期刊
JOURNAL OF IMMUNOLOGY
卷 182, 期 5, 页码 3032-3038出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0803402
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资金
- National Institute of Child Health and Human Development/National Institutes of Health [K08HD51584]
- March of Dimes Basil O'Conner Research Award
- Minnesota Vikings Children's Fund
- Minnesota Medical Foundation
The Foxp3-expressing subset of regulatory CD4(+) T cells have defined Ag specificity and play essential roles in maintaining peripheral tolerance by suppressing the activation of self-reactive T cells. Similarly, during chronic infection, pathogen-specific Foxp3-expressing CD4(+) T cells expand and actively suppress pathogen-specific effector T cells. Herein, we used MHC class II tetramers and Foxp3(gfp) knockin mice to track the kinetics and magnitude whereby pathogen-specific Foxp3(+)CD4(+) and Foxp3(-)CD4(+) cells are primed and expand after acute infection with recombinant Listeria monocytogenes (Lm) expressing the non-self-Ag 2W1S(52-68). We demonstrate that Lm infection selectively primes proliferation, expansion, and subsequent contraction of Lm-specific Foxp3(-) effector CD4(+) cells, while the numbers of Lm-specific Foxp3(+)CD4(+) regulatory cells remain essentially unchanged. In sharp contrast, purified 2W1S(52-68) peptide primes coordinated expansion of both Foxp3(+) regulatory and Foxp3(-) effector T cells with the same Ag specificity. Taken together, these results indicate selective priming and expansion of Foxp3(-) CD4 T cells is a distinguishing feature for acute bacterial infection. The Journal of Immunology, 2009, 182: 3032-3038.
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