Interleukin-10 promotes Mycobacterium tuberculosis disease progression in CBA/J mice

被引:165
作者
Beamer, Gillian L. [1 ,2 ]
Flaherty, David K. [4 ]
Assogba, Barnabe D. [1 ]
Stromberg, Paul [2 ]
Gonzalez-Juarrero, Mercedes [5 ]
Malefyt, Rene de Waal [6 ]
Vesosky, Bridget [1 ]
Turner, Joanne [1 ,3 ]
机构
[1] Ohio State Univ, Ctr Microbial Interface Biol, Columbus, OH 43210 USA
[2] Ohio State Univ, Dept Vet Biosci, Columbus, OH 43210 USA
[3] Ohio State Univ, Dept Internal Med, Div Infect Dis, Columbus, OH 43210 USA
[4] Vanderbilt Univ, Med Ctr, Nashville, TN 37212 USA
[5] Colorado State Univ, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA
[6] Schering Plough Biopharma, Dept Immunol, Palo Alto, CA 94304 USA
基金
美国国家卫生研究院;
关键词
D O I
10.4049/jimmunol.181.8.5545
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 is a potent immunomodulatory cytokine that affects innate and acquired immune responses. The immunological consequences of IL-10 production during pulmonary tuberculosis (TB) are currently unknown, although IL-10 has been implicated in reactivation TB in humans and with TB disease in mice. Using Mycobacterium tuberculosis-susceptible CBA/J mice, we show that blocking the action of IL-10 in vivo during chronic infection stabilized the pulmonary bacterial load and improved survival. Furthermore, this beneficial outcome was highly associated with the recruitment of T cells to the lungs and enhanced T cell IFN-gamma production. Our results indicate that IL-10 promotes TB disease progression. These findings have important diagnostic and/or therapeutic implications for the prevention of reactivation TB in humans.
引用
收藏
页码:5545 / 5550
页数:6
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