Many autoimmune diseases are characterized by B-cell hyperactivity, marked by a proliferation of B cells and autoantibodies and by hypergammaglobulinemia. B-cell hyperactivity is probably related to T-cell abnormalities, but the molecular basis for autoimmunity is poorly understood. Hormonal and genetic factors strongly influence the incidence of autoimmune disorders. for example, lupus erythematosus predominantly affects females of childbearing age. “Certain HLA (histocompatibility leukocyte antigen) haplotypes are associated with an increased risk of specific autoimmune disorders” (Harold, 2008: 437).
Autoimmune disorders may not follow a clear pattern of symptoms. therefore a definitive diagnosis may be delayed. Diagnosis may rely on the patient’s medical history, family history, physical examination, including signs and symptoms and laboratory tests. Autoantibodies are usually found with such disorders as rheumatoid arthritis or systemic lupus erythematosus. However, confusion may result because individuals with these disorders may have false-negative results in laboratory tests. Treatment for autoimmune disorders focuses on relieving symptoms, preserving organ function, and providing medication that can target the immune system such as cyclophosphamide and cyclosporine. Autoimmune and immunological disorders are being further researched (Harold, 2008: 438).
In most autoimmune diseases, mutligenic factors play a significant role in pathogenesis. Considerable progress has been made in identifying thesw genetic factors, many of which are located outside the major histocompatibility complex. Most autoimmune diseases are multigenic disorders in which genes of the major histocompatibility complex (MHC) play an important role. To define the other genes of importance several .genetic methods can be used. .