gp130 on macrophages/granulocytes modulates inflammation during experimental tuberculosis.
gp130 on macrophages/granulocytes modulates inflammation during experimental tuberculosis.
复制标题
巨噬细胞/粒细胞上的 gp130 可调节实验性结核病期间的炎症。
DOI：
10.1016/j.ejcb.2010.10.010
复制
发表时间：
2011
影响因子：
6.6
通讯作者：
C. Hölscher
中科院分区：
文献类型：
--
作者：
J. Sodenkamp;J. Behrends;I. Förster;Werner Müller;S. Ehlers;C. Hölscher
gp130 是白细胞介素 (IL)-27 和 IL-6 等细胞因子的常见受体链。在实验性结核病 (TB) 期间，IL-27 会阻止最佳的抗分枝杆菌保护并限制慢性炎症的病理后遗症。 IL-27 的抗炎特性主要归因于其对辅助性 T (TH) 细胞的抑制作用。然而，由于 gp130 细胞因子也会抑制巨噬细胞的炎症免疫反应，因此 IL-27 也可能通过限制促炎细胞因子的分泌来调节炎症。为了明确 gp130 细胞因子对巨噬细胞的作用，在巨噬细胞/中性粒细胞特异性 gp130 缺陷 (LysMcregp130loxP/loxP) 小鼠中分析了实验性结核病的结果。在这些小鼠中，炎症细胞因子的诱导增强以及诱导型一氧化氮合酶 (NOS2) 和 LRG47 表达的增加与 TH17 免疫反应和基质金属蛋白酶 (MMP)-9 表达的大大增强有关。然而，Mtb 感染的 LysMcregp130loxP/loxP 小鼠中这种增强的炎症免疫反应与细菌负荷减少和/或病理加速无关。我们的研究揭示了 gp130 细胞因子对巨噬细胞/粒细胞的免疫调节功能，但这对于调节结核病的结果并不重要。
gp130 is a common receptor chain for cytokines such as interleukin (IL)-27 and IL-6. During experimental tuberculosis (TB), IL-27 prevents optimal antimycobacterial protection and limits the pathological sequelae of chronic inflammation. The anti-inflammatory properties of IL-27 have been attributed mainly to its suppressive effect on T helper (TH) cells. However, because gp130 cytokines also suppress the inflammatory immune response of macrophages, IL-27 may also regulate inflammation by limiting the secretion of pro-inflammatory cytokines. To specifically address the role of gp130 cytokines on macrophages, the outcome of experimental TB was analysed in macrophage/neutrophil-specific gp130-deficient (LysMcregp130loxP/loxP) mice. In these mice, the enhanced induction of inflammatory cytokines and increased expression of the inducible nitric oxide synthase (NOS2) and LRG47 was linked to a greatly augmented TH17 immune response and matrix metalloproteinase (MMP)-9 expression. However, this amplified inflammatory immune response in Mtb-infected LysMcregp130loxP/loxPmice was not associated with reduced bacterial loads and/or accelerated pathology. Our study revealed an immunoregulatory function of gp130 cytokines on macrophages/granulocytes, which is, however, not critical for modulating the outcome of TB.
Interleukin-11 抑制巨噬细胞 IL-12 的产生。
DOI：
--
发表时间：
1997
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Leng,SX;Elias,JA
通讯作者：
Elias,JA