**6. Conclusions**

Since the development of the hybridoma technique several monoclonal antibodies have been approved for the treatment of autoimmune diseases. Immunogenicity of murine sequences caused initial complications, which could be attenuated and finally overcome by the production of chimeric and humanized antibodies and with the generation of transgenic mouse strains for human Ig-sequences. One of the crucial steps by the design of a monoclonal antibody for therapeutic applications is the selection of the right target molecule. In autoimmune disorders several options exist: the blockade of the proinflammatory cytokines TNF, IL-1 or IL-6, the inhibition of T cell-B cell interactions, B cell depletion to reduce autoantibody production and the establishment of ectopic lymphoid structures or the blockade of B cell survival factors. Although we still need to face adverse events upon the application of these therapeutic antibodies, targeting specific molecules will help us to reduce the severity of occurring side effects and provide more efficient medications.
