Interleukins in Experimental Autoimmune Disease
Abstract
In autoimmune disorders, the organism’s ability to discriminate self from foreign antigens is disturbed, leading to tissue destruction due to a variety of immunopathologic mechanisms. Autoantibodies and immune complexes may be present in the serum, and target organs may undergo vasculitic destruction or become infiltrated with lymphocytes and plasma cells. Recognition of histocompatibility antigens and Ia antigens on lymphocyte and macrophage membranes is an important regulatory mechanism allowing the immune system to react against viral and other foreign antigens. The immune system is exquisitely regulated. In part, this regulation is dependent upon specific immune response genes which are located within the major histocompatibility complex. Genetic factors influence specialized subpopulations of T-lymphocytes, which function either to suppress or enhance immune responses. Recognition of idiotypic receptors on lymphocyte membranes by antibody or by other lymphocytes can also result in either suppression or priming of an immune response. Since these regulatory mechanisms play an important role in immunologic control, one must look to some derangement in their function to explain the existence of autoimmunity and autoimmune disorders.
Keywords
Systemic Lupus Erythematosus Spleen Cell Tritiated Thymidine Rheumatoid Arth Autoimmune MousePreview
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