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									<identifier>oai:www.peertechzpublications.org:10.17352/raoa.000003</identifier>
									<datestamp>2017-03-02</datestamp>
									<setSpec>PTZ.RAOA:VOL1</setSpec>
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										<dc:title>
										The Biological Effects of Interleukin-6 and Their Clinical Applications in Autoimmune Diseases and Cancers
										</dc:title><dc:creator>Deng-Ho Yang</dc:creator><dc:description>&lt;p&gt;Interleukin-6 (IL-6) is one of the pro-infl ammatory cytokines involved in pathogenesis of various&amp;nbsp; autoimmune and chronic infl ammatory diseases. IL-6 through binding to its cellular receptor can transduce both classical- and trans-signaling pathways. Overproduction of circulating IL-6 can be&amp;nbsp; detected in patients with different autoimmune diseases. Tocilizumab, a humanized monoclonal antibody against IL-6 receptor, can block IL-6-mediated signaling and has been approved for the treatment of rheumatoid arthritis and Castleman’s disease. Besides, expression of IL-6 may promote tumorigenesis and has been detected in various tumors, including multiple myeloma, colorectal cancer, breast cancer, lymphoma, breast cancer and lung cancer. Furthermore, increased levels of circulating IL-6 are&amp;nbsp; associated with poor prognosis and cachexia in cancer patients. Monotherapy with IL-6 blockade or a combination therapy with both IL-6 blockade and conventional chemotherapy may reduce the progression of cancer and improve the status of cachexia in cancer patients. Finally, based upon the known biological effects of IL-6, diseases, other than autoimmune diseases and cancers, potentially to be anti-IL-6 candidates will be briefl y discussed.&lt;/p&gt;</dc:description>
										<dc:publisher>Rheumatica Acta: Open Access - Peertechz Publications</dc:publisher>
										<dc:date>2017-03-02</dc:date>
										<dc:type>Review Article</dc:type>
										<dc:identifier>https://doi.org/10.17352/raoa.000003</dc:identifier>
										<dc:language>en</dc:language>
										<dc:rights>Copyright © Deng-Ho Yang et al.</dc:rights>
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