Do KATP channels have a role in immunity?

Front Immunol. 2024 Nov 28:15:1484971. doi: 10.3389/fimmu.2024.1484971. eCollection 2024.

Abstract

Ion channels, exchangers and pumps are expressed ubiquitously in cells from all phyla of life. In mammals, their role is best described in excitable cells, where they regulate the initiation and propagation of action potentials. There are over 70 different types of K+ channels subunits that contribute to these processes. In non-excitable cells, K+ channels set the resting membrane potential, which in turn drives the activity of other translocators. K+ channels also help maintain cell volume, influence cell proliferation and apoptosis and regulate Ca2+ signaling, which in turn is crucial for many cellular processes, including metabolism, secretion, and gene expression. K+ channels play crucial roles in the activation, proliferation and a variety of other functions in cells of the innate and adaptive immune system. The ATP-sensitive K+ (KATP) channel has an established role in diverse cells, but its presence and function in immunity is scantly described. Public gene expression databases show that KATP channel subunits are highly expressed in NKT and NK cells, and that they are significantly upregulated after infection in CD8+ T cells and macrophages. We discuss these findings in the light of the available literature and propose a role for KATP channels in cytotoxicity of cells that are primed for a rapid immune response. Possible underlying molecular mechanisms are discussed.

Keywords: CD8+ T lymphocyte subsets; K+; KATP channels; NK cells; cytotoxic lymphocyte; immunity; ion channels.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • KATP Channels* / genetics
  • KATP Channels* / metabolism
  • Killer Cells, Natural / immunology
  • Killer Cells, Natural / metabolism
  • Macrophages / immunology
  • Macrophages / metabolism

Substances

  • KATP Channels

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by National Institutes of Health grants R01HL146514 and 1R01HL148609 to WC, R01 AI097302, R01 AI130143, and R01 DE027981 to SF, R03 TR004157 and R03 TR004459 to WC and SF and Wellcome Trust grant 200841/Z/16/Z to FC.