Characterization of Dendritic Cells and Myeloid-Derived Suppressor Cells Expressing Major Histocompatibility Complex Class II in Secondary Lymphoid Organs in Systemic Lupus Erythematosus-Prone Mice

系统性红斑狼疮易感小鼠次级淋巴器官中表达主要组织相容性复合物 II 类的树突状细胞和髓系抑制细胞的表征

阅读:9
作者:Felipe R Uribe, Fabián González-Martínez, Sebastián A Echeverría-Araya, Alison Sepúlveda-Pontigo, Karissa Chávez-Villacreses, Andrés Díaz-Bozo, Isabel Méndez-Pérez, Valentina P I González, Karen Bohmwald, Alexis M Kalergis, Jorge A Soto

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by self-antibody production and widespread inflammation affecting various body tissues. This disease is driven by the breakdown of immune tolerance, which promotes the activation of autoreactive B and T cells. A key feature of SLE is dysregulation in antigen presentation, where antigen-presenting cells (APCs) play a central role in perpetuating immune responses. Dendritic cells (DCs) are highly specialized for antigen presentation among APCs. At the same time, myeloid-derived suppressor cells (MDSCs) can also express MHC-II molecules, although their role in SLE is less understood. Utilizing the SLE model, MRL/MpJ-Faslpr/J, we determined the presence of different phenotypes of DCs and MDSCs expressing MHC-II in secondary lymphoid organs, along with the gene expression of ICOSL, CD80 and CD86 in the spleen. Our study determined that the most abundant population of APCs in secondary lymphoid organs corresponds to cDC CD103-CD11b+ MHC-II+ throughout SLE development. Additionally, ICOSL expression increased over time, becoming more preponderant in week 16 in the SLE model, which could indicate that it is a crucial pathway for the development and progression of the pathology. In week 16, we observed a positive correlation between M-MDSC MHC-II and IFN-γ-producing CD4+ T cells.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。