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International Immunology, Vol. 13, No. 3, 305-312, March 2001
© 2001 Japanese Society for Immunology

A potential role for protein tyrosine kinase p56lck in rheumatoid arthritis synovial fluid T lymphocyte hyporesponsiveness

Paola Romagnoli1, Donna Strahan1, Michele Pelosi2, Alain Cantagrel1,3 and Joost P. M. van Meerwijk1,4

1 Tolerance and Autoimmunity Section, INSERM U395, IFR 30, CHU Purpan, BP 3028, 31024 Toulouse Cedex 3, France
2 Molecular Immunology Unit, Institut Pasteur, 75724 Paris Cedex 15, France
3 Department of Rheumatology, Rangueil Hospital, 31403 Toulouse Cedex 4, France
4 Faculty of Life Sciences (UFR-SVT), University Toulouse III, 31062 Toulouse Cedex 4, France

Correspondence to: P. Romagnoli

Rheumatoid arthritis (RA) synovial fluid (SF)-T lymphocytes appear relatively inactive in situ and respond only weakly to diverse stimuli ex vivo. To characterize the molecular defects underlying this hyporesponsiveness we analyzed the expression level of several proteins involved in TCR-proximal signal transduction. As compared to peripheral blood (PB)-T lymphocytes, SF-T cells from some (but not all) of the patients analyzed expressed lower levels of TCR{alpha}ß, CD3{varepsilon}, TCR{zeta}, p56lck and LAT, while p59fyn, phospholipase C-{gamma}1 and ZAP-70 expression was unaltered. Semi-quantitative analysis of T cells from several patients revealed that the degree of TCR{zeta} chain and p56lck modulation correlated statistically significantly with the level of SF-T cell hyporesponsiveness. The differential reactivity of p56lck specific monoclonal and polyclonal antibodies in SF-T but not PB-T lymphocytes indicated that p56lck modulation consists of a conformational change rather than loss of expression. Our results indicate that multiple signaling molecules can be modulated in RA SF-T cells and show for the first time a direct quantitative correlation between T cell hyporesponsiveness and modulation of TCR{zeta} and of p56lck, a critical protein tyrosine kinase required for T cell activation.

Keywords: TCR{zeta}, LAT

Transmitting editor: T. Saito


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