Open AccessExpression and functional role of 1F7 (CD26) antigen on peripheral blood and synovial fluid T cells in rheumatoid arthritis patients
Author(s) -
MUSCAT C.,
BERTOTTO A.,
AGEA E.,
BISTONI O.,
ERCOLANI R.,
TOGNELLINI R.,
SPINOZZI F.,
CESAROTTI M.,
GERLI R.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06134.x
Subject(s) - lymphokine , t cell , antigen , immunology , synovial fluid , t lymphocyte , rheumatoid arthritis , tcirg1 , peripheral blood mononuclear cell , immune system , biology , medicine , endocrinology , antigen presenting cell , in vitro , pathology , biochemistry , alternative medicine , osteoarthritis
SUMMARY The expression and the functional role of the CD26 (1F7) T cell surface molecule, an ectoenzyme which seems to represent a functional collagen receptor of T lymphocytes and to have a role in T cell activation, were analysed in both peripheral blood (PB) and synovial fluid (SF) T cell samples from patients with active and inactive rheumatoid arthritis (RA). Although patients with active disease displayed higher percentages of PB CD26 + CD4 + T cells than inactive RA and control subjects, CD26 antigen expression on RA SF T lymphocytes was low. The anti‐1F7 binding to the T cell surface, that led to CD26 antigen modulation and enhancement of both IL‐2 synthesis by, and 3 H‐TdR incorporation of, anti‐CD3‐ or anti‐CD2‐triggered PB T cells in RA and control subjects, was unable to affect significantly both expression and functional activity of RA SF T lymphocytes. Since the 1F7 antigen spontaneously reappeared on the surface of unstimulated SFT cells after 2‐5 days of culturing, the low IF7 antigen expression of anti‐lF7 in the SF T cell compartment may be the result of in vivo molecule modulation exerted by the natural ligand in the joint, with important implications for T cell activation and lymphokine synthesis.