To facilitate functional genomics in the nervous system, an appropriate methodology should be taken for conditional genetic manipulation to the purpose. Our system has the potential to be a tool with which to elucidate the in vivo molecular mechanisms of later stages of development. Rheumatoid arthritis is a chronic autoimmune disease that features persistent synovial inflammation and proliferation along with infiltration of predominantly T lymphocytes, plasma cells and macrophages. A central role for the B lymphocytes in the pathogenesis of RA is supported by the presence of 4′-Chloropropiophenone autoantibodies, which are locally produced in the inflamed synovium and may promote tissue inflammation and destruction by forming immune complexes. Moreover, a significant percentage of RA patients display ectopic lymphoid structures in the synovial membrane that could sustain T and B cell interaction. Finally, effector B cells produce cytokines and other immunological mediators thereby promoting the extent and direction of immune responses. The observation that therapeutic B cell depletions using rituximab treatment disrupts synovial lymphoid neogenesis and decreases macrophages infiltration supports the notion that B cells orchestrate synovial inflammation in RA. In the rheumatoid joint, the synovial fluid contains a variety of cytokines, chemokines, growth factors and lipid-derived mediators, which potentially mediate B cells effector functions. Of the prostaglandins, high levels are reached by prostaglandin E2, which plays a prominent role in the rheumatoid Eupalinilide-D pathogenic process by promoting tissue damaging and autoimmunity. Microsomal prostaglandin E2 synthase 1 catalyses its formation from cyclooxygenase-derived PGH2 and is an inflammation-induced enzyme overexpressed in synovial tissue of RA patients. MPGES1 is mostly found in fibroblast-like synoviocytes and macrophages. Cyclooxygenase enzymes known as COX-1 and COX-2 are also widely expressed in the inflamed synovium. COX-1 is present in intimal lining layer and synovial sublining mononuclear cells and FLS. COX2 has a similar localization, but is also highly expressed by endothelial cells. Furthermore, whereas COX-1 expression is independent of the inflammatory status in the joint tissue, COX-2 is markedly upregulated at sites of inflammation.