| First Author | Di Nardo A | Year | 2023 |
| Journal | Cell Rep | Volume | 42 |
| Issue | 5 | Pages | 112453 |
| PubMed ID | 37120813 | Mgi Jnum | J:351837 |
| Mgi Id | MGI:7485654 | Doi | 10.1016/j.celrep.2023.112453 |
| Citation | Di Nardo A, et al. (2023) Mast cell tolerance in the skin microenvironment to commensal bacteria is controlled by fibroblasts. Cell Rep 42(5):112453 |
| abstractText | Activation and degranulation of mast cells (MCs) is an essential aspect of innate and adaptive immunity. Skin MCs, the most exposed to the external environment, are at risk of quickly degranulating with potentially severe consequences. Here, we define how MCs assume a tolerant phenotype via crosstalk with dermal fibroblasts (dFBs) and how this phenotype reduces unnecessary inflammation when in contact with beneficial commensal bacteria. We explore the interaction of human MCs (HMCs) and dFBs in the human skin microenvironment and test how this interaction controls MC inflammatory response by inhibiting the nuclear factor kappaB (NF-kappaB) pathway. We show that the extracellular matrix hyaluronic acid, as the activator of the regulatory zinc finger (de)ubiquitinating enzyme A20/tumor necrosis factor alpha-induced protein 3 (TNFAIP3), is responsible for the reduced HMC response to commensal bacteria. The role of hyaluronic acid as an anti-inflammatory ligand on MCs opens new avenues for the potential treatment of inflammatory and allergic disorders. |
