title: Auto-immunity and prostaglandins.
abstract: Several auto-immune diseases have been described in human beings. Though the exact aetiological agent(s) is not known, clinical or subclinical viral infections and certain drugs are known to induce them. Hyperactivity of B-cells, possibly due to the loss of normal regulatory control by T-cells may account for the increased synthesis of auto-antibodies in these diseases. Prostaglandins (PGs) are known to regulate immune response and fibrous tissue formation. Deficiency of PGE1 and/or thromboxane A2 (TxA2) and excess PGE2 seem to activate B-cells and suppress T-Cell function and enhance fibrosis. Viruses are known to block the enzyme delta-6-desaturase necessary for PGE1 synthesis and thus depress cell-mediated immune response. Drugs known to cause autoimmune disorders also seem to block PGE1 and/or TxA2 synthesis and enhance PGE2 formation which may lead to excess auto-antibody formation. Drugs like colchicine known to enhance TxA2 formation and the  biological actions of PGE1 were found to be of benefit in Behcet's syndrome, vasculitis, amyloidosis, scleroderma and in controlling the auto-immune disease in adjuvant arthritis in rats, the renal disease in NZB/W mice and passively transferred vasculitis. Thus altered PG function may play a major role in auto-immunity.
mesh_terms: D000818:Animals; D000917:Antibody Formation; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D006680:HLA Antigens / Q000235:genetics; D006801:Humans; D051379:Mice; D011453:Prostaglandins / Q000276:immunology*; D051381:Rats; D013601:T-Lymphocytes / Q000276:immunology; D014777:Virus Diseases / Q000150:complications
chemical_list: D006680:HLA Antigens; D011453:Prostaglandins