Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 101, Issue 43, Pages 15434-15439Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0404444101
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Funding
- NIAID NIH HHS [R01 AI044880, R01 AI44880] Funding Source: Medline
- NINDS NIH HHS [R01 NS030843, P01 NS038037, P01 NS38037, R01 NS046414, R01 NS30843, NS 046414] Funding Source: Medline
- PHS HHS [P01 A145757] Funding Source: Medline
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SJL mice are highly susceptible to experimental autoimmune encephalomyelitis (EAE) induced with myelin proteolipid protein (PLP) peptide 139-151, whereas H-2 congenic B10.S mice are resistant. Immunodominance and susceptibility to EAE are associated with a high precursor frequency of PLP 139-151-specific T cells in the naive repertoire of SA mice. To understand the mechanism of EAE resistance in B10.S mice, we determined the precursor frequency of PLP 139-151-reactive T cells in both strains by using IA(s)/PLP 139-151 tetramers. SJL and B10.S mice had similar frequencies of tetra mer-reactive T cells in the naive peripheral repertoire. However, in SJL mice, the majority of PLP 139-151 tetramer-positive cells were in the CD4(+)CD25(-) population, whereas there were more tetra mer-positive cells in the CD4(+)CD25(+) population of B10.S mice. Depletion of CD4(+)CD25(+) cells in vivo facilitated the expansion of PLP 139-151-reactive cells with production of T helper 1 cytokines in EAE-resistant B10.S mice. Furthermore, anti-CD25 Ab treatment before immunization resulted in EAE induction in these otherwise resistant mice. These data indicate an important role for autoantigen-specific CD4(+)CD25(+) cells in genetic resistance to autoimmunity.
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