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Published in: BMC Immunology 1/2020

Open Access 01-12-2020 | Research article

A regulatory role for CD72 expression on B cells and increased soluble CD72 in primary Sjogren’s syndrome

Authors: Yuqi Shen, Yuhua Ma, Jingyuan Xie, Li Lin, Yifan Shi, Xiao Li, Pingyan Shen, Xiaoxia Pan, Hong Ren

Published in: BMC Immunology | Issue 1/2020

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Abstract

Background

CD72, a co-receptor of B cell receptor (BCR), has been reported to have both positive and negative effects on B cell functions in several immunological diseases. The B cell plays an important role in the pathogenesis of primary Sjogren’s syndrome (pSS). However, whether CD72 is involved in the process remains unknown. This study aimed to observe the possible role of CD72 in the pathogenesis of pSS.

Results

A total of 60 cases who fulfilled the American-European Consensus Group (AECG) criteria for the diagnosis of pSS and 61 gender and age-matched healthy controls were recruited in this study. The percentage of CD72+ B cells was 85.31 ± 8.37% in pSS patients and 76.91 ± 8.50% in healthy controls(p < 0.001). The percentage of CD72+ B cells was correlated to serum IgG levels in patients [β = 0.018(0.001–0.036), p = 0.034]. The level of serum soluble CD72 was significantly higher in pSS patients than the one in healthy controls (0.41 (0.29) vs 0.07 (0.08) ng/mL, p < 0.001).

Conclusions

The percentage of CD72+ B cells was upregulated in pSS patients and was correlated to the serum IgG level, which revealed the hyperactivity of B cells in this disease. The serum soluble CD72 level was also increased in pSS patients. These results indicated a potential role of CD72 in the pathogenesis of pSS.
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Metadata
Title
A regulatory role for CD72 expression on B cells and increased soluble CD72 in primary Sjogren’s syndrome
Authors
Yuqi Shen
Yuhua Ma
Jingyuan Xie
Li Lin
Yifan Shi
Xiao Li
Pingyan Shen
Xiaoxia Pan
Hong Ren
Publication date
01-12-2020
Publisher
BioMed Central
Published in
BMC Immunology / Issue 1/2020
Electronic ISSN: 1471-2172
DOI
https://doi.org/10.1186/s12865-020-00351-2

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