Buffering Adaptive Immunity by Hydrogen Sulfide

Cells. 2022 Jan 19;11(3):325. doi: 10.3390/cells11030325.

Abstract

T cell-mediated adaptive immunity is designed to respond to non-self antigens and pathogens through the activation and proliferation of various T cell populations. T helper 1 (Th1), Th2, Th17 and Treg cells finely orchestrate cellular responses through a plethora of paracrine and autocrine stimuli that include cytokines, autacoids, and hormones. Hydrogen sulfide (H2S) is one of these mediators able to induce/inhibit immunological responses, playing a role in inflammatory and autoimmune diseases, neurological disorders, asthma, acute pancreatitis, and sepsis. Both endogenous and exogenous H2S modulate numerous important cell signaling pathways. In monocytes, polymorphonuclear, and T cells H2S impacts on activation, survival, proliferation, polarization, adhesion pathways, and modulates cytokine production and sensitivity to chemokines. Here, we offer a comprehensive review on the role of H2S as a natural buffer able to maintain over time a functional balance between Th1, Th2, Th17 and Treg immunological responses.

Keywords: NaHS; cystathionine-lyase; cystathionine-synthase; gasotransmitters; sulphurous waters.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Disease
  • Adaptive Immunity
  • Cystathionine gamma-Lyase / metabolism
  • Humans
  • Hydrogen Sulfide* / metabolism
  • Pancreatitis*

Substances

  • Cystathionine gamma-Lyase
  • Hydrogen Sulfide