کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10962151 | 1102338 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Anti-tuberculosis treatment enhances the production of IL-22 through reducing the frequencies of regulatory B cell
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
میکروبیولوژی و بیوتکنولوژی کاربردی
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![عکس صفحه اول مقاله: Anti-tuberculosis treatment enhances the production of IL-22 through reducing the frequencies of regulatory B cell Anti-tuberculosis treatment enhances the production of IL-22 through reducing the frequencies of regulatory B cell](/preview/png/10962151.png)
چکیده انگلیسی
IL-22 has been suggested to play an important role in immune response against Mycobacterium tuberculosis infection. However, the exact role of IL-22 in human tuberculosis (TB) infection remains unclear and the regulatory mechanism of IL-22 response in human TB is unknown. In this study, we observed that successful anti-tuberculosis treatment induced an enhanced and sustained M. tuberculosis antigen-specific IL-22 response, correlated with the decrease of the frequencies of CD19+CD5+CD1d+ regulatory B cells. We also found that depletion of CD19+ B cells significantly enhanced M. tuberculosis antigen-specific IL-22 production by peripheral blood mononuclear cells. More importantly, we observed that purified CD19+ B cells, and more efficiently, CD19+CD5+CD1d+ regulatory B cells, suppressed IL-22 production. In summary, we showed here for the first time that effective anti-tuberculosis treatment restores M. tuberculosis antigen-specific IL-22 response through a novel mechanism by reducing the frequencies of CD19+CD5+CD1d+ regulatory B cells in human TB.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Tuberculosis - Volume 94, Issue 3, May 2014, Pages 238-244
Journal: Tuberculosis - Volume 94, Issue 3, May 2014, Pages 238-244
نویسندگان
Mingxia Zhang, Gucheng Zeng, Qianting Yang, Jieyun Zhang, Xiuyun Zhu, Qi Chen, Pichaimuthu Suthakaran, Ying Zhang, Qunyi Deng, Haiying Liu, Boping Zhou, Xinchun Chen,