Enhanced protection to Mycobacterium tuberculosis infection in IL-10-deficient mice is accompanied by early and enhanced Th1 responses in the lung

被引：200

作者：

Redford, Paul S. ^{[1
]}

Boonstra, Andre ^{[1
,2
]}

Read, Simon ^{[1
,3
]}

Pitt, Jonathan ^{[1
]}

Graham, Christine ^{[1
]}

Stavropoulos, Evangelos ^{[1
]}

Bancroft, Gregory J. ^{[4
]}

O'Garra, Anne ^{[1
]}

机构：

[1] Natl Inst Med Res, MRC, Div Immunoregulat, London NW7 1AA, England

[2] Erasmus MC, Dept Gastroenterol & Hepatol, Rotterdam, Netherlands

[3] Biopharmaceut Res Unit, Malov, Denmark

[4] London Sch Hyg & Trop Med, Immunol Unit, Dept Infect & Trop Dis, London WC1, England

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 2010年 / 40卷 / 08期

关键词：

Granulocytes; IL-10; IL-17; Mycobacterium tuberculosis; Th1; DRAINING LYMPH-NODES; T-CELL RESPONSES; IMMUNE-RESPONSES; PULMONARY TUBERCULOSIS; INTERFERON-GAMMA; IN-VIVO; ANTIMYCOBACTERIAL IMMUNITY; INTERLEUKIN-10; RECEPTOR; DENDRITIC CELLS; C57BL/6; MICE;

D O I：

10.1002/eji.201040433

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

IL-10 regulates the balance of an immune response between pathogen clearance and immunopathology. We show here that Mycobacterium tuberculosis (Mtb) infection in the absence of IL-10 (IL-10(-/-) mice) results in reduced bacterial loads in the lung. This reduction was preceded by an accelerated and enhanced IFN-gamma response in the lung, an increased influx of CD4(+) T cells into the lung, and enhanced production of chemokines and cytokines, including CXCL10 and IL-17, in both the lung and the serum. Neutralization of IL-17 affected neither the enhanced production of CXCL10 nor the accumulation of IFN-gamma-producing T cells in the lungs, but led to reduced numbers of granulocytes in the lung and reduced bacterial loads in the spleens of Mtb-infected mice. This suggests that IL-17 may contribute to dissemination of Mtb.

引用

页码：2200 / 2210

页数：11

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