作者: David P. Andrew
DOI: 10.1007/978-1-59259-473-3_12
关键词: Experimental autoimmune encephalomyelitis 、 Immunology 、 Leukocyte Rolling 、 Receptor 、 Cell adhesion molecule 、 Autoimmune encephalitis 、 MHC class I 、 Inflammation 、 Multiple sclerosis 、 Medicine
摘要: Strategies to control neurological diseases with antagonists of cell-adhesion molecules (CAMs) target predominantly leukocytes and endothelial cells, two different approaches currently in use. In the first approach, attempts are being made block accumulation at site inflammation by targeting various CAMs that involved leukocyte rolling, arrest, trans-endothelial migration. this area investigated clinic both for acute diseases, such as stroke, also management chronic relapsing disorder multiple sclerosis. The second approach utilizes involvement several T-lymphocyte activation, which there points intervention. During a expressing an appropriate T-cell receptor recognizes autoimmune peptide associated MHC I or II on antigen-presenting cell (APC). addition signal, requires additional signals, transmitted via termed costimulation molecules. These represent point absence these costimulatory is anergized enters resting state it refractory further activation. This thought result from changes cell-signaling pathway, since T-lymphocytes show defective phosphorylation proteins cross-linking. intervention role adhesion T-cells APCs. Certain CAM pairs, LFA-1:ICAM-1 CD2:LFA-3, utilized T:APC interaction, blockade pairs inhibits Several be costimulation. LFA-1 ICAM-1 examples. initial activation their expansion using evaluated models disease known play important role, experimental encephalitis (EAE).