948 infliximab, ANA developed in 29-76.7% and anti-dsDNA in 10-29% (7, 8, 16, 17). Also in etanercept treated RA pati- ents, 11-36.3% patients had developed ANA, and 5-15% developed anti-dsDNA (16, 18, 19). In Crohn’s disease, auto- antibody development and infliximab-induced SLE were reported (20-24). Shakoor et al. first reported four cases of etan- ercept-induced SLE in a series of RA patients in 2002 (9). Swale et al. also reported a case of SLE following 12 months of etanercept therapy in the following year (10). In the pre- vious reports, timing of the onset and offset of the SLE fea- tures strongly supported a drug related effect of etanercept. In these patients, SLE developed after mean 7.7 months (range 3-24) of commencing etanercept therapy, and were all women. Most common clinical feature of SLE was skin rash. There was no significant life threatening organ involvement such as kidney, lung, heart and central nervous system. The SLE features were resolved rapidly on stopping the treatment. The British Society for Rheumatology recommends stopping anti- TNF therapy and appropriate treatment if symptoms of an SLE-like syndrome develop on anti-TNF treatment (25). The pathogenesis of anti-TNF in development of SLE has not been yet clarified. Cairns et al. explained that TNF may up-regulate the cellular expression of the adhesion molecule CD44, which has a role in the clearance of apoptotic neutro- phil by phagocyte. Reduced CD44 expression by anti-TNF can potentially induce SLE by abnormal clearance and expo- sure to apoptotic materials (12, 26). Long term exposure over 30 weeks to infliximab has been suggested as a factor that can lead to SLE in one study (17). 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