Depletion of Vbeta4 TCR does not induce resistance to EAN--further evidence for diversity of TCR usage.
In EAN, TCR variable (V) gene usage is still controversial. A dominant usage of a TCR Vbeta4-associated idiotype has been reported. To assess the role of TCR Vbeta4 positive T-cells in susceptibility to induction of EAN, we suppressed the selection of this idiotype by neonatal treatment of Lewis rats with anti-TCR Vbeta4 monoclonal antibody (mAb). Anti-Vbeta4 treatment had no effect on development of clinical disease after immunization with the neuritogenic P2-peptide amino acids (aa) 53-78. Furthermore, lymph node cells from anti-Vbeta4 treated animals isolated after immunization with P2-peptide did not exhibit a reduced proliferative response towards whole P2-protein or P2-peptide. Our results indicate that T-cells utilizing other TCR V chains can functionally replace the neuritogenic cell population, which is dominant in stable T-cell lines.
Stienekemeier
M
M
Department of Neurology, Clinical Research Group for Multiple Sclerosis and Neuroimmunology, Julius-Maximilians Universität, Würzburg, Germany.
Weishaupt
A
A
Gold
R
R
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D002478:Cells, Cultured; D005260:Female; D007114:Immunization; D008212:Lymphocyte Depletion; D009444:Neuritis, Autoimmune, Experimental / Q000209:etiology*; D051381:Rats; D011917:Rats, Inbred Lew; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000502:physiology*
D000911:Antibodies, Monoclonal; D016693:Receptors, Antigen, T-Cell, alpha-beta