Ovalbumin (OVA) and Mycobacterium tuberculosis bacilli cooperatively polarize anti-OVA T-helper (Th) cells toward a Th1-dominant phenotype and ameliorate murine tracheal eosinophilia
Ovalbumin (OVA) and Mycobacterium tuberculosis bacilli cooperatively polarize anti-OVA T-helper (Th) cells toward a Th1-dominant phenotype and ameliorate murine tracheal eosinophilia
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DOI：
10.1165/ajrcmb.20.6.3546
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发表时间：
1999-06-01
影响因子：
6.4
通讯作者：
Shirato, K
中科院分区：
文献类型：
--
作者：
Sano, K;Haneda, K;Shirato, K
最近过敏性疾病的增加与包括结核病在内的感染的减少相吻合。虽然结核菌素反应和特应性疾病之间的负相关的报道，它是不知道如何辅助性T细胞（Th）1偏向免疫反应结核分枝杆菌影响Th 2优势的过敏原反应。我们研究了结核分枝杆菌是否能以超越抗原特异性屏障的方式调节卵清蛋白（OVA）诱导的小鼠气管嗜酸性粒细胞炎症。我们发现，用完全弗氏佐剂（CFA）中的OVA致敏的CD 4（+）T细胞通过分泌干扰素（IFN）-γ抑制OVA诱导的气管嗜酸性粒细胞增多。用CFA中的不相关抗原或用不完全弗氏佐剂中的OVA免疫未能诱导抑制细胞。体外实验证实，M.结核病和OVA（与单独的任何一种相反）对于通过白细胞介素-12分泌引起向Th 1样表型的极化发展是必要的。这些结果表明，接触过敏原沿着M.结核病将过敏原特异性T细胞的发育转向Th 1表型，这反过来又以抗原特异性方式下调过敏性表现。这些结果的可能影响的背景下，结核病的减少和过敏性疾病的增加之间的因果关系进行了讨论。
A recent increase in allergic disorders has coincided with a decrease in infections, including tuberculosis. Although an inverse association between tuberculin responses and atopic disorders was reported, it was not known how T-helper (Th)l-biased immune responses to Mycobacterium tuberculosis influenced Th2-dominant responses to allergens. We examined whether M, tuberculosis could modulate ovalbumin (OVA)-induced eosinophilic inflammation in the murine trachea in a manner that transcended the barrier of antigen specificity, We found that CD4(+) T cells primed with OVA in complete Freund's adjuvant (CFA) inhibited OVA-induced tracheal eosinophilia through interferon (IFN)-gamma secretion. Immunization with an irrelevant antigen in CFA or with OVA in incomplete Freund's adjuvant failed to induce suppressor cells. In vitro experiments confirmed that both M. tuberculosis and OVA (as opposed to either one alone) were necessary to evoke polarized development toward a Th1-like phenotype through interleukin-12 secretion. These results indicate that exposure to an allergen along with M. tuberculosis switches development of allergen-specific T cells toward a Th1 phenotype, which, in turn, downregulates allergic manifestations in an antigen-specific manner. The possible implications of these results are discussed in the context of the causal relationship between a decrease in tuberculosis and an increase in allergic disorders.