CD4+CD25+ T(R) cells suppress innate immune pathology through cytokine-dependent mechanisms.

CD4+CD25+ T(R) cells suppress innate immune pathology through cytokine-dependent mechanisms.
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CD4+ CD25+ T(R)细胞通过细胞因子依赖性机制抑制先天的免疫病理。

DOI:
10.1084/jem.20021345
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发表时间:
2003-01-06
影响因子:
15.3
通讯作者:
Powrie, F
Powrie, F
中科院分区:
医学1区
文献类型:
--
作者:
Maloy, KJ;Salaun, L;Cahill, R;Dougan, G;Saunders, NJ;Powrie, F

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CD 4 + CD 25+调节性T(TR)细胞可以抑制多种自身免疫性和炎症性疾病,但它们抑制体内免疫应答的确切机制仍未解决。在这里,我们使用肝螺杆菌感染的T细胞重组激活基因(RAG)−/−小鼠作为模型,研究CD 4 + CD 25 + TR细胞抑制细菌引发的肠道炎症的能力。H.肝吸虫感染引起T细胞介导的和T细胞非依赖性的肠道炎症,这两种炎症都被过继转移的CD 4 + CD 25 + TR细胞抑制。T细胞非依赖性病理学伴随着先天免疫系统的激活,其也被CD 4 + CD 25 + TR细胞抑制。先天免疫病理学的抑制依赖于T细胞来源的白细胞介素10,也依赖于转化生长因子β的产生。因此,CD 4 + CD 25 + TR细胞不仅抑制适应性T细胞应答,而且还能够控制由先天免疫机制介导的病理。
CD4+CD25+ regulatory T (TR) cells can inhibit a variety of autoimmune and inflammatory diseases, but the precise mechanisms by which they suppress immune responses in vivo remain unresolved. Here, we have used Helicobacter hepaticus infection of T cell–reconstituted recombination-activating gene (RAG)−/− mice as a model to study the ability of CD4+CD25+ TR cells to inhibit bacterially triggered intestinal inflammation. H. hepaticus infection elicited both T cell-mediated and T cell–independent intestinal inflammation, both of which were inhibited by adoptively transferred CD4+CD25+ TR cells. T cell–independent pathology was accompanied by activation of the innate immune system that was also inhibited by CD4+CD25+ TR cells. Suppression of innate immune pathology was dependent on T cell–derived interleukin 10 and also on the production of transforming growth factor β. Thus, CD4+CD25+ TR cells do not only suppress adaptive T cell responses, but are also able to control pathology mediated by innate immune mechanisms.
DOI: 10.1093/intimm/5.11.1461
发表时间: 1993-11-01
影响因子: 4.4
作者:
POWRIE, F;LEACH, MW;COFFMAN, RL
通讯作者: COFFMAN, RL
DOI: 10.1128/iai.69.7.4232-4241.2001
发表时间: 2001-07-01
影响因子: 3.1
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发表时间: 1999-10-04
影响因子: 15.3
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DOI: 10.1128/iai.69.9.5914-5920.2001
发表时间: 2001-09-01
影响因子: 3.1
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通讯作者: Riley, LK
DOI: 10.1016/1074-7613(94)90045-0
发表时间: 1994-10-01
期刊: IMMUNITY
影响因子: 32.4
作者:
POWRIE, F;LEACH, MW;COFFMAN, RL
通讯作者: COFFMAN, RL