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Mol Cell Neurosci. 2016 Jul;74:106-13. doi: 10.1016/j.mcn.2016.05.001. Epub 2016 May 7.

ROCK inhibitor abolishes the antibody response in experimental autoimmune myasthenia gravis.

Author information

1
Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
2
Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
3
Department of Neurology, Jinan General Military Hospital, Second Military Medical University, Jinan 250031, PR China.
4
College of Basic Medical Sciences, Shandong University of Traditional Chinese Medicine, Jinan 250355, PR China.
5
Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China. Electronic address: ruisheng_duan@yahoo.com.

Abstract

The Rho/Rho kinase (ROCK) pathway serves as molecular switches in many biological processes including the immune response. ROCK inhibitors lead to amelioration of some autoimmune diseases. The present study was designed to define whether a selective ROCK inhibitor, fasudil, was effective in experimental autoimmune myasthenia gravis (EAMG) and investigate the underlying mechanisms. Here we found fasudil effectively attenuated the development of ongoing EAMG. Fasudil abolished the antibody production and function by decreasing follicular helper T cells and CD19(+) B cells, especially germinal center B cells. Moreover, fasudil reduced the expression of CD80 on lymph node mononuclear cells. These findings suggest the inhibition of ROCK might be a potential therapeutic strategy for antibody-mediated autoimmune diseases.

KEYWORDS:

Antibody; Experimental autoimmune myasthenia gravis; Follicular helper T cells; Germinal center; Rho kinase inhibitor

PMID:
27168379
DOI:
10.1016/j.mcn.2016.05.001
[Indexed for MEDLINE]

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