| Literature DB >> 17391915 |
Miri Blank1, Yehuda Shoenfeld.
Abstract
Autoimmunity results from a break in self-tolerance involving humoral and/or cell-mediated immune mechanisms. Part of the pathological consequence of a failure in central and/or peripheral tolerance, results from survival and activation of self-reactive B cells. Such B cells produce tissue-damaging pathogenic autoantibodies, and subsequent formation of complement-fixing immune complexes that contribute to tissue damage. Current pharmacological strategies for treating autoimmune diseases involve global use of broad-acting immunosuppressants that with long term use have associated toxicities. The present drive in drug development is towards therapies that target a specific biological pathway or pathogenic cell population. This review focuses on some of the emerging therapies based on co-stimulation blockers, and compounds which contribute to a specific B cells depletion, based on studies in animal models and human clinical studies.Entities:
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Year: 2007 PMID: 17391915 DOI: 10.1016/j.jaut.2007.02.001
Source DB: PubMed Journal: J Autoimmun ISSN: 0896-8411 Impact factor: 7.094