In vivo preferential usage of TCR V beta 8 in Torpedo acetylcholine receptor immune response in the murine experimental model of myasthenia gravis

• Published in: Journal of neuroimmunology 1995-05, Vol.58 (2), p.191-200
• Main Authors: Aimé-Sempé, C, Cohen-Kaminsky, S, Bruand, C, Klingel-Schmitt, I, Truffault, F, Berrih-Aknin, S
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Monoclonal - immunology; Cell Division; Immunity, Cellular; Lymph Nodes - cytology; Male; Mice; Mice, Inbred C57BL; Myasthenia Gravis - immunology; Myasthenia Gravis - metabolism; Myasthenia Gravis - pathology; Receptors, Antigen, T-Cell, alpha-beta - immunology; Receptors, Antigen, T-Cell, alpha-beta - metabolism; Receptors, Cholinergic - immunology; Torpedo
• ISSN: 0165-5728
• DOI: 10.1016/0165-5728(95)00017-V

The aim of our study was to determine the T cell receptor (TCR) V beta gene usage involved in the T cell response to Torpedo AChR in C57BL/6 mice. The specific proliferation towards AChR was found to be blocked by anti-V beta 8.1,2,3 and to a lesser extent by anti-V beta 5 mAbs, but not by the other antibodies used (anti-V beta 2, V beta 6, V beta 9). In addition, a significant expansion of CD4+ V beta 8+ cells was observed when lymph node cells from these primed mice were stimulated in vitro with purified AChR. Involvement of V beta 8 subfamilies was also explored in vivo. After 7 days of treatment, there was a striking inhibition of the proliferative response of cells from anti-V beta 8.1,2,3-treated mice and a moderate inhibition when using anti-V beta 8.1,2 and anti-V beta 8.2 antibodies. Thus our in vitro and in vivo analysis indicate that in C57Bl/6 mice, T cell response to AChR is restricted to few V beta TCR, mostly belonging to the V beta 8 sub-families.