Cross-reactivity between peptide mimics of the immunodominant myelin proteolipid protein epitope PLP139-151:: Comparison of peptide priming in CFA vs. viral delivery

被引:7
作者
Ercolini, Anne M.
Croxford, J. Ludovic
Degutes, Mathew
Miller, Stephen D.
机构
[1] Northwestern Univ, Feinberg Sch Med, Dept Immunol Microbiol, Chicago, IL 60611 USA
[2] Northwestern Univ, Feinberg Sch Med, Interdept Immunobiol Ctr, Chicago, IL 60611 USA
关键词
multiple sclerosis; T cell; autoimmunity; EAE; molecular mimicry; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; T-CELLS; BASIC-PROTEIN; CHLAMYDIA-PNEUMONIAE; MOLECULAR MIMICRY; INFECTIONS; DISEASE; MECHANISMS;
D O I
10.1016/j.jneuroim.2007.02.002
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Epidemiological evidence suggests that pathogens may trigger the development of autoimmune diseases such as multiple sclerosis (MS). Pathogens may trigger disease via molecular mimicry, wherein T cells generated against foreign epitopes are also cross-reactive with self-epitopes. Five pathogen-derived molecular mimics of PLP139-151 (the immunodominant CD4(+) T cell myelin epitope in SJL mice) were previously identified. This study examines the degree of cross-reactivity between the different mimics, comparing mice primed with mimic peptide in CFA with mice infected with recombinant mimic-expressing viruses. The pattern of in vitro reactivity and ability to induce CNS disease differs between peptide priming and virus infection. (c) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:5 / 18
页数:14
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