Adenosine is a purine metabolite that can mediate anti-inflammatory responses in the digestive tract through the A2A adenosine Receptor (A_2AAR). Here we examined the role of this receptor in the control of inflammation in the adoptive transfer model of colitis. Infection of A_2AAR^-/- mice with Helicobacter hepaticus increased colonic inflammation scores compared to uninfected A_2AAR controls. Comparison of T cell subsets in wildtype and A_2AAR^-/- mice revealed differences in markers associated with activated helper T (Th) cells and Treg. Past studies have shown that expression of A_2AAR on CD45RB^HI and CD45RB^LO Th cells is essential for the proper regulation of colonic inflammation. Adoptive transfer of CD45RB^HI with CD45RB^LO from wildtype mice into RAG1^-/-/A_2AAR^-/- mice induced severe disease within 3 weeks, although transfer of the same subsets into RAG1^-/- mice does not induce colitis. This suggests that the presence of A_2AAR on recipient cells is also important for controlling colitis. To investigate the role of A_2AAR on myeloid cells, chimeric recipients were generated by giving RAG1^-/- or RAG1^-/-/A_2AAR^-/- bone marrow to irradiated RAG1^-/- mice. After adoptive transfer, these recipients did not develop colitis regardless of the A_2AAR expression by the donor. Together, our results suggest that the control of inflammation in vivo is dependent on A_2AAR signaling through multiple cell types that collaborate in the regulation of colitis by responding to extracellular adenosine.