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Activation of HLA‐DR and Interleukin‐6 Gene Transcription in Resting T Cells via the CD2 Molecule: Relevance to Chronic Immune‐Mediated Inflammation
Author(s) -
LINARDOPOULOS S.,
CORRIGALL V.,
PANAYI G. S.
Publication year - 1992
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1992.tb02962.x
Subject(s) - biology , immune system , immunology , cytotoxic t cell , t cell , zap70 , interleukin 21 , antigen presenting cell , inflammation , il 2 receptor , antigen , interleukin 2 , tcirg1 , human leukocyte antigen , microbiology and biotechnology , in vitro , biochemistry
Only a minority of T cells at cell‐mediated immune lesions are antigen specific. In the lesions of human autoimmune disease, such as the synovial membrane in rheumatoid arthritis, the T cells are activated as shown by a variety of phenotypic and functional changes including the expression of HLA‐DR and the production of interleukin‐6 (IL‐6). The stimulatory pathway involved is unknown but does not seem to involve the T‐cell receptor. Alternative pathways of activation which may be involved include the CD2 molecule. It is shown that the formation of sheep red blood cell (SRBC) rosettes with resting T cells from human peripheral blood, which is equivalent to CD2/LFA‐3 binding, leads to the de novo transcription ofthe HLA‐DR and IL‐6 genes and the expression of HLA‐DR on the surface of the T cells. There was no transcription of the interleukin‐2 (IL‐2) or the interleukin‐2 receptor (IL‐2R) genes and Tac expression was not seen. The rosetted T cells did not proliferate. These are all characteristics of T cells at chronic inflammatory sites. It is concluded that receptor‐ligand interactions between CD2/LFA‐3, which are expressed in increased amounts in the rheumatoid Joint, may be one pathway by which antigen non‐specific T cells are recruited as effector cells in lesions of human autoitnmune disease.