TLR2型
生物
CD8型
脾脏
细胞因子
结核分枝杆菌
细胞毒性T细胞
体内
T细胞
免疫学
微生物学
免疫系统
肺结核
先天免疫系统
体外
医学
病理
生物化学
生物技术
作者
Scott M. Reba,Qing Li,Sophia Onwuzulike,Nancy Nagy,Shane Fletcher,Kyle Parker,Rachel J Shaw,Katharine Umphred‐Wilson,Supriya Shukla,Clifford V. Harding,W. Henry Boom,Roxana E. Rojas
标识
DOI:10.1002/eji.202350715
摘要
Abstract Although a role for TLR2 on T cells has been indicated in prior studies, in vivo stimulation of TLR2 on T cells by Mtb and its impact on Mtb infection has not been tested. Furthermore, it is not known if the enhanced susceptibility to Mtb of Tlr2 gene knockout mice is due to its role in macrophages, T cells, or both. To address TLR2 on T cells, we generated Tlr2 fl/fl xCd4 cre/cre mice, which lack expression of TLR2 on both CD4 and CD8 T cells, to study the in vivo role of TLR2 on T cells after aerosol infection with virulent Mtb . Deletion of TLR2 in CD4+ and CD8+ T cells reduces their ability to be co‐stimulated by TLR2 ligands for cytokine production. These include both pro‐ (IFN‐γ, TNF‐α) and anti‐inflammatory cytokines (IL‐10). Deletion of TLR2 in T cells affected control of Mtb in the lungs and spleens of infected mice. This suggests that T‐cell co‐stimulation by mycobacterial TLR2 ligands in vivo contributes to the control of Mtb infection in the lung and spleen.
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