Vol 49 No. 4: 328-337 [PDF] [Full Text]
Decreased CD1d level is associated with CD86 over-expression in B cells from systemic lupus erythematosus
Fei Liu1, Jianjian Ji1, Xiujun Li2, Xiaojing Li1, Jingjing Xu1, Huimin Yue1, Shuli Zhao3, Hongye Fan4,*, and Yayi Hou1,5,*

1State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing 210093, China,
2Department of Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing 210008, China,
3State Key Laboratory of Reproductive Medicine, Central Laboratory of Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China,
4School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China, and
5Jiangsu Key Laboratory of Molecular Medicine, Nanjing 210093, China

Abstract  The disorder of B cells is one of the hallmarks of systemic lupus erythematosus (SLE). The activation state indicated by CD86 of B cells from SLE is well known, while the defect of regulatory B cells mediated by CD1d is also responsible for the process of SLE. In the present study, we focused on the relationship between B cell activation mediated by CD86 and B cell regulatory function mediated by CD1d. Our results showed that the level of CD1d in B cells was decreased during the early stages of B6.MRLlpr SLE mice and imiquimod-treated (IMQ-treated) mice, while the level of CD86 was significantly increased at the late stage. Moreover, the expression of CD1d showed a significantly negative correlation with CD86 level in B cells from IMQ-treated mice (r = −05741; P = 0.0022), B6.MRLlpr mice (r = −0.7091; P = 0.0268), and SLE patients (r = −0.4125; P = 0.0404). The in vivo and in vitro experiments with splenocytes demonstrated that CD1d signaling pathway could inhibit toll-like receptor 7 (TLR7)-induced CD86 expression of B cells. Further studies showed that this relationship also affected antibody production. Thus, our results confirmed the association of CD1d and CD86 levels in B cells from SLE, and demonstrated the importance to preserve the immunoregulatory function of B cells mediated by CD1d in the progression of SLE.


Keywords   systemic lupus erythematosus, B cells, CD1d, CD86, toll-like receptor 7


Received   2016-9-5  


Funding  This work was supported by the grants from the National Natural Science Foundation of China (Nos. 31570909, 91542113, and 81501403) and the Natural Science Foundation for Young Scholars of Jiangsu Province (No. SBK2015041401).


* Correspondence address  Tel/Fax: +86-2583686441; E-mail: yayihou@nju.edu.cn (Y.H.)/changqingshu2004@126.com (H.F.)

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