Further, pharmacological blocking of the A2A adenosine receptor, the down-stream target of the liberated adenosine, also did not reverse the immunomodulatory activity of the Lr-CFS, suggesting that these receptors, although potentially important in certain microbe-host interactions, are not involved in the effects of the Lr-CFS on IEC. This evidence concerns the gene ADORA2A and myalgic encephalomeyelitis/chronic fatigue syndrome.