| First Author | Erdogmus S | Year | 2022 |
| Journal | Nat Commun | Volume | 13 |
| Issue | 1 | Pages | 2033 |
| PubMed ID | 35440113 | Mgi Jnum | J:324618 |
| Mgi Id | MGI:7265937 | Doi | 10.1038/s41467-022-29725-3 |
| Citation | Erdogmus S, et al. (2022) Cavbeta1 regulates T cell expansion and apoptosis independently of voltage-gated Ca(2+) channel function. Nat Commun 13(1):2033 |
| abstractText | TCR stimulation triggers Ca(2+) signals that are critical for T cell function and immunity. Several pore-forming alpha and auxiliary beta subunits of voltage-gated Ca(2+) channels (VGCC) were reported in T cells, but their mechanism of activation remains elusive and their contribution to Ca(2+) signaling in T cells is controversial. We here identify CaVbeta1, encoded by Cacnb1, as a regulator of T cell function. Cacnb1 deletion enhances apoptosis and impairs the clonal expansion of T cells after lymphocytic choriomeningitis virus (LCMV) infection. By contrast, Cacnb1 is dispensable for T cell proliferation, cytokine production and Ca(2+) signaling. Using patch clamp electrophysiology and Ca(2+) recordings, we are unable to detect voltage-gated Ca(2+) currents or Ca(2+) influx in human and mouse T cells upon depolarization with or without prior TCR stimulation. mRNAs of several VGCC alpha1 subunits are detectable in human (CaV3.3, CaV3.2) and mouse (CaV2.1) T cells, but they lack transcription of many 5' exons, likely resulting in N-terminally truncated and non-functional proteins. Our findings demonstrate that although CaVbeta1 regulates T cell function, these effects are independent of VGCC channel activity. |
