In vitro induction of T cells that are resistant to A2 adenosine receptor-mediated immunosuppression

Br J Pharmacol. 2009 Jan;156(2):297-306. doi: 10.1111/j.1476-5381.2008.00019.x. Epub 2008 Dec 9.

Abstract

Background and purpose: The increased levels of extracellular adenosine in inflamed tissues down-regulate activated immune cells via the A(2A) adenosine receptor. This A(2A) adenosine receptor-mediated immunosuppression is a disqualifying obstacle in cancer immunotherapy as it protects cancerous tissues from adoptively transferred anti-tumour T cells. The aim of this study was to test whether the negative selection of T cells will produce T cells that are resistant to inhibition by extracellular adenosine.

Experimental approach: Cytotoxic T lymphocytes (CTL) were developed by mixed lymphocyte culture in the presence or absence of the adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA). The sensitivity of CTL to adenosine analogues was characterized by cAMP induction, interferon-gamma production and cytotoxicity.

Key results: CTL that could proliferate even in the presence of NECA were less susceptible to inhibition by A(2A) adenosine receptor agonists, as shown by a much smaller accumulation of cAMP and less inhibition of interferon-gamma production compared with control CTL. The successful protocol to produce CTL that are both resistant to adenosine-mediated immunosuppression and maintain strong cytotoxicity and interferon-gamma secretion required NECA to be added only during the expansion stage after the establishment of CTL. In contrast, the priming of resting T cells in the presence of NECA resulted in T cells with impaired effector functions.

Conclusions and implications: Adenosine-resistant effector T cells were successfully obtained by exposure of activated T cells to NECA. These in vitro studies form the basis for future attempts to produce anti-tumour T cells that are more effective in adoptive immunotherapy.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adenosine / metabolism
  • Adenosine A2 Receptor Agonists
  • Adenosine-5'-(N-ethylcarboxamide) / pharmacology
  • Animals
  • Cell Line, Tumor
  • Cyclic AMP / biosynthesis
  • Cytotoxicity, Immunologic
  • Extracellular Space / metabolism
  • Immune Tolerance* / drug effects
  • Interferon-gamma / biosynthesis
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred DBA
  • Receptor, Adenosine A2A / physiology*
  • Receptor, Adenosine A2B / physiology*
  • T-Lymphocytes, Cytotoxic / cytology*
  • T-Lymphocytes, Cytotoxic / drug effects
  • T-Lymphocytes, Cytotoxic / immunology

Substances

  • Adenosine A2 Receptor Agonists
  • Receptor, Adenosine A2A
  • Receptor, Adenosine A2B
  • Adenosine-5'-(N-ethylcarboxamide)
  • Interferon-gamma
  • Cyclic AMP
  • Adenosine