期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 44, 期 7, 页码 2013-2024出版社
WILEY
DOI: 10.1002/eji.201343680
关键词
Cytokine; Human; IL-17; M. tuberculosis
类别
资金
- National Institutes of Health [AI085135, AI094692]
- Cain Foundation for Infectious Disease Research
- Center for Pulmonary and Infectious Disease Control, Department of Biotechnology, GoI, India [BT/01/COE/07/02]
- Potts Memorial Foundation
- Council of Scientific and Industrial Research, GoI, India [09/0980(001)09/EMR-1]
We studied the factors that regulate IL-23 receptor expression and IL-17 production in human tuberculosis infection. Mycobacterium tuberculosis (M. tb)-stimulated CD4(+) T cells from tuberculosis patients secreted less IL-17 than did CD4(+) T cells from healthy tuberculin reactors (PPD+). M. tb-cultured monocytes from tuberculosis patients and PPD+ donors expressed equal amounts of IL-23p19 mRNA and protein, suggesting that reduced IL-23 production is not responsible for decreased IL-17 production by tuberculosis patients. Freshly isolated and M. tb-stimulated CD4(+) T cells from tuberculosis patients had reduced IL-23 receptor and phosphorylated STAT3 (pSTAT3) expression, compared with cells from PPD+ donors. STAT3 siRNA reduced IL-23 receptor expression and IL-17 production by CD4(+) T cells from PPD+ donors. Tuberculosis patients had increased numbers of PD-1(+) T cells compared with healthy PPD+ individuals. Anti-PD-1 antibody enhanced pSTAT3 and IL-23R expression and IL-17 production by M. tb-cultured CD4(+) T cells of tuberculosis patients. Anti-tuberculosis therapy decreased PD-1 expression, increased IL-17 and IFN-gamma production and pSTAT3 and IL-23R expression. These findings demonstrate that increased PD-1 expression and decreased pSTAT3 expression reduce IL-23 receptor expression and IL-17 production by CD4(+) T cells of tuberculosis patients.
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