POLYCLONAL TH1 CELLS TRANSFER OIL-INDUCED ARTHRITIS

T-cells play a critical role in oil-induced arthritis (OIA) in DA rats . The present study focuses on the involvement of CD4/CD8 T cells in O IA by using adoptive transfer. Mitogen-activated T cells from DA rats previously injected with incomplete Freund's adjuvant (IFA) were deple ted of CD4(+) T cells or CD8(+) T cells before transfer to irradiated naive receipients. The results indicate that CD4(+) T cells are essent ial for the induction of passively induced OIA. However, in vitro bloc king experiments with monoclonal antibodies (mAb) to the CD4 molecule of the T cells before transfer did not affect the passive OIA. Neither was passive OIA inhibited by treating the CD4(+) T cells with mAb to intracellular adhesion molecule-1 (ICAM-1) in order to block cell-cell interactions or migration. The arthritogenic CD4(+) T cells were sens itive, however, to in vitro treatment with mAb to the interleukin-2 re ceptor, which inhibited the disease or delayed the onset of passive OI A in recipients. The arthritogenic CD4(+) T cells were also analysed f or expression of specific T-cell receptor (TCR) variable (V)beta chain s, critical for recognition of autoantigen, by utilizing V beta gene-s pecific polymerase chain reaction (PCR. The results show a heterogeneo us expression of V beta segments of the TCR, indicating a polyclonal o rigin of the pathogenic cells. Moreover, an investigation of the T hel per (Th)1/Th2 status of the CD4(+) T cells, defined by cytokine expres sion was made at the mRNA level by using ill situ hybridization, High numbers of interleukin-2 (IL-2) mRNA expressing cells and also interfe ron-gamma (IFN-gamma) and tumour necrosis factor-alpha (TNF-alpha)-exp ressing cells could be identified. We conclude from this study that no nimmunogenic IFA triggers polyclonal, IL-2-dependent Th1 cells which i nduce arthritis, The contribution of the CD4 or ICAM-1 molecules for a rthritis induction seem to be of minor importance.