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Immunological alterations mediated by adenosine during host-microbial interactions

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Abstract

Adenosine accumulates in inflammation and ischemia but it is more than an end-product of ATP catabolism. Signaling through different receptors with distinct, cell-specific cytoplasmic pathways, adenosine is now recognized as an inducible switch that regulates the immune system. By acting through the A2AAR, adenosine shapes T cell function, largely by conferring an anti-inflammatory tone on effector Th cells (Teff) and natural killer (NK)T cells. In contrast, both the A2AAR and A2BAR are expressed by antigen-presenting cells (APC) which have been shown to regulate innate responses and the transition to adaptive immunity. There is also emerging evidence that adenosine production is one mechanism that allows some pathogens as well as neoplasms to evade host defenses. This review discusses the immunoregulatory functions of adenosine and some of the interactions it may have in regulating host–microbial interactions.

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Abbreviations

AdsA:

Adenosine synthase A

αCD3/CD28:

Anti-CD3/anti-CD28

ADA:

Adenosine deaminase

APC:

Antigen-presenting cells

AR:

Adenosine receptor

DC:

Dendritic cell

KO:

Knock-out

NKT:

Natural killer T cell

TcR:

T cell receptor

Teff:

Effector T cell

Th:

Helper T cell

Thpp:

Primed precursor helper T cell

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Acknowledgments

This work was supported by NIH grants AI 070491 to PBE and IJG and AI 079145 to PBE. DL is supported by T32AI007046.

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Correspondence to Peter B. Ernst.

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Drygiannakis, I., Ernst, P.B., Lowe, D. et al. Immunological alterations mediated by adenosine during host-microbial interactions. Immunol Res 50, 69–77 (2011). https://doi.org/10.1007/s12026-011-8207-0

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