Tuyển tập các báo cáo nghiên cứu khoa học ngành y học tạp chí Medical Sciences dành cho các bạn sinh viên ngành y tham khảo đề tài: Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta. | Int. J. Med. Sci. 2009 6 85 International Journal of Medical Sciences 2009 6 2 85-92 Ivyspring International Publisher. All rights reserved Research Paper Induction and effector phase of allergic lung inflammation is independent of CCL21 CCL19 and LT-beta Corinne Ploix1 Riaz I. Zuberi2 Fu-Tong Liu3 Monica J. Carson4 and David D. Lo4 H 1. Roche Ltd. Basel Switzerland 2. La Jolla Institute for Molecular Medicine La Jolla CA USA 3. Department of Dermatology School of Medicine University of California Davis CA USA 4. Division of Biomedical Sciences University of California Riverside CA USA H Correspondence to David D. Lo . . Division of Biomedical Sciences University of California Riverside CA. phone 951-827-4553 fax 951-827-5504 email Received Accepted Published Abstract The chemokines CCL21 and CCL19 and cell bound TNF family ligand lymphotoxin beta LTP have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however in the case of allergic inflammatory disease CCL21 CCL19 and LTP have not been associated with the induction recruitment or effector function of Th2 cells nor dendritic cells to the lung. We have examined the induction of allergic inflammatory lung disease in mice deficient in CCL21 CCL19 or LTP and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice adoptive transfers of Th2 cells were also performed and they showed that such effector cells had equivalent effects on airway hyper-responsiveness in both knockout background recipients. Moreover class II positive antigen presenting cells B cells and CD11c dendritic cells showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop
