International Immunology Advance Access originally published online on March 29, 2004
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International Immunology, Vol. 16, No. 5, pp. 655-663,
May 2004
© 2004 Japanese Society for Immunology
Contrasting contributions of complementarity-determining region 2 and hypervariable region 4 of rat BV8S2+ (Vß8.2) TCR to the recognition of myelin basic protein and different types of bacterial superantigens
1 Institute for Virology and Immunobiology, University of Würzburg, Würzburg 97078, Germany 2 Institute of Virology, University of Dresden, Dresden 01307, Germany 3 Department of Microbiology and Immunology, Tokyo Women’s Medical University School of Medicine, Tokyo 162-8666, Japan 4 Institute of Immunology, University Hospital, RWTH-Aachen, Aachen 52074, Germany 5 Institute of Infectious Diseases and Immunology, University of Utrecht, Utrecht 3584 CL, The Netherlands
The first two authors contributed equally to this work; this work is dedicated to the memory of C. P. M. Broeren.
Correspondence to: T. Herrmann, Institute for Virology and Immunobiology, Versbacherstrasse 7, Würzburg 97078, Germany. E-mail: herrmann-t{at}vim.uni-wuerzburg.de
Transmitting editor: H. R. MacDonald
In experimental autoimmune encephalomyelitis (EAE) of LEW rats, BV8S2+ (Vß8.2) T cells dominate the RT1Bl-restricted response to guinea pig myelin basic protein (gpMBP), and respond to the superantigens (SAg) Staphylococcus enterotoxin C1 (SEC1), Mycoplasma arthritidis SAg (MAS) and Yersinia pseudotuberculosis mitogen (YPM). T cells expressing the closely related BV8S4 differ from BV8S2 T cells in their response to gpMBP, and the SAg SEC1 and MAS, but not in their response to YPM. The functional differences between BV8S2 and BV8S4, which vary in complementarity-determining/hypervariable region 4 (CDR4/HV4) and CDR2, were analyzed by cloning and mutating a TCR with features typical for gpMBP-specific BV8S2+ TCR. The wild-type BV8S2 receptor and the BV8S4-like CDR2 + 4ß double mutant of BV8S2 showed the same differences in ligand specificity as polyclonal BV8S2+ and BV8S4+ lymphocyte populations. The CDR2ß mutant lost its reactivity for SEC1 and gpMBP68–88, but the CDR4/HV4ß mutation abolished only activation by SEC1. Thus, CDR2 and HV4 contribute not only differently to recognition of peptide antigens, but also to recognition of different types of bacterial SAg.
Keywords: autoimmunity, experimental autoimmune encephalomyelitis, LEW, T cell repertoire
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