阿巴塔克普
CD80
CD86
医学
细胞生物学
T细胞
免疫学
B细胞
癌症研究
体外
生物
免疫系统
调节性T细胞
白细胞介素2受体
化学
CD40
细胞毒性T细胞
抗体
生物化学
美罗华
作者
Guillermo Carvajal Alegria,Divi Cornec,Alain Saraux,Valérie Devauchelle‐Pensec,Christophe Jamin,Sophie Hillion,Julien Demoersman,Pierre Pochard
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2021-07-15
卷期号:207 (2): 470-482
被引量:8
标识
DOI:10.4049/jimmunol.2000455
摘要
Abatacept mimics natural CD152 and competes with CD28 for binding to CD80/CD86 on APC, such as B cells, thereby preventing T cell activation. However, its potential impact on B cells has not been identified. The aim of this study was to assess whether abatacept can potentiate the immunoregulatory properties of B cells in vitro and in patients with rheumatoid arthritis (RA). T and B cells from healthy controls were purified. The suppressor properties of B cells in the presence of abatacept or control IgG1 were evaluated based on the ability of these cells to inhibit the polyclonal expansion (anti-CD3/CD28 stimulation) of T cells or their differentiation into Th1 or Th17 cells. Similar analyses were also performed with cells from RA patients before and 3 mo after abatacept initiation. Abatacept significantly potentiated regulatory B cell regulatory functions by enhancing their ability to produce IL-10 and TGF-β, resulting in the increased generation of regulatory T cells and limited T cell proliferation and differentiation into Th1 and Th17 cells. Interestingly, B cells isolated from patients that received a 3-mo treatment with abatacept had an increased ability to reduce T cell functions, confirming the above observations. Abatacept binding to CD80/CD86 induces and promotes regulatory B cell functions by enhancing the ability of these cells to produce IL-10 and TGF-β in vitro and in RA patients.
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