Depletion of Vbeta4 TCR does not induce resistance to EAN--further evidence for diversity of TCR usage |
| |
Authors: | Stienekemeier M Weishaupt A Gold R |
| |
Affiliation: | Department of Neurology, Clinical Research Group for Multiple Sclerosis and Neuroimmunology, Julius-Maximilians Universit?t, Würzburg, Germany. |
| |
Abstract: | 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. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|