Affiliation:
1. Center for Clinical Laboratory Affiliated Hospital of Guizhou Medical University Guiyang 550004 P. R. China
2. School for Clinical Laboratory Guizhou Medical University Guiyang 550004 P. R. China
3. Department of Health Technology and Informatics Faculty of Health and Social Sciences Hong Kong Polytechnic University Hong Kong P. R. China
4. Department of Microbiology and Immunology Mucosal Immunobiology and Vaccine Research Center Institute of Biomedicine University of Gothenburg Gothenburg Sweden
Abstract
AbstractRodent mast cells can be divided into two major subtypes: the mucosal mast cell (MMC) and the connective tissue mast cell (CTMC). A decade‐old observation revealed a longer lifespan for CTMC compared with MMC. The precise mechanisms underlying such differential tissue persistence of mast cell subsets have not been described. In this study, we have discovered that mast cells expressing only one receptor, either FcγRIIB or FcγRIIIA, underwent caspase‐independent apoptosis in response to IgG immune complex treatment. Lower frequencies of CTMC in mice that lacked either FcγRIIB or FcγRIIIA compared with WT mice were recorded, especially in aged mice. We proposed that this paradigm of FcγR‐mediated mast cell apoptosis could account for the more robust persistence of CTMC, which express both FcγRIIB and FcγRIIIA, than MMC, which express only FcγRIIB. Importantly, we reproduced these results using a mast cell engraftment model, which ruled out possible confounding effects of mast cell recruitment or FcγR expression by other cells on mast cell number regulation. In conclusion, our work has uncovered an FcγR‐dependent mast cell number regulation paradigm that might provide a mechanistic explanation for the long‐observed differential mast cell subset persistence in tissues.
Subject
Immunology,Immunology and Allergy