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Uemura Y, Senju S, Fujii S, et al. Specificity, degeneracy, and molecular mimicry in antigen recognition by HLA-Class II restricted T cell receptors: implications for clinical medicine. Mod Rheumatol. 2003;13(3):205-14doi: 10.3109/s10165-003-0225-x.
Uemura, Y., Senju, S., Fujii, S., Iwai, L. K., Maenaka, K., Tabata, H., Kanai, T., Chen, Y. Z., & Nishimura, Y. (2003). Specificity, degeneracy, and molecular mimicry in antigen recognition by HLA-Class II restricted T cell receptors: implications for clinical medicine. Modern rheumatology, 13(3), 205-14. https://doi.org/10.3109/s10165-003-0225-x
Uemura, Yasushi, et al. "Specificity, degeneracy, and molecular mimicry in antigen recognition by HLA-Class II restricted T cell receptors: implications for clinical medicine." Modern rheumatology vol. 13,3 (2003): 205-14. doi: https://doi.org/10.3109/s10165-003-0225-x
Uemura Y, Senju S, Fujii S, Iwai LK, Maenaka K, Tabata H, Kanai T, Chen YZ, Nishimura Y. Specificity, degeneracy, and molecular mimicry in antigen recognition by HLA-Class II restricted T cell receptors: implications for clinical medicine. Mod Rheumatol. 2003 Sep;13(3):205-14. doi: 10.3109/s10165-003-0225-x. PMID: 24387206.
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Mod Rheumatol. 2003 Sep;13(3):205-14. doi: 10.3109/s10165-003-0225-x.

Specificity, degeneracy, and molecular mimicry in antigen recognition by HLA-Class II restricted T cell receptors: implications for clinical medicine.

Modern rheumatology

Yasushi Uemura, Satoru Senju, Shinji Fujii, Leo Kei Iwai, Katsumi Maenaka, Hiroki Tabata, Takayuki Kanai, Yu-Zhen Chen, Yasuharu Nishimura

Affiliations

  1. Department of Immunogenetics, Graduate School of Medical Sciences, Kumamoto University , 1-1-1 Honjo, Kumamoto 860-8556 , Japan.

PMID: 24387206 DOI: 10.3109/s10165-003-0225-x

Abstract

Abstract In humans, increased susceptibility to specific autoimmune diseases is closely associated with specific HLA-class II alleles. CD4(+) T cells that recognize short self-peptides in the context of HLA-class II molecules via their T cell receptor (TCR) are considered to mediate the central role of pathogenesis in autoimmunity. Although both self- and nonself-peptides are presented on HLA-class II molecules under physiological conditions, several mechanisms exist to avoid the T cell response to the self-peptide/HLA-class II complex. One of the mechanisms that account for the breakdown in immune tolerance is cross-recognition by TCR between a pathogen-derived antigen and a host antigen (molecular mimicry theory). Epidemiological studies have indicated that a number of autoimmune diseases are developed or exacerbated after infections. Therefore, elucidating the recognition nature of HLA-class II restricted TCR in detail is necessary in order to understand disease processes. A large body of evidence indicates that T cell recognition is highly degenerate, and many different peptides can activate an individual T cell. Degeneracy of TCR recognition also can appear in various physiological outcomes, ranging from full activation to strong antagonism. Here, we review the clinical implications of our findings on T cell recognition, as well as a new direction of future applications for analyses in molecular mimicry. We also describe the latest developments in methods of mapping TCR epitopes for CD4(+) T cells using a peptide epitope expression library generated in the class II-associated invariant chain peptide substituted invariant chain gene format.

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