期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 3, 页码 1962-1970出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.3.1962
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- FIC NIH HHS [D43TW007115, D43 TW007115] Funding Source: Medline
- Medical Research Council [MC_U117588499, U117588499(88499)] Funding Source: Medline
- NIAID NIH HHS [R01AI065653, R01 AI065653, N01AI70022] Funding Source: Medline
- Wellcome Trust [080929/Z/06/Z, 072070, 080929] Funding Source: Medline
- Medical Research Council [MC_U117588499] Funding Source: researchfish
- MRC [MC_U117588499] Funding Source: UKRI
- Wellcome Trust [080929/Z/06/Z] Funding Source: Wellcome Trust
We investigated whether the proinflammatory T cell cytokines IL-17 and IL-22 are induced by human mycobacterial infection. Remarkably, >20% of specific cytokine-producing CD4(+) T cells in peripheral blood of healthy, mycobacteria-exposed adults expressed IL-17 or IL-22. Specific IL-17- and IL-22-producing CD4(+) T cells were distinct from each other and from Th1 cytokine-producing cells. These cells had phenotypic characteristics of long-lived central memory cells. In patients with tuberculosis disease, peripheral blood frequencies of these cells were reduced, whereas bronchoalveolar lavage fluid contained higher levels of IL-22 protein compared with healthy controls. IL-17 was not detected in this fluid, which may be due to suppression by Th1 cytokines, as PBMC IL-17 production was inhibited by IFN-gamma in vitro. However, Th1 cytokines had no effect on IL-22 production in vitro. Our results imply that the magnitude and complexity of the anti-mycobacterial immune response have historically been underestimated. IL-17- and IL-22-producing CD4(+) T cells may play important roles in the human immune response to mycobacteria.
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