Akbari O, DeKruyff R H, Umetsu D T
Division of Immunology and Allergy, Department of Pediatrics, School of Medicine, Stanford University, Stanford, CA 94305-5208, USA.
Nat Immunol. 2001 Aug;2(8):725-31. doi: 10.1038/90667.
Respiratory exposure to allergen induces T cell tolerance and protection against the development of airway hyperreactivity and asthma. However, the specific mechanisms by which tolerance is induced by respiratory allergen are not clear. We report here that pulmonary dendritic cells (DCs) from mice exposed to respiratory antigen transiently produced interleukin 10 (IL-10). These phenotypically mature pulmonary DCs, which were B-7(hi) as well as producing IL-10, stimulated the development of CD4(+) T regulatory 1--like cells that also produced high amounts of IL-10. In addition, adoptive transfer of pulmonary DCs from IL-10(+/+), but not IL-10(-/-), mice exposed to respiratory antigen induced antigen-specific unresponsiveness in recipient mice. These studies show that IL-10 production by DCs is critical for the induction of tolerance, and that phenotypically mature pulmonary DCs mediate tolerance induced by respiratory exposure to antigen.
呼吸道暴露于变应原可诱导T细胞耐受，并预防气道高反应性和哮喘的发生。然而，呼吸道变应原诱导耐受的具体机制尚不清楚。我们在此报告，暴露于呼吸道抗原的小鼠肺树突状细胞（DCs）短暂产生白细胞介素10（IL-10）。这些表型成熟的肺DCs，其B-7（高）且产生IL-10，刺激了同样产生大量IL-10的CD4（+）调节性T1样细胞的发育。此外，来自暴露于呼吸道抗原的IL-10（+/+）而非IL-10（-/-）小鼠的肺DCs的过继转移在受体小鼠中诱导了抗原特异性无反应性。这些研究表明，DCs产生IL-10对于耐受的诱导至关重要，并且表型成熟的肺DCs介导呼吸道暴露于抗原所诱导的耐受。
