Acquired resistance to experimental autoimmune encephalomyelitis is independent of V beta usage

被引：11

作者：

Johnson, BD ^{[1
]}

Nardella, JP ^{[1
]}

McConnell, TJ ^{[1
]}

Mannie, MD ^{[1
]}

机构：

[1] E CAROLINA UNIV,DEPT BIOL,GREENVILLE,NC 27858

来源：

CELLULAR IMMUNOLOGY | 1997年 / 179卷 / 01期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1006/cimm.1997.1143

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

In Lewis rats, activated encephalitogenic T-helper cells elicit a single bout of experimental autoimmune encephalomyelitis (EAE). Recovery from EAE is marked by reduced susceptibility to disease reinduction. The purpose of this study was to determine whether a dominant expression of VP gene segments by encephalitogenic T cells was required for development of recovery-associated resistance. Several polyclonal and monoclonal T cell lines were derived from Lewis rats sensitized with R72-86, a synthetic peptide representing the 72-to 86-amino-acid sequence of rat myelin basic protein (RMBP). The results revealed broad heterogeneity among encephalitogenic T cells specific for R72-86 in regard to V beta expression and CDR3 sequence. Encephalitogenic clones exclusively bearing either V beta 4 or V beta 10 TCR or polyclonal T cells bearing heterogeneous TCR transferred EAE to recipient rats and elicited resistance to EAE as revealed by subsequent challenge with guinea pig (GP)MBP in complete Freund's adjuvant (CFA). Nonpathogenic V beta 3(+) and V beta 8.6(+) clones specific for the 68-86 and 55-66 regions of MBP, respectively, did not elicit effective protection from EAE. These data indicate that induction of postrecovery resistance to EAE does not depend upon a particular V beta usage. (C) 1997 Academic Press.

引用

页码：55 / 65

页数：11

共 65 条

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