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.
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Authors | Miri Blank, Yehuda Shoenfeld |
Journal | Journal of autoimmunity
(J Autoimmun)
2007 Mar-May
Vol. 28
Issue 2-3
Pg. 62-8
ISSN: 0896-8411 [Print] England |
PMID | 17391915
(Publication Type: Journal Article, Review)
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Chemical References |
- Antibodies, Monoclonal
- Autoantibodies
- Immunosuppressive Agents
- Receptors, Antigen, B-Cell
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Topics |
- Animals
- Antibodies, Monoclonal
(therapeutic use)
- Autoantibodies
(biosynthesis, immunology)
- Autoimmune Diseases
(immunology, therapy)
- B-Lymphocytes
(drug effects, immunology)
- Humans
- Immunosuppressive Agents
(adverse effects, therapeutic use)
- Immunotherapy
(methods)
- Lymphocyte Activation
- Lymphocyte Depletion
- Receptors, Antigen, B-Cell
(immunology, metabolism)
- Self Tolerance
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