ab2006

Interleukin-10 expression: Is there a neglected contribution of CD8+ T cells in rheumatoid arthritis joints ?

B. Möller, T.T. Nguyen, U. Kessler, J.P. Kaltwasser, D. Hoelzer, O.G. Ottmann

Klinikum der Johann Wolfgang Goethe-UniversitŠt, Medizinische Klinik III, Frankfurt, Germany

ABSTRACT
Objective
To search for RA specific processes among T cell accumulation, T cell activation, or cytokine expression in CD4+ and CD8+ synovial fluid (SF) T cells

Methods
Flow cytometry of CD4+, CD8+, CD45RA+, CD45RO+, CD69 double or triple stained peripheral blood (PB) and SF T cells. IL-2, IL-10, and IFN-g expression was determined in PMA + ionomycin stimulated T cells on the single cell level. Concentrations of secreted IL-2, IL-4, IL-10, and IFN-g were quantified in the sera and synovial fluids by enzyme linked immunosorbent assay (ELISA).

Results
A preferential recruitment of CD45RO+ memory T cells was found for CD4+ helper T cells, and in similar also for CD8+ suppressor T cells. An elevated CD69 expression was detected in memory, but also in CD45RA+ naive CD4+ and CD8+ SF T cells, whilst IL-2 expression was only demonstrable in a minor proportion of T cells populations. Preferential recruitment of memory T cells, but incomplete activation of naive and memory, CD4+ and CD8+ T cells were in similar found in RA and control patients. In RA but not in the control patients, a relevant proportion of CD4+ and CD8+ PB and SF T cells expressed IL-10 and IFN-g. High concentrations of IL-10, that were correlated with the amounts of secreted TNF-a, were only detected in RA joints.

Conclusion
Memory and naive T cell state of CD4+ and CD8+ T cell accumulates in the joints, and early T cell activation occur in similar patterns in RA and control patients. High IL-10 SF concentrations in contrast, and elevated percentages of IFN-g and IL-10 expressing CD4+ and CD8+ T cells in the PB and SF were characteristic for RA. Here, CD8+ T cells may contribute to high IL-10 concentrations in RA joints.

Key words
Arthritis, interleukin-10, T cell, suppressor, cytotoxic.

This work was supported by grants from the Riese and Klein foundations, Johann Wolfgang Goethe University of Frankfurt, Germany.
Please address correspondence and reprint requests to: Dr. Burkhard Mšller, Rheumazentrum Rhein-Main, UniversitŠtsklinik, Marienburgstra§e 2, D-60528 Frankfurt/Main, Germany.
E-mail: B.Moeller@em.uni-frankfurt.de