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Adenosine and IFN‐α synergistically increase IFN‐γ production of human NK cells
Author(s) -
Jeffe Florian,
Stegmann Kerstin A.,
Broelsch Felix,
Manns Michael P.,
Cornberg Markus,
Wedemeyer Heiner
Publication year - 2009
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0108046
Subject(s) - biology , adenosine , immune system , adenosine receptor , microbiology and biotechnology , adenosine a3 receptor , effector , receptor , interleukin 12 , immunology , cytotoxic t cell , agonist , endocrinology , biochemistry , in vitro
Prevention of overwhelming immune reactions is essential for an organism to survive. Adenosine, a ribonucleoside produced by various cell types during inflammatory processes, has been shown to inhibit effector functions of different immune cells. Here, we show that the adenosine A 3 receptor agonist iodobenzyl methylcarboxamidoadenosine potently inhibited proliferation, IFN‐γ production, and cytotoxicity of activated human lymphoid cells. Stimulation of the A 3 receptor also caused apoptosis of activated PBMC. However, when PBMC were stimulated with IFN‐α, adenosine did not decrease, but synergistically increased, the IFN‐γ production of NK cells. This effect was also mediated mainly via the A 3 receptor. Thus, our data suggest that adenosine differentially contributes to the regulation of immune responses during inflammatory processes: It may increase effector functions of NK cells in combination with IFN‐α but also prevents overwhelming immune responses by inhibiting proliferation and induction of apoptosis of activated lymphoid cells. Future studies need to define the role of the different adenosine receptors in more detail.