Open AccessA2B adenosine receptor activation switches differentiation of bone marrow cells to a CD11c + Gr‐1 + dendritic cell subset that promotes the Th17 response
Author(s) -
Liang Dongchun,
Zuo Aijun,
Shao Hui,
Chen Mingjiazi,
Kaplan Henry J.,
Sun Deming
Publication year - 2015
Publication title -
immunity, inflammation and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 18
ISSN - 2050-4527
DOI - 10.1002/iid3.74
Subject(s) - agonist , cd11c , adenosine , bone marrow , dendritic cell , microbiology and biotechnology , t cell , immunology , receptor , medicine , chemistry , endocrinology , biology , immune system , biochemistry , gene , phenotype
Adenosine is one of the major molecules associated with inflammation. We have previously reported that an adenosine receptor (AR) agonist has an enhancing effect on Th17 autoimmune responses, even though it suppressed Th1 responses. To determine the mechanism involved, we have examined the effect of AR agonists on mouse bone marrow dendritic cell (BMDC) differentiation and function. We show that mouse bone marrow cells (BMCs) differentiated into CD11c + Gr‐1 + dentritic cells (DCs) when cultured in granulocyte macrophage colony‐stimulating factor (GM‐CSF)‐containing medium containing an AR agonist. The non‐selective AR agonist NECA and an A2BR‐specific agonist had a similar effect, and the effect of NECA could be blocked by an A2BR‐specific antagonist. Unlike CD11c + Gr‐1 − BMDCs, which have a greater stimulatory effect on Th1 T cells than Th17 cells, CD11c + Gr‐1 + BMDCs had a greater stimulatory effect on Th17 autoreactive T cells than on Th1 autoreactive T cells and this effect depended on γδ T cell activation.