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Regulatory T Cells Modulate Staphylococcal Enterotoxin B-Induced Effector T-Cell Activation and Acceleration of Colitis

机译:调节性T细胞调节葡萄球菌肠毒素B诱导效应性T细胞活化和加速结肠炎。

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Oral administration of bacterial superantigen Staphylococcus aureus enterotoxin B (SEB) activates mucosal T cells but does not cause mucosal inflammation. We examined the effect of oral SEB on the development of mucosal inflammation in mice in the absence of regulatory T (Treg) cells. SCID mice were fed SEB 3 and 7 days after reconstitution with CD4+ CD45RBhigh or CD4+ CD45RBhigh plus CD4+ CD45RBlow T cells. Mice were sacrificed at different time points to examine changes in tissue damage and in T-cell phenotypes. Feeding SEB failed to produce any clinical effect on SCID mice reconstituted with CD4+ CD45RBhigh and CD4+ CD45RBlow T cells, but feeding SEB accelerated the development of colitis in SCID mice reconstituted with CD4+ CD45RBhigh T cells alone. The latter was associated with an increase in the number of CD4+ Vβ8+ T cells expressing CD69 and a significantly lower number of CD4+ CD25+ Foxp3+ T cells. These changes were not observed in SCID mice reconstituted with both CD45RBhigh and CD45RBlow T cells. In addition, SEB impaired the development of Treg cells in the SCID mice reconstituted with CD4+ CD45RBhigh T cells alone but had no direct effect on Treg cells. In the absence of Treg cells, feeding SEB induced activation of mucosal T cells and accelerated the development of colitis. This suggests that Treg cells prevent SEB-induced mucosal inflammation through modulation of SEB-induced T-cell activation.
机译:口服细菌超抗原金黄色葡萄球菌肠毒素B(SEB)可以激活粘膜T细胞,但不会引起粘膜炎症。我们检查了在没有调节性T(Treg)细胞的情况下口服SEB对小鼠粘膜炎症发展的影响。用CD4 + CD45RB high 或CD4 + CD45RB high plus重建后,SCID小鼠在SEB后第3天和第7天进食CD4 + CD45RB 低 T细胞。在不同时间点处死小鼠以检查组织损伤和T细胞表型的变化。 SEB喂养对用CD4 + CD45RB high 和CD4 + CD45RB low 重构的SCID小鼠没有产生任何临床效果T细胞,但饲喂SEB可以加速仅用CD4 + CD45RB 高 T细胞重构的SCID小鼠的结肠炎的发展。后者与表达CD69的CD4 + Vβ8 + T细胞数量增加和CD4 + CD25 < sup> + Foxp3 + T细胞。在用CD45RB high 和CD45RB low T细胞重构的SCID小鼠中未观察到这些变化。此外,SEB损害了单独用CD4 + CD45RB 高 T细胞重建的SCID小鼠中Treg细胞的发育,但对Treg细胞没有直接作用。在没有Treg细胞的情况下,喂食SEB会诱导粘膜T细胞活化并加速结肠炎的发展。这表明Treg细胞通过调节SEB诱导的T细胞活化来预防SEB诱导的粘膜炎症。

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