Impaired Function of CD5+CD19+CD1dhi B10 Cells on IgE Secretion in an Atopic Dermatitis-Like Mouse Model

被引：26

作者：

Li, Jieqiong ^{[1
]}

Shen, Chunping ^{[2
]}

Liu, Ying ^{[2
]}

Li, Yunzhu ^{[2
]}

Sun, Lin ^{[1
]}

Jiao, Lei ^{[2
]}

Jiao, Weiwei ^{[1
]}

Xiao, Jing ^{[1
]}

Shen, Chen ^{[1
]}

Qi, Hui ^{[1
]}

Xu, Fang ^{[1
]}

Ma, Lin ^{[2
]}

机构：

[1] Capital Med Univ, Key Lab Major Dis Children,Beijing Childrens Hosp, Beijing Key Lab Pediat Resp Infect Dis,Minist Edu, Natl Key Discipline Pediat,Beijing Pediat Res Ins, Beijing 100045, Peoples R China

[2] Capital Med Univ, Beijing Childrens Hosp, Dept Dermatol, Beijing 100045, Peoples R China

来源：

PLOS ONE | 2015年 / 10卷 / 08期

基金：

北京市自然科学基金;

关键词：

REGULATORY B-CELLS; SUPPRESSIVE ROLE; T-CELLS; AUTOIMMUNITY; INITIATION; TOLERANCE; RESPONSES; PATHWAYS; COLITIS; ROLES;

D O I：

10.1371/journal.pone.0132173

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Atopic dermatitis (AD) is a chronic inflammatory pruritic skin disease in which the pathogenic mechanism is complicated and not completely understood. Reports on the role of regulated cells in AD have recently evolved to regulate B cells, which may play a role in allergic inflammation as well. In the present study, we examined the frequency and regulatory function of CD5(+)CD19(+)CD1d(hi) B10 cells in an AD-like mouse model. Our results showed that the percentage of CD5(+)CD19(+)CD1d(hi) B10 cells increased while the frequency of IL-10-producing B cells in CD19(+)B cells decreased in the mice of AD group. Moreover, no difference in the percentage of B10pro+B10 cells was observed between the AD and control groups. Strikingly, B10 cells from control mice effectively inhibited IgE secretion, whereas the suppressive function of B10 cells from the AD mice was significantly decreased, which was similar to that observed in the group without B10. Altogether, these results suggest that the number of IL-10-producing B cells decreased in the AD group and these cells showed a defective regulatory function on IgE secretion.

引用

页数：11

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