Activation of α7nAChR by nicotine reduced the Th17 response in CD4(+)T lymphocytes

nAChRs play an important role in the regulation and modulation of immune cell proliferation, differentiation, migration and cell-cell interactions. The present study was to characterize the expression of α7nAChR on human peripheral blood mononuclear cells (hPBMC) and CD4(+)T lymphocytes, and to explore the change of Th17 expression after activation of α7nAChR on human CD4(+)T lymphocytes.

A Ficoll gradient was used to separate hPBMC from whole blood, and then CD4(+)T lymphocytes were isolated by magnetic bead separation. The expression of α7nAChR on PBMC and CD4(+)T lymphocytes was analyzed using flow cytometry before and after stimulation with phytohemagglutinin (PHA). The effect of α7nAChR stimulation by nicotine or inhibition by α-bungarotoxin (α-BTX), as well as Th17 expression on the phenotype of CD4(+)T cells was evaluated using flow cytometric analysis.

The percentage of CD4(+)T cells in reduced PBMC, while the expression of α7nAChR increased when cells were stimulated by nicotine. This effect vanished when co-treated with nicotine and α-BTX. α7nAChR was found to expressed in about 90% of CD4(+)T cells. However, α7nAChR expression reduced to 80% on CD4(+)T cells after stimulation with PHA for 24 h. Stimulation of α7nAChR with nicotine increased the expression of Th17 cells, and this upregulation reduced when AChRα7 was inhibited by α-BTX.

α7nAChR was ubiquitously expressed by CD4(+)T lymphocytes, which was correlated with the cell activation status. Meanwhile, activation of nAChRα7 by nicotine in CD4 cells reduced the Th17 response.