Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Trans-dominant cellular inhibition of DC-SIGN-mediated HIV-1 transmission | Retrovirology BioMed Central Research Open Access Trans-dominant cellular inhibition of DC-SIGN-mediated HIV-1 transmission Li Wu1 Thomas D Martin1 Yoon-Chi Han1 2 Sabine KJ Breun1 and Vineet N KewalRamani 1 Address 1Model Development Section HIV Drug Resistance Program National Cancer Institute at Frederick National Institutes of Health Frederick Maryland 21702 USA and 2Department of Microbiology College of Physicians and Surgeons Columbia University New York New York 10032 USA Email Li Wu - liwu@ Thomas D Martin - tmartin@ Yoon-Chi Han - yh2029@ Sabine KJ Breun - sbreun@ VineetN KewalRamani - vineet@ Corresponding author Published 28 June 2004 Received 23 March 2004 Retrovirology 2004 1 14 doi 1742-4690-1-14 Accepted 28 June 2004 This article is available from http content 1 1 14 2004 Wu et al licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Background Dendritic cell DC transmission of human immunodeficiency virus HIV to CD4 T cells occurs across a point of cell-cell contact referred to as the infectious synapse. The relationship between the infectious synapse and the classically defined immunological synapse is not currently understood. We have recently demonstrated that human B cells expressing exogenous DC-SIGN DC-specific intercellular adhesion molecule-3 ICAM-3 -grabbing nonintegrin efficiently transmit captured HIV type 1 HIV-1 to CD4 T cells. K562 another human cell line of hematopoietic origin that has been extensively used in functional analyses of DC-SIGN and related molecules lacks the principal molecules involved in the formation of immunological synaptic junctions namely major histocompatibility complex MHC class II molecules and leukocyte function-associated antigen-1 LFA-1 . We .
