Hirosako S, Goto E, Fujii K, Tsumori K, Hirata N, Tsumura S, Kamohara H, Kohrogi H
Department of Respiratory Medicine, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University Hospital, Honjo, Kumamota, Japan.
Clin Exp Immunol. 2009 Feb;155(2):266-74. doi: 10.1111/j.1365-2249.2008.03811.x. Epub 2008 Nov 26.
Intraepithelial lymphocytes (IELs) can be identified among epithelial cells in systemic mucosal tissues. Although intestinal IELs play a crucial role in mucosal immunity, their bronchial counterparts have not been well studied. The purpose of this study was to determine the immunological functions of human bronchial IELs, which interact directly with epithelial cells, unlike lamina propria lymphocytes (LPLs). We isolated successfully bronchial IELs and LPLs using a magnetic cell separation system from the T cell suspensions extracted from bronchial specimens far from the tumours of resected lungs. Human bronchial IELs showed an apparent type 1 cytokine profile and proliferated more actively in response to CD2 signalling than did bronchial LPLs. CD8(+) IELs were identified as the most significant sources of interferon (IFN)-gamma. Human bronchial epithelial cells constitutively produced the T cell growth factors interleukin (IL)-7 and IL-15, and levels of those factors increased when cells were stimulated by IFN-gamma. Bronchial epithelial cells expressed cell surface proteins CD58 and E-cadherin, possibly enabling adhesion to IELs. In summary, human bronchial IELs have immunological functions distinct from bronchial LPLs and may interact with epithelial cells to maintain mucosal homeostasis.
上皮内淋巴细胞(IELs)可在全身黏膜组织的上皮细胞中被识别。尽管肠道IELs在黏膜免疫中发挥关键作用,但其在支气管中的对应细胞尚未得到充分研究。本研究的目的是确定人支气管IELs的免疫功能,与固有层淋巴细胞(LPLs)不同,支气管IELs可直接与上皮细胞相互作用。我们使用磁珠细胞分选系统,从切除肺肿瘤远处的支气管标本提取的T细胞悬液中成功分离出支气管IELs和LPLs。人支气管IELs表现出明显的1型细胞因子谱,且相较于支气管LPLs,其对CD2信号的反应增殖更为活跃。CD8(+) IELs被确定为干扰素(IFN)-γ的最重要来源。人支气管上皮细胞组成性地产生T细胞生长因子白细胞介素(IL)-7和IL-15,当细胞受到IFN-γ刺激时,这些因子的水平会升高。支气管上皮细胞表达细胞表面蛋白CD58和E-钙黏蛋白,这可能使其能够与IELs黏附。总之,人支气管IELs具有与支气管LPLs不同的免疫功能,并且可能与上皮细胞相互作用以维持黏膜稳态。