Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: T-cell contact-dependent regulation of CC and CXC chemokine production in monocytes through differential involvement of NFκB: implications for rheumatoid arthritis. | Available online http content 8 6 R168 Research article T-cell contact-dependent regulation of CC and CXC chemokine production in monocytes through differential involvement of NFkB implications for rheumatoid arthritis Jonathan T Beech1 Evangelos Andreakos2 Cathleen J Ciesielski1 Patricia Green1 Brian MJ Foxwell1 and Fionula M Brennan1 Open Access Kennedy Institute of Rheumatology Division Imperial College School of Medicine 1 Aspenlea Road Hammersmith London W6 8LH UK foundation for Biomedical Research of the Academy of Athens Center for Immunology and Transplantations 4 Soranou tou Ephessiou 11527 Athens Greece Contributed equally Corresponding author Jonathan T Beech Received 7 Jun 2006 Revisions requested 28 Jun 2006 Revisions received 28 Sep 2006 Accepted 13 Nov 2006 Published 13 Nov 2006 Arthritis Research Therapy 2006 8 R168 doi ar2077 This article is online at http content 8 6 R168 2006 Beech 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 We and others have reported that rheumatoid arthritis RA synovial T cells can activate human monocytes macrophages in a contact-dependent manner to induce the expression of inflammatory cytokines including tumour necrosis factor alpha TNFa . In the present study we demonstrate that RA synovial T cells without further activation can also induce monocyte CC and CXC chemokine production in a contact-dependent manner. The transcription factor NFkB is differentially involved in this process as CXC chemokines but not CC chemokines are inhibited after overexpression of IKBa the natural inhibitor of NFkB. This effector function of RA synovial T cells is also shared by T cells activated with a cytokine .
