Genetic control of experimental autoimmune myasthenia gravis in mice. III. Ia molecules mediate cellular immune responsiveness to acetylcholine receptors

P. Christadoss, V. A. Lennon, C. J. Krco, C. S. David

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

When MHC congenic and recombinant mice are inoculated with Torpedo acetylcholine receptors (AChR) with adjuvants, the magnitude of autoantibody responses to muscle AChR and the defect of neuromuscular transmission closely parallel in vitro lymphocyte proliferative responses to Torpedo AChR. All of these responses are controlled by gene(s) at the I-A subregion of the H-2 complex. Data presented in this report confirm in backcross mice that T lymphocyte proliferative responses to AChR are controlled by a Mendelian dominant gene linked to H-2, at the I-A subregion. Lymphocyte responses were eliminated by blocking Ia antigens on lymph node cell surfaces with appropriate anti-I-A allo-antisera and by removal of adherent cells. A spontaneous mutation at the I-A subregion in the B6 strain, which resulted in structural alteration of the Aβ chain of Ia, converted high responsiveness to AChR to a state of low responsiveness. These data implicate a macrophage-associated Ia molecule in induction of autoimmune responses to AChR, probably in the presentation of AChR to helper T lymphocytes that thereby help B lymphocytes to differentiate into anti-AChR antibody-forming cells.

Original languageEnglish (US)
Pages (from-to)1141-1144
Number of pages4
JournalJournal of Immunology
Volume128
Issue number3
StatePublished - 1982
Externally publishedYes

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Autoimmune Experimental Myasthenia Gravis
Cholinergic Receptors
Torpedo
Lymphocytes
Congenic Mice
Dominant Genes
Histocompatibility Antigens Class II
Helper-Inducer T-Lymphocytes
Autoimmunity
Autoantibodies
Immune Sera
B-Lymphocytes
Lymph Nodes
Macrophages
T-Lymphocytes
Muscles
Mutation

ASJC Scopus subject areas

  • Immunology

Cite this

Genetic control of experimental autoimmune myasthenia gravis in mice. III. Ia molecules mediate cellular immune responsiveness to acetylcholine receptors. / Christadoss, P.; Lennon, V. A.; Krco, C. J.; David, C. S.

In: Journal of Immunology, Vol. 128, No. 3, 1982, p. 1141-1144.

Research output: Contribution to journalArticle

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AU - Lennon, V. A.

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AU - David, C. S.

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AB - When MHC congenic and recombinant mice are inoculated with Torpedo acetylcholine receptors (AChR) with adjuvants, the magnitude of autoantibody responses to muscle AChR and the defect of neuromuscular transmission closely parallel in vitro lymphocyte proliferative responses to Torpedo AChR. All of these responses are controlled by gene(s) at the I-A subregion of the H-2 complex. Data presented in this report confirm in backcross mice that T lymphocyte proliferative responses to AChR are controlled by a Mendelian dominant gene linked to H-2, at the I-A subregion. Lymphocyte responses were eliminated by blocking Ia antigens on lymph node cell surfaces with appropriate anti-I-A allo-antisera and by removal of adherent cells. A spontaneous mutation at the I-A subregion in the B6 strain, which resulted in structural alteration of the Aβ chain of Ia, converted high responsiveness to AChR to a state of low responsiveness. These data implicate a macrophage-associated Ia molecule in induction of autoimmune responses to AChR, probably in the presentation of AChR to helper T lymphocytes that thereby help B lymphocytes to differentiate into anti-AChR antibody-forming cells.

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