Cell-mediated immunity in idiopathic polyneuritis.
The role of cell-mediated immunity (CMI) in the pathogenesis of idiopathic polyneuritis (IP) is discussed. Of significance has been the finding of a decreased suppressor T cell response in IP. This may provide an important common denominator linking the numerous antecedent events which trigger IP to the disease. The role of humoral immunity in IP and chronic relapsing inflammatory polyneuritis (CRIP) remains controversial, but has awakened renewed interest in view of recent reports of favorable response to plasmapheresis in IP and CRIP patients. P2 protein is an important neuritogenic factor in experimental allergic neuritis (EAN), but we failed to find antibody directed against P2 in either IP or CRIP even though anti-P2 antibody was regularly detected in EAN. Whether CMI response to P2 occurs in IP or CRIP remains controversial. We did not detect CMI response to P2 in IP or CRIP. It may be that the neuritogenic factor (or factors) in IP and CRIP remains to be found.
D000818:Animals; D000917:Antibody Formation; D001327:Autoimmune Diseases / Q000276:immunology; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology; D006801:Humans; D007105:Immune Complex Diseases / Q000276:immunology; D007111:Immunity, Cellular; D009185:Myelin Proteins / Q000276:immunology; D011115:Polyneuropathies / Q000276:immunology*; D011817:Rabbits; D051381:Rats; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D009185:Myelin Proteins