CD11c participates in triggering acute graft-versus-host disease during bone marrow transplantation.

ABSTRACT: CD11c is a canonical dendritic cell (DC) marker with poorly defined functions in the immune system. Here, we found that blocking CD11c on human peripheral blood mononuclear cell-derived DCs (MoDCs) inhibited the proliferation of CD4⁺ T cells and the differentiation into IFN-γ-producing T helper 1 (Th1) cells, which were critical in acute graft-versus-host disease (aGVHD) pathogenesis. Using allogeneic bone marrow transplantation (allo-BMT) murine models, we consistently found that CD11c-deficient recipient mice had alleviated aGVHD symptoms for the decreased IFN-γ-expressing CD4⁺ Th1 cells and CD8⁺ T cells. Transcriptional analysis showed that CD11c participated in several immune regulation functions including maintaining antigen presentation of APCs. CD11c

SUBMITTER: Wang Q 

PROVIDER: S-EPMC8358721 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature