학술논문

Human bronchial intraepithelial T cells produce interferon-[gamma] and stimulate epithelial cells
Document Type
Report
Source
Clinical and Experimental Immunology. Feb, 2009, Vol. 155 Issue 2, p266, 9 p.
Subject
Biological response modifiers
T cells
Interferon gamma
Universities and colleges
Respiratory agents
Language
English
ISSN
0009-9104
Abstract
To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1365-2249.2008.03811.x Byline: S. Hirosako (*), E. Goto (*), K. Fujii (*), K. Tsumori (*), N. Hirata (*), S. Tsumura (*), H. Kamohara ([dagger]), H. Kohrogi (*) Keywords: bronchial epithelial cells; CD103; intraepithelial lymphocytes; lamina propria lymphocytes; mucosal immunity Abstract: Summary 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.sup.+ 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. Author Affiliation: (*)Department of Respiratory Medicine, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University Hospital, and ([dagger])Department of Gastroenterological Surgery, Graduate School of Medical Sciences, Kumamoto University, Honjo, Kumamoto, Japan Article History: Accepted for publication 7 October 2008 Article note: H. Kohrogi, Department of Respiratory Medicine, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University Hospital, Kumamoto University, 1-1-1, Honjo, Kumamoto, 860-8556, Japan., E-mail: kohrogi@kumamoto-u.ac.jp