Journal
IMMUNITY
Volume 35, Issue 5, Pages 832-844Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.09.015
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Funding
- ERC [233074]
- DFG [754-2-3]
- SFB 938-project
- Medical Faculty Ulm [ETH 0-20400-07, R01 AR055271]
- European Research Council (ERC) [233074] Funding Source: European Research Council (ERC)
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Immunological functions of mast cells remain poorly understood. Studies in Kit mutant mice suggest key roles for mast cells in certain antibody- and T cell-mediated autoimmune diseases. However, Kit mutations affect multiple cell types of both immune and nonimmune origin. Here, we show that targeted insertion of Cre-recombinase into the mast cell carboxypeptidase A3 locus deleted mast cells in connective and mucosal tissues by a genotoxic Trp53-dependent mechanism. Ore-mediated mast cell eradication (Ore-Master) mice had, with the exception of a lack of mast cells and reduced basophils, a normal immune system. Ore-Master mice were refractory to IgE-mediated anaphylaxis, and this defect was rescued by mast cell reconstitution. This mast cell-deficient strain was fully susceptible to antibody-induced autoimmune arthritis and to experimental autoimmune encephalomyelitis. Differences comparing Kit mutant mast cell deficiency models to selectively mast cell-deficient mice call for a systematic re-evaluation of immunological functions of mast cells beyond allergy.
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