tailieunhanh - Báo cáo y học: "IL-4 increases type 2, but not type 1, cytokine production in cells from mild atopic asthmatics"

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: "IL-4 increases type 2, but not type 1, cytokine production in cells from mild atopic asthmatics. | Respiratory Research BioMed Central Research Open Access IL-4 increases type 2 but not type I cytokine production in CD8 T cells from mild atopic asthmatics Luminita A Stanciu 1 Kevan Roberts2 Nikolaos G Papadopoulos2 Sang-Heon Cho2 Stephen T Holgate2 Anthony J Coyle3 and Sebastian L Johnston1 Address Department of Respiratory Medicine National Heart and Lung Institute Wright Fleming Institute for Infection and Immunity Imperial College London Norfolk Place London UK 2Respiratory Cell and Molecular Biology Research Division University of Southampton Southampton UK and 3MedImmune Gaithersburg USA Email Luminita A Stanciu - Kevan Roberts - kroberts@ Nikolaos G Papadopoulos - ngp@ Sang-Heon Cho - shcho@ Stephen T Holgate - Anthony J Coyle - coylea@ Sebastian L Johnston - Corresponding author Published 07 July 2005 Received 07 February 2005 Respiratory Research 2005 6 67 doi 1465-9921 -6-67 Accepted 07 July 2005 This article is available from http content 6 1 67 2005 Stanciu 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 Virus infections are the major cause of asthma exacerbations. CD8 T cells have an important role in antiviral immune responses and animal studies suggest a role for CD8 T cells in the pathogenesis of virus-induced asthma exacerbations. We have previously shown that the presence of IL-4 during stimulation increases the frequency of IL-5-positive cells and CD30 surface staining in CD8 T cells from healthy normal subjects. In this study we investigated whether excess IL-4 during repeated TCR CD3 stimulation of CD8 T cells from atopic