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Acta Biochim Biophys Sin (Shanghai). 2017 Apr 1;49(4):328-337. doi: 10.1093/abbs/gmx011.

Decreased CD1d level is associated with CD86 over-expression in B cells from systemic lupus erythematosus.

Liu F1, Ji J1, Li X2, Li X1, Xu J1, Yue H1, Zhao S3, Fan H4, Hou Y1,5.

Author information

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

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

PMID:
28338767
DOI:
10.1093/abbs/gmx011
[Indexed for MEDLINE]

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