinsic factors (eg, AIDS). 

Inflammation is characterized by the orderly occurrence of several processes initiation of the event by a foreign substance or physical injury, recruitment and chemoattraction of inflammatory cells, and activation of these cells to release inflammatory mediators capable of damaging or killing an invading microbe or tumor. In some instances, the inflammatory response is initiated by an otherwise harmless foreign material (e.g., pollen). Inflammation can also result from an autoimmune response to the host s own tissue, as occurs in rheumatoid arthritis. 

The typical pancreatic lesion of type 1 diabetes is the selective loss of almost all 3-cells, whereas other islet cell types (a, 8, and pancreatic polypeptide cells) remain intact. The most common mechanism for 3-cell destruction is thought to be autoimmune-mediated inflammatory damage. Prospective family studies strongly support a genetic basis for susceptibility to this autoimmune process and suggest that the underlying immune abnormalities precede clinical insulin deficiency by many years. However, not all spontaneous type 1 diabetes is the result of autoimmune mechanisms. 

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