Buffering Adaptive Immunity by Hydrogen Sulfide.
Giulia PozziGiuliana GobbiElena MasselliCecilia CarubbiValentina PrestaLuca AmbrosiniMarco VitalePrisco MirandolaPublished in: Cells (2022)
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 (H 2 S) 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 H 2 S modulate numerous important cell signaling pathways. In monocytes, polymorphonuclear, and T cells H 2 S 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 H 2 S as a natural buffer able to maintain over time a functional balance between Th1, Th2, Th17 and Treg immunological responses.
Keyphrases
- signaling pathway
- induced apoptosis
- dendritic cells
- intensive care unit
- single cell
- acute kidney injury
- regulatory t cells
- endoplasmic reticulum stress
- lung function
- epithelial mesenchymal transition
- cell proliferation
- cell death
- septic shock
- mesenchymal stem cells
- staphylococcus aureus
- gram negative
- multidrug resistant
- allergic rhinitis
- genetic diversity