International Immunology, Vol 9, 281-290, Copyright © 1997 by Oxford University Press
MH Wauben, M van der Kraan, MC Grosfeld-Stulemeyer and I Joosten
The Lewis rat, an inbred rat strain susceptible to several well-
characterized experimental autoimmune diseases, provides a good model to
study peptide-mediated immunotherapy. Peptide immunotherapy focussing on
the modulation of T cell responses by interfering with TCR- peptide-MHC
complex formation requires the elucidation of the molecular basis of
TCR-peptide-MHC interactions for an efficient design of modulatory
peptides. In the Lewis rat most autoimmune-associated CD4+ T cell responses
are MHC class II RT1.BL restricted. In this study, the characteristics of
RT1.BL-peptide interactions were explored. A series of substitution analogs
of two Lewis rat T cell epitopes was examined in a direct peptide-MHC
binding assay on isolated RT1.BL molecules. Furthermore, other
autoimmune-related as well as non-disease-related T cell epitopes were
tested in the binding assay. This has led to the definition of an extended
RT1.BL-peptide binding motif. The RT1.BL- peptide binding motif established
in this study is the first described rat MHC-peptide binding motif based on
direct MHC-peptide binding experiments. To predict good or intermediate
RT1.BL binding peptides, T cell epitope search profiles were deduced from
this motif. The motif and search profiles will greatly facilitate the
prediction of modulatory peptides based on autoimmune-associated T cell
epitopes and the identification of target structures in experimental
autoimmune diseases in Lewis rats.
ARTICLES
Definition of an extended MHC class II-peptide binding motif for the autoimmune disease-associated Lewis rat RT1.BL molecule
Institute of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, The Netherlands.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
K. L. de Graaf, S. Barth, M. M. Herrmann, M. K. Storch, C. Otto, T. Olsson, A. Melms, G. Jung, K.-H. Wiesmuller, and R. Weissert MHC Class II Isotype- and Allele-Specific Attenuation of Experimental Autoimmune Encephalomyelitis J. Immunol., August 15, 2004; 173(4): 2792 - 2802. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. G. A. Paul, R. van der Zee, L. S. Taams, and W. van Eden A self-hsp60 peptide acts as a partial agonist inducing expression of B7-2 on mycobacterial hsp60-specific T cells: a possible mechanism for inhibitory T cell regulation of adjuvant arthritis? Int. Immunol., July 1, 2000; 12(7): 1041 - 1050. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. Wendling, L. Paul, R. van der Zee, B. Prakken, M. Singh, and W. van Eden A Conserved Mycobacterial Heat Shock Protein (hsp) 70 Sequence Prevents Adjuvant Arthritis upon Nasal Administration and Induces IL-10-Producing T Cells That Cross-React with the Mammalian Self-hsp70 Homologue J. Immunol., March 1, 2000; 164(5): 2711 - 2717. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. L. de Graaf, R. Weissert, P. Kjellen, R. Holmdahl, and T. Olsson Allelic variations in rat MHC class II binding of myelin basic protein peptides correlate with encephalitogenicity Int. Immunol., December 1, 1999; 11(12): 1981 - 1988. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. B. Smeltz, M. H. M. Wauben, N. A. Wolf, and R. H. Swanborg Critical Requirement for Aspartic Acid at Position 82 of Myelin Basic Protein 73-86 for Recruitment of V{beta}8.2+ T Cells and Encephalitogenicity in the Lewis Rat J. Immunol., January 15, 1999; 162(2): 829 - 836. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Weissert, A. Svenningsson, A. Lobell, K. L. de Graaf, R. Andersson, and T. Olsson Molecular and Genetic Requirements for Preferential Recruitment of TCRBV8S2+ T Cells in Lewis Rat Experimental Autoimmune Encephalomyelitis J. Immunol., January 15, 1998; 160(2): 681 - 690. [Abstract] [Full Text] [PDF] |
||||

