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Levels of anti-inflammatory extracellular adenosine are controlled by the sequential action of the ectonucleotidases CD39 and CD73, whose expression in CD4(+) T cells has been associated with natural regulatory T cells (nTregs). We here show that CD73 expression on activated murine CD4(+) T cells is induced by TGF-β independently of Foxp3 expression, operates at the transcriptional level and translates into gain of functional capacity to generate adenosine. In the presence of AMP, CD73 induced by TGF-β generates adenosine able to suppress proliferation of activated CD4(+) T cells in vitro. These effects are contextual and opposed by proinflammatory cytokines. CD73 is also upregulated by TGF-β in CD8(+) T cells, DCs and macrophages, so providing an amplification mechanism for adenosine generation in tissue microenvironments. Together, these findings expose a novel anti-inflammatory role for TGF-β.

Original publication




Journal article


Eur J Immunol

Publication Date





2955 - 2965


5'-Nucleotidase, Adenosine, Adenosine Monophosphate, Animals, Antigens, CD, Antigens, Surface, Apyrase, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cell Proliferation, Cytokines, Dendritic Cells, Forkhead Transcription Factors, Inflammation Mediators, Leukocytes, Lymphocyte Activation, Macrophages, Mice, Mice, Inbred C57BL, Mice, Transgenic, T-Lymphocytes, Regulatory, Transforming Growth Factor beta