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Int Immunopharmacol. 2016 Feb;31:1-8. doi: 10.1016/j.intimp.2015.12.007. Epub 2015 Dec 11.

BAFF and its receptors involved in the inflammation progress in adjuvant induced arthritis rats.

Author information

1
Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine of Education Ministry of China, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, China; Department of Pharmacy, Bengbu Medical College, Bengbu 233000, China. Electronic address: weifangmailbox@126.com.
2
Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine of Education Ministry of China, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, China.
3
Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine of Education Ministry of China, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, China. Electronic address: wwei@ahmu.edu.cn.
4
Institute of Clinical Pharmacology, Anhui Medical University, Key Laboratory of Anti-inflammatory and Immune Medicine of Education Ministry of China, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Hefei 230032, China. Electronic address: changyan318@126.com.

Abstract

This study is in order to clear the roles of BAFF and its receptors in the inflammation course of autoimmune arthritis. We used a T cell-mediated experimental autoimmune model adjuvant-induced arthritis (AA) rat to study the profiles of BAFF and its receptors in spleen during the inflammation arthritis induction and the effects of BAFF on DCs functions. In vivo, the levels of BAFF and the expression of BAFF-R, TACI were increased in spleen from very early stage of AA. The lesions of spleen were definite correlated with increased levels of BAFF in homogenization. The mature of DCs and increased number in spleen were mainly at early stage of arthritis. In addition, the levels of Interleukin (IL)-12 were found highest and IL-10 were found lowest at this time too. In vitro recombinant BAFF promoted maturation of DCs and inhibited the phagocytosis of DCs. Under stimulation of BAFF on DCs, the levels of tumor necrosis factor (TNF)-α, IL-6, IL-12 were increased, IL-10 and transforming growth factor (TGF)-β1 were decreased. Moreover, BAFF-treated DCs induced proliferation of CD4(+) T cell. These findings support the crucial pathogenic role of DCs, BAFF, and its receptors in the development of experimental arthritis.

KEYWORDS:

Adjuvant-induced arthritis; B cell activating factor; Dendritic cells; Receptors; Spleen

PMID:
26688104
DOI:
10.1016/j.intimp.2015.12.007
[Indexed for MEDLINE]

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