Activation of the adenosine A2A receptor exacerbates experimental autoimmune neuritis in Lewis rats in association with enhanced humoral immunity

• The A2A receptor agonist, CGS21680, exacerbated experimental autoimmune neuritis.
• CGS21680 inhibited lymphocyte proliferation and IL-2 secretion.
• CGS21680 decreased Treg cells, while it increased Tfh cells, B cells and autoantibodies.
• The enhanced humoral immunity induced by CGS21680 possibly related to IL-2 deficiency.

Accumulated evidence demonstrated that Adenosine A2A receptor (A2AR) is involved in the inflammatory diseases. In the present study, we showed that a selective A2AR agonist, CGS21680, exacerbated experimental autoimmune neuritis in Lewis rats induced with bovine peripheral myelin. The exacerbation was accompanied with reduced CD4+ Foxp3+ T cells, increased CD4+ CXCR5+ T cells, B cells, dendritic cells and antigen-specific autoantibodies, which is possibly due to the inhibition of IL-2 induced by CGS21680. Combined with previous studies, our data indicate that the effects of A2AR stimulation in vivo are variable in different diseases. Caution should be taken in the use of A2AR agonists.

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