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首页> 外文期刊>International immunology. >IL-1beta, but not IL-1alpha, is required for antigen-specific T cell activation and the induction of local inflammation in the delayed-type hypersensitivity responses.
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IL-1beta, but not IL-1alpha, is required for antigen-specific T cell activation and the induction of local inflammation in the delayed-type hypersensitivity responses.

机译：抗原特异性T细胞激活和延迟型超敏反应中的局部炎症诱导需要IL-1beta，但不是IL-1alpha。

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摘要

As IL-1 expression is augmented in delayed-type hypersensitivity (DTH) responses, we analyzed the role of IL-1 in this response. DTH responses against methyl BSA (mBSA) were significantly suppressed in IL-1beta-deficient (IL-1beta-/-) and IL-1alpha/beta-/- mice, but not in IL-1alpha-/- mice. In contrast, responses in IL-1R antagonist-/- (IL-1Ra-/-) mice were exacerbated. Lymph node cells derived from mBSA-sensitized IL-1beta-/-, IL-1alpha/beta-/- and IL-1R type I (IL-1RI)-/- mice, but not from IL-1alpha-/- mice, exhibited reduced proliferative responses against mBSA, while these from IL-1Ra-/- mice demonstrated augmented responses. DTH responses in wild-type mice following adoptive transfer of CD4+ T cells from mBSA-sensitized IL-1alpha/beta-/- mice were also reduced, while those in mice given cells derived from IL-Ra-/- mice were increased. DTH responses in IL-1RI-/-, but not IL-1alpha/beta-/-, mice were reduced upon transplantation of mBSA-sensitized CD4+ T cells from wild-type mice. The recall response of mBSA-sensitized CD4+ T cells against mBSA decreased upon co-culture with dendritic cells (DCs) from IL-1RI-/- mice, while the responses were normal with DCs from IL-1alpha/beta-/- mice. DTH responses in tumor necrosis factor alpha-/- (TNF-/-) mice were also suppressed; the magnitude of the suppression in IL-1alpha/beta-/-TNF-/- mice, however, was similar to that observed in IL-1alpha/beta-/- mice. These observations indicate that IL-1 possesses dual functions during the DTH response. IL-1beta is necessary for the efficient priming of T cells. In addition, CD4+ T cell-derived IL-1 plays an important role in the activation of DCs during the elicitation phase, resulting in the production of TNF, that activate allergen-specific T cells.
机译：由于IL-1表达在迟发型超敏反应（DTH）应答中增加，因此我们分析了IL-1在该应答中的作用。在IL-1beta缺陷（IL-1beta-/-）和IL-1alpha / beta-/-小鼠中，对甲基BSA（mBSA）的DTH应答被显着抑制，而在IL-1alpha-/-小鼠中则没有。相反，IL-1R拮抗剂-/-（IL-1Ra-/-）小鼠的反应加剧。来自mBSA致敏的IL-1beta-/-，IL-1alpha / beta-/-和IL-1R I型（IL-1RI）-/-小鼠的淋巴结细胞，但不是来自IL-1alpha-/-小鼠，表现出降低的针对mBSA的增殖反应，而来自IL-1Ra-/-小鼠的增殖反应增强。从mBSA敏感的IL-1alpha / beta-/-小鼠过继转移CD4 + T细胞后，野生型小鼠中的DTH响应也降低了，而接受IL-Ra-/-小鼠细胞的小鼠中的DTH响应也有所提高。从野生型小鼠移植mBSA致敏的CD4 + T细胞后，IL-1RI-/-，但IL-1alpha / beta-/-小鼠的DTH反应降低。与来自IL-1RI-/-小鼠的树突状细胞（DC）共培养时，mBSA敏感的CD4 + T细胞对mBSA的召回反应降低，而对于来自IL-1alpha / beta-/-小鼠的DC则反应正常。肿瘤坏死因子α-/-（TNF-/-）小鼠中的DTH反应也被抑制;但是，在IL-1alpha / beta-/-TNF-/-小鼠中抑制的幅度与在IL-1alpha / beta-/-小鼠中观察到的相似。这些观察表明IL-1在DTH反应期间具有双重功能。 IL-1beta是有效引发T细胞所必需的。此外，CD4 + T细胞来源的IL-1在诱导阶段的DC激活中起着重要作用，导致TNF的产生，后者激活了过敏原特异性T细胞。

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