2. Academic Validation
  3. Activation of the adenosine A2A receptor exacerbates experimental autoimmune neuritis in Lewis rats in association with enhanced humoral immunity

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

  • J Neuroimmunol. 2016 Apr 15;293:129-136. doi: 10.1016/j.jneuroim.2016.03.002.
Min Zhang 1,  Xiao-Li Li 1,  Heng Li 1,  Shan Wang 1,  Cong-Cong Wang 1,  Long-Tao Yue 2,  Hua Xu 3,  Peng Zhang 1,  Hui Chen 1,  Bing Yang 1,  Rui-Sheng Duan 4
Affiliations

Affiliations

  • 1 Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
  • 2 Central Laboratory, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
  • 3 Department of Neurology, Taian City Central Hospital, Taian 271000, PR China.
  • 4 Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China. Electronic address: [email protected].
PMID: 27049573 DOI: 10.1016/j.jneuroim.2016.03.002
Abstract

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.

Keywords

A(2A) receptor; CGS21680; Experimental autoimmune neuritis.

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