| First Author | Lory NC | Year | 2021 |
| Journal | Front Immunol | Volume | 12 |
| Pages | 778916 | PubMed ID | 35095852 |
| Mgi Jnum | J:319727 | Mgi Id | MGI:6864831 |
| Doi | 10.3389/fimmu.2021.778916 | Citation | Lory NC, et al. (2021) TRPM2 Is Not Required for T-Cell Activation and Differentiation. Front Immunol 12:778916 |
| abstractText | Antigen recognition by the T-cell receptor induces a cytosolic Ca(2+) signal that is crucial for T-cell function. The Ca(2+) channel TRPM2 (transient receptor potential cation channel subfamily M member 2) has been shown to facilitate influx of extracellular Ca(2+) through the plasma membrane of T cells. Therefore, it was suggested that TRPM2 is involved in T-cell activation and differentiation. However, these results are largely derived from in vitro studies using T-cell lines and non-physiologic means of TRPM2 activation. Thus, the relevance of TRPM2-mediated Ca(2+) signaling in T cells remains unclear. Here, we use TRPM2-deficient mice to investigate the function of TRPM2 in T-cell activation and differentiation. In response to TCR stimulation in vitro, Trpm2 (-/-) and WT CD4(+) and CD8(+) T cells similarly upregulated the early activation markers NUR77, IRF4, and CD69. We also observed regular proliferation of Trpm2 (-/-) CD8(+) T cells and unimpaired differentiation of CD4(+) T cells into Th1, Th17, and Treg cells under specific polarizing conditions. In vivo, Trpm2 (-/-) and WT CD8(+) T cells showed equal specific responses to Listeria monocytogenes after infection of WT and Trpm2 (-/-) mice and after transfer of WT and Trpm2 (-/-) CD8(+) T cells into infected recipients. CD4(+) T-cell responses were investigated in the model of anti-CD3 mAb-induced intestinal inflammation, which allows analysis of Th1, Th17, Treg, and Tr1-cell differentiation. Here again, we detected similar responses of WT and Trpm2 (-/-) CD4(+) T cells. In conclusion, our results argue against a major function of TRPM2 in T-cell activation and differentiation. |
