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Antigen-specific tolerogenic dendritic cells ameliorate the severity of murine collagen-induced arthritis
Ning, Bin Wei, Jianlu Zhang, Aijun Gong, Weiming Fu, Jinqiu Jia, Tanghong Yang, Shang-You
Ning, Bin
Wei, Jianlu
Zhang, Aijun
Gong, Weiming
Fu, Jinqiu
Jia, Tanghong
Yang, Shang-You
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Ning_2015
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2015-06-24
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Article
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Regulatory t-cells,Rheumatoid-arthritis,Immune thrombocytopenia,Tolerance,Therapy,Mice,Methotrexate,Cytokines,Targets,Anergy
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Ning, Bin; Wei, Jianlu; Zhang, Aijun; Gong, Weiming; Fu, Jinqiu; Jia, Tanghong; Yang, Shang-You. 2015. Antigen-specific tolerogenic dendritic cells ameliorate the severity of murine collagen-induced arthritis. PLOS ONE, vol. 10:no. 6: Article Number: e0131152
Abstract
Dendritic cells (DCs) play important roles in initiation of the pathogenic processes of autoimmune disorders, such as rheumatoid arthritis (RA). Tolerogenic dendritic cells (tolDCs) are generated from naive DCs and induce T cell tolerance; thus, they represent a promising strategy for specific cellular therapy for autoimmune diseases. In this study, we generated green fluorescent protein (GFP)-labeled tolDCs and confirmed their phenotypes and biological functions. We found that tolDCs suppressed the memory lymphocyte response and exhibited strong tolerogenic potential; thus, these cells show promise for the treatment of autoimmune diseases. Additionally, a collagen-induced arthritis (CIA) mouse model was used to test the role of tolDCs in vivo. The results of a further mechanistic experiment revealed that tolDCs suppressed inflammatory arthritis at least partially by up-regulating regulatory T (Treg) cells. Collectively, our data suggest that tolDCs may be used as a promising alternative therapy for inflammatory arthritis.
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Copyright: © 2015 Ning et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Public Library Science
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PLoS ONE
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1932-6203