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FcRI Aggregation Promotes Survival of Connective Tissue-Like Mast Cells but Not Mucosal-Like Mast Cells¹

Maria Ekoff^*, Andreas Strasser and Gunnar Nilsson^2,*

^* Department of Medicine, Clinical Immunology and Allergy Unit, Karolinska Institutet, Stockholm, Sweden; and Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia

Mast cells play a critical role in IgE-dependent immediate hypersensitivity reactions. This is facilitated by their capacity to release inflammatory mediators and to undergo activation-induced survival upon cross-linking of the high-affinity IgE-receptor (FcRI). Due to their heterogeneity, mast cells can be divided into two major groups: the connective tissue mast cells and the mucosal mast cells. We have previously shown that IL-3-dependent bone marrow-derived mast cells can undergo activation-induced survival that is dependent on the prosurvival gene A1. In this study, we have used two different protocols to develop murine connective tissue-like mast cells (CTLMC) and mucosal-like mast cells (MLMC) to investigate their capacity to survive an allergic reaction in vitro. In this study, we demonstrate that FcRI stimulation promotes survival of CTLMC but not MLMC. Similarly, a prominent induction of A1 is observed only in CTLMC but not MLMC. MLMC have a higher basal level of the proapoptotic protein Bim compared with CTLMC. These findings demonstrate a difference among mast cell populations in their ability to undergo activation-induced survival after FcRI stimulation, which might explain the slower turnover of CTMC in IgE-dependent reactions.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Swedish Research Council-Medicine; the Swedish Cancer Foundation, Cancer and Allergy Foundation; Ellen, Walter and Lennart Hesselmans Foundation for Scientific Research; Consul Th C Berghs Foundation; Ollie and Elof Ericsson’s Foundation; and King Gustav V’s 80-year foundation (all from Sweden); the National Health and Medical Research Council (Canberra, Australia, Grant 257502); the JDRF/National Health and Medical Research Council (Australia); the National Cancer Institute (National Institutes of Health Grants CA80188 and CA43540); and the Leukemia and Lymphoma Society of America (Specialized Center of Research Grant 7015).

² Address correspondence and reprint requests to Dr. Gunnar Nilsson, Department of Medicine, Karolinska Institutet, Clinical Immunology and Allergy Unit, KS L2:04, Stockholm, Sweden. E-mail address: gunnar.p.nilsson{at}ki.se

³ Abbreviations used in this paper: SCF, stem cell factor; MC_T, mast cells containing tryptase; MC_TC, MC containing tryptase and chymase; CTMC, connective tissue MC; MMC, mucosal MC; BMMC, bone marrow-derived MC; BH, Bcl-2 homology; wt, wild type; Bim, Bcl-2 interacting mediator of cell death; CTLMC, connective tissue-like MC; MLMC, mucosal-like MC; mMCP, mouse MC protease; RPA, RNase protection assay.

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