Anti-CD11b antibody treatment suppresses the osteoclast generation, inflammatory cell infiltration, and autoantibody production in arthritis-prone FcγRIIB-deficient mice

Anti-CD11b antibody treatment suppresses the osteoclast generation, inflammatory cell infiltration, and autoantibody production in arthritis-prone FcγRIIB-deficient mice

Abstract Background Previously we established an arthritis-prone FcγRIIB-deficient mouse strain (designated KO1). Anti-mouse CD11b mAb (5C6) has been reported to inhibit the recruitment of peripheral CD11b+ myelomonocytic cells from the blood to the inflammatory site. These cells include neutrophils...

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Bibliographic Details
Main Authors: Mareki Ohtsuji, Qingshun Lin, Hideki Okazaki, Kazuko Takahashi, Hirofumi Amano, Hideo Yagita, Hiroyuki Nishimura, Sachiko Hirose
Format: Article
Language:English
Published: BMC 2018-02-01
Series:Arthritis Research & Therapy
Subjects:
Rheumatoid arthritis
FcγRIIB deficiency
Osteoclast
Monocytes
B cell activation
Online Access:http://link.springer.com/article/10.1186/s13075-018-1523-1

Internet

http://link.springer.com/article/10.1186/s13075-018-1523-1

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