期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 9, 页码 6361-6369出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.9.6361
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- NIAID NIH HHS [R01 AI067731-01, R01 AI 47171, R56 AI067731, R01 AI047171, R01 AI067731, AI 067731] Funding Source: Medline
Whether true memory T cells develop in the face of chronic infection such as tuberculosis remains controversial. To address this question, we studied CD8(+) T cells specific for the Mycobacterium tuberculosis ESAT6-related Ags TB10.3 and TB10.4. The shared epitope TB10.3/10.4(20-28) is presented by H-2 K-d, and 20-30% of the CD8(+) T cells in the lungs of chronically infected mice are specific for this Ag following respiratory infection with M. tuberculosis. These TB10.3/10.4(20-28)-specific CD8(+) T cells produce IFN-gamma and TNF and express CD107 on their cell surface, which indicates their likely role as CTL in vivo. Nearly all of the Ag-specific CD8(+) T cells in the lungs of chronically infected mice had a T effector cell phenotype based on their low expression of CD62L and CD45RB. In contrast, a population of TB10.3/10.4(20-28)-specific CD8(+) T cells was identified in the lymphoid organs that express high levels of CD62L and CD45RB. Antibiotic treatment to resolve the infection led to a contraction of the Ag-specific CD8(+) T cell population and was accompanied by an increase in the proportion of CD8(+) T cells with a central memory phenotype. Finally, challenge of memory-immune mice with M. tuberculosis was accompanied by significant expansion of TB10.3/10.4(20-28)-specific CD8(+) T cells, which suggests that these cells are in fact functional memory T cells.
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