Premium
Cell‐mediated immunity in idiopathic polyneuritis
Author(s) -
Iqbal Aleem,
Oger Joel J.F.,
Arnason Barry G. W.
Publication year - 1981
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410090711
Subject(s) - immunology , pathogenesis , medicine , antibody , antecedent (behavioral psychology) , disease , immunity , humoral immunity , neuritis , cell mediated immunity , plasmapheresis , immune system , pathology , psychology , developmental psychology , psychiatry
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.