FRI0086 Characterisation of ra33 (hnrnp-a2/b1)- autoreactive t cells in sle-patients

Background SLE is a systemic autoimmune disease with distinct immunological characteristics including defective T cell functions, especially concerning IL2 production and proliferation. Furthermore, B-cell hyperactivity is observed leading to the formation of several characteristic autoantibodies (ab), among them ab to the heterogenous nuclear ribonucleoprotein A2/B1 (hnRNP/RA33). These antibodies are known to occur in over 20% of SLE patients. Objectives In order to elucidate the role of T cells and their influence in antibody production in SLE, we studied proliferation of PBMC to purified hnRNP-A2/B1 in SLE patients and healthy controls. Methods Stimulation assays with PBMC of 34 SLE patients and 21 healthy controls were performed. We then proceeded to draw RA33-specific T cell clones (TCC) by cultivation and limiting-dilution cloning of T cell lines. Results While the stimulation indices (SI) in the healthy control group ranged from 0.5 to 3.5 (mean SI: 1.5 ± 0.9), the proliferative response of PBMC of the patient group ranged from 0.7 to 17 with a mean SI of 4.8 ± 4.0 (only 6 of 34 patients had an SI Conclusion Our data reveal that more than 80% of SLE-patients have a significant T cell reactivity (SI >2) to the nuclear protein hnRNP-A2/B1 indicating that the antibody response might be T cell driven. Furthermore, almost 60% of TCC derived from SLE patients were CD8+, which supports the importance of these T cells in SLE. Further studies will have to elucidate the pathogenetic implications of these findings.