The Mechanism Of JAM-A On Lymphocytes In Rheumatoid Arthritis

Rheumatoid Arthritis belong to autoimmune diseases, Synovial inflammation is the basic pathology of rheumatoid Arthritis which belong to autoimmune diseases.Patients appear Joint swelling along with synovisis membrane and bone Multiple factors involved in RA.JAM-A lies on tight junctions between endothelial cells.cell membrane, distributed in the close connection between the help to form the complete physical barrier, prevent free water and macromolecular substances through the gaps between cells. Much more attention were paied to the study in JAM-A’s role in maintaining immune barrier, but less study were reported on lymphocyte function.This research from clinical patients with RA, collagen induced arthritis animal models in mice and the Angle of JAM-A protein function in RA is an autoimmune disease were discussed. We focus on functions of JAM-A in RA by clinical patients and CIA models and cell and molecular biology of lymphocyte.There is broad spectrum expression of JAMs family, JAM-A mRNA and protein levels are very high, JAM-A high mRNA expression was detected in B cells with low level of protein expression.It showed that the T cells may be the major types of cells which JAM-A gene and protein expressed.JAM-A in patients increased compared with healthy people.There is no significant change of JAM-A between RA and untreated patients while MTX increase JAM-A level(especially in T cells).There is negative correlation of JAM-A and disease activity score. Regulation of JAM-A maybe one of the treatment mechanism of MTX.No differences were found in JAM-A protein levels in CIA mice and the control group. Joint swelling were relieved when levels of JAM-A protein elevated by MTX.Lymphocytes were cultured for researching the JAM-A in the pathogenesis of RA. Results showed that the migration ability of lymphocytes in RA was higher than that of healthy people. MTX inhibited the migration of lymphocytes in RA patients in vitro and could be opposed by J10.4.MTX raiseed the expression of Jam-a gene and JAM-A protein too.Regulation of lymphocytes migration process maybe is one of the mechanism of JAM-A. It is suggested that JAM-A could be the target for the treatment of RA. This study will provide theoretical reference for exploring pathogenesis of RA and screening of new drugs.