AUTOIMMUNE RESPONSESNormally a pers

AUTOIMMUNE RESPONSES
Normally a person is tolerized to self-antigens during the development of T cells and B cells and by Treg cells. However, deregulation of the immune response may be initiated by cross-reactivity with microbial antigens (e.g., group A streptococcal infection, rheumatic fever), polyclonal activation of lymphocytes induced by tumors or infection (e.g., malaria, Epstein-Barr virus infection), excessive cytokine production (e.g., type 1 interferons and systemic lupus erythematosus), or a genetic predisposition toward expression of self-antigenic peptides (MHC association) or lack of tolerization to specific antigens.
Autoimmune diseases result from the presence of autoantibodies, activated T cells, and hypersensitivity reactions. People with certain MHC antigens are at higher risk for autoimmune responses (e.g., HLAB27: juvenile rheumatoid arthritis, ankylosing spondylitis). Once initiated, a cycle is established between antigen-presenting cells and T cells, which produce cytokines to promote inflammation and tissue damage and more self-antigen. TH17 responses are responsible for rheumatoid arthritis and other diseases.