B7-1 costimulatory molecule is critical for the development of experimental autoimmune myasthenia gravis

Mathilde A. Poussin, Erdem Tüzün, Elzbieta Goluszko, Benjamin G. Scott, Huan Yang, Juan U. Franco, Premkumar Christadoss

Research output: Contribution to journalArticle

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Abstract

Following immunization with acetylcholine receptor (AChR), MHC class II-restricted, AChR-specific CD4 cell activation is critical for the development of experimental autoimmune myasthenia gravis (EAMG) in C57BL/6 mice. To study the contributions of B7-1 and B7-2 costimulatory molecules in EAMG, B7-1, B7-2, and B7-1/B7-2 gene knockout (KO) mice were immunized with Torpedo AChR in CFA. Compared with wild-type C57BL6 mice, B7-1 and B7-1/2 KO mice were resistant to EAMG development. B7-1 KO mice had reduced anti-AChR Ab compared with C57BL/6 mice. However, neither B7-1 nor B7-2 gene disruption impaired AChR-induced or dominant α146-162 peptide-induced in vitro lymphoproliferative responses. Blocking of the B7-1 or B7-2 molecule by specific mAbs in vivo led to a reduction in the AChR-specific lymphocyte response, and the reduction was more pronounced in mice treated with anti-B7-2 Ab. The findings implicate B7-1 molecules as having a critical role in the induction of EAMG, and the resistance of B7-1 KO mice is associated with suppressed humoral, rather than suppressed AChR-specific, T cell responses. The data also point to B7-2 molecules as being the dominant costimulatory molecules required for AChR-induced lymphocyte proliferation.

Original languageEnglish (US)
Pages (from-to)4389-4396
Number of pages8
JournalJournal of Immunology
Volume170
Issue number8
StatePublished - Apr 15 2003

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CD80 Antigens
Autoimmune Experimental Myasthenia Gravis
Cholinergic Receptors
B7 Antigens
Knockout Mice
Inbred C57BL Mouse
CD86 Antigens
Lymphocytes
Torpedo
Gene Knockout Techniques
Immunization
T-Lymphocytes
Peptides

ASJC Scopus subject areas

  • Immunology

Cite this

Poussin, M. A., Tüzün, E., Goluszko, E., Scott, B. G., Yang, H., Franco, J. U., & Christadoss, P. (2003). B7-1 costimulatory molecule is critical for the development of experimental autoimmune myasthenia gravis. Journal of Immunology, 170(8), 4389-4396.

B7-1 costimulatory molecule is critical for the development of experimental autoimmune myasthenia gravis. / Poussin, Mathilde A.; Tüzün, Erdem; Goluszko, Elzbieta; Scott, Benjamin G.; Yang, Huan; Franco, Juan U.; Christadoss, Premkumar.

In: Journal of Immunology, Vol. 170, No. 8, 15.04.2003, p. 4389-4396.

Research output: Contribution to journalArticle

Poussin, MA, Tüzün, E, Goluszko, E, Scott, BG, Yang, H, Franco, JU & Christadoss, P 2003, 'B7-1 costimulatory molecule is critical for the development of experimental autoimmune myasthenia gravis', Journal of Immunology, vol. 170, no. 8, pp. 4389-4396.
Poussin MA, Tüzün E, Goluszko E, Scott BG, Yang H, Franco JU et al. B7-1 costimulatory molecule is critical for the development of experimental autoimmune myasthenia gravis. Journal of Immunology. 2003 Apr 15;170(8):4389-4396.
Poussin, Mathilde A. ; Tüzün, Erdem ; Goluszko, Elzbieta ; Scott, Benjamin G. ; Yang, Huan ; Franco, Juan U. ; Christadoss, Premkumar. / B7-1 costimulatory molecule is critical for the development of experimental autoimmune myasthenia gravis. In: Journal of Immunology. 2003 ; Vol. 170, No. 8. pp. 4389-4396.
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