A battle with my skin

Abstract

a humanized monoclonal antibody against the CD11a chain of LFA-1. This rapidly acting drug has recently gained approval. Once activated, T-cells result in release of cytokines, including tumor necrosis factor a (TNF-a), which initiates a cascade of events ultimately leading to inflammation and proliferation of keratinocytes. Two TNF-a blocking agents previously used to treat rheumatoid arthritis and Crohn’s disease are in advanced stages of testing for psoriasis and have proven highly effective. Etanercept, a fusion protein consisting of the Fc portion of human IgG1 fused with the human p75 TNF receptor, targets the trimer form of soluble TNF-a. This agent is highly effective for psoriasis and provides not only a dramatic remission of psoriatic arthritis, but prevents radiographic progression of disease. It is already approved for the treatment of psoriatic arthritis and is likely to gain approval for psoriasis in the near future. Infliximab, a chimeric monoclonal antibody to TNF-a, targets both monomer and trimer forms of soluble as well as cell-bound TNF-a. This drug has proven to be one of the most effective psoriasis therapies available. Do we still have more to do? We still don’t have the ideal treatment for psoriasis, a therapy that is entirely harmless, very convenient, and entirely safe. We still haven’t found the gene or genes responsible for psoriasis, and the search for those genes will undoubtedly speed up over the next decade. Hopefully, with the discovery of new genes, we will gain insights into new targets for more effective and safer therapies.