tailieunhanh - Báo cáo y học: " Antigen-sensitized CD4+CD62Llow memory/effector T helper 2 cells can induce airway hyperresponsiveness in an antigen free setting"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: Antigen-sensitized CD4+CD62Llow memory/effector T helper 2 cells can induce airway hyperresponsiveness in an antigen free setting. | Respiratory Research BioMed Central Research Open Access Antigen-sensitized CD4 CD62Llow memory effector T helper 2 cells can induce airway hyperresponsiveness in an antigen free setting Kazuyuki Nakagome Makoto Dohi Katsuhide Okunishi Yasuo To Atsushi Sato Yoshinori Komagata Katsuya Nagatani Ryoichi Tanaka and Kazuhiko Yamamoto Address Department of Allergy and Rheumatology Graduate School of Medicine University of Tokyo Tokyo Japan Email Kazuyuki Nakagome - nakagomek-tky@ Makoto Dohi - mdohi-tky@ Katsuhide Okunishi - okunishik-int@ Yasuo To - ym-to@ Atsushi Sato - asatoh@ Yoshinori Komagata - y@ Katsuya Nagatani - nagatani-tky@ Ryoichi Tanaka - tanakar-phy@ Kazuhiko Yamamoto - yamamoto-tky@ Corresponding author Published 28 May 2005 Received 13 September 2004 Respiratory Research 2005 6 46 doi 1465-9921 -6-46 Accepted 28 May 2005 This article is available from http content 6 1 46 2005 Nakagome et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Airway hyperresponsiveness AHR is one of the most prominent features of asthma however precise mechanisms for its induction have not been fully elucidated. We previously reported that systemic antigen sensitization alone directly induces AHR before development of eosinophilic airway inflammation in a mouse model of allergic airway inflammation which suggests a critical role of antigenspecific systemic immune response itself in the induction of AHR. In the present study we examined this possibility by cell transfer experiment and then analyzed which cell source was essential for this process. Methods BALB c mice were .