Neonatal tolerance to an immunodominant T cell reactivity does not confer resistance to EAMG induction in Lewis rats.
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| Abstract |
The overall goal of this study was to determine, during induction of experimental autoimmune myasthenia gravis (EAMG) in Lewis rats, the relative importance of acetylcholine receptor (AChR)-reactive helper T cells associated with one particular immunodominant fine specificity. Thus, experiments presented below were designed to evaluate the immunopathological role played by helper T cells with reactivity against the AChR alpha subunit region associated with amino acid residues 100-116 (i.e., alpha 100-116); in particular, the relationship between T cell reactivity with this specificity and disease induction was assessed. In order to examine the importance of this T cell reactivity, Lewis rat neonates were made T cell tolerant to a synthetic peptide alpha 100-116 and subsequently evaluated for anti-AChR antibody production and resulting neuromuscular dysfunction. Results indicated that although T cell reactivity against the alpha 100-116 peptide could be effectively removed from the Lewis T cell repertoire, tolerized Lewis rats immunized with AChR could undergo an active anti-AChR antibody response that produced symptoms of EAMG. Thus, other AChR T cell reactivities appeared capable of providing adequate help to B cells leading to production of anti-AChR antibodies with pathogenic potential.
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| Authors | T E Zoda, K Brandon, K A Krolick |
| Journal | Journal of neuroimmunology (J Neuroimmunol) Vol. 57 Issue 1-2 Pg. 35-44 (Mar 1995) ISSN: 0165-5728 [Print] Netherlands |
| PMID | 7535790 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.) |
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