Cutting edge: Adenosine a2a receptor signals inhibit germinal center T follicular helper cell differentiation during the primary response to vaccination

Shirdi E. Schmiel, Jessica A. Yang, Marc K. Jenkins, Daniel L. Mueller

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Adenosine A2a receptor (A2aR) signaling acts as a barrier to autoimmunity by promoting anergy, inducing regulatory T cells, and inhibiting effector T cells. However, in vivo effects of A2aR signaling on polyclonal CD4 T cells during a primary response to foreign Ag has yet to be determined. To address this problem, we immunized mice with peptide Ag 2W1S coupled to PE in CFA and treated with the selective A2aR agonist CGS-21680 (CGS). 2W1S:I-Ab-specific tetramerbinding CD4 T cells did not become anergic or differentiate into Foxp3+ regulatory T cells. Additionally, CGS treatment did not inhibit Th1 or Th17 differentiation. However, CGS did abrogate germinal center T follicular helper cells, and blunted PE-specific germinal center B cell responses. The use of A2aRdeficient CD4 T cells established that this CGS effect was T cell intrinsic. Therefore, this study has identified a unique role for A2aRs in regulating CD4 T cell differentiation during vaccination.

Original languageEnglish (US)
Pages (from-to)623-628
Number of pages6
JournalJournal of Immunology
Volume198
Issue number2
DOIs
StatePublished - Jan 15 2017

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