1. Anti-B7-H3 monoclonal antibody ameliorates the damage of acute experimental pancreatitis by attenuating the inflammatory response.
- Author
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Zhuang, Xiaohui, Shen, Jiaqing, Jia, Zhengyu, Wu, Airong, Xu, Ting, Shi, Yuqi, and Xu, Chunfang
- Subjects
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THERAPEUTIC use of monoclonal antibodies , *T cells , *INFLAMMATION , *PANCREATITIS treatment , *THERAPEUTIC use of cytokines , *MACROPHAGES , *ARGININE , *NUCLEAR factor of activated T-cells - Abstract
B7-H3, a recently discovered B7 family member, is documented as a regulator in the inflammatory response as well as T cell-mediated immune responses. In this paper, we find that patients with acute pancreatitis revealed overwhelming levels of serum soluble B7-H3 (sB7-H3) associated with the clinical outcomes. Furthermore, B7-H3 protein was marked increased in l -arginine-induced acute experimental pancreatitis. Anti-B7-H3 monoclonal antibody treatment attenuated the proinflammatory cytokine production, downregulated the activation of the NF-κB signaling pathway, and ameliorated the pancreas disruption in l -arginine-induced pancreatitis. In addition, although l -arginine alone failed to induce the production of proinflammatory cytokine and anti-B7-H3 mAb had no effect on the proinflammatory cytokine production of acinar cells, administration of anti-B7-H3 mAb in the coculture model of acinar cells and macrophages stimulated by l -arginine displayed the similar effects. On the whole, B7-H3 participates in the development of acute pancreatitis, and anti-B7-H3 monoclonal antibody ameliorates severity of acute experimental pancreatitis via attenuation of the inflammatory response. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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