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A20-Deficient Mast Cells Exacerbate Inflammatory Responses In Vivo

MPS-Authors
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Heger,  Klaus
Schmidt-Supprian, Marc / Molecular Immunology and Signaltransduction, Max Planck Institute of Biochemistry, Max Planck Society;

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Vahl,  J. Christoph
Schmidt-Supprian, Marc / Molecular Immunology and Signaltransduction, Max Planck Institute of Biochemistry, Max Planck Society;

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Schmidt-Supprian,  Marc
Schmidt-Supprian, Marc / Molecular Immunology and Signaltransduction, Max Planck Institute of Biochemistry, Max Planck Society;

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journal.pbio.1001762.pdf
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Citation

Heger, K., Fierens, K., Vahl, J. C., Aszodi, A., Peschke, K., Schenten, D., et al. (2014). A20-Deficient Mast Cells Exacerbate Inflammatory Responses In Vivo. PLOS BIOLOGY, 12(1): e1001762. doi:10.1371/journal.pbio.1001762.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-DBC6-F
Abstract
Mast cells are implicated in the pathogenesis of inflammatory and autoimmune diseases. However, this notion based on studies in mast cell-deficient mice is controversial. We therefore established an in vivo model for hyperactive mast cells by specifically ablating the NF-kappa B negative feedback regulator A20. While A20 deficiency did not affect mast cell degranulation, it resulted in amplified pro-inflammatory responses downstream of IgE/Fc epsilon RI, TLRs, IL-1R, and IL-33R. As a consequence house dust mite- and IL-33-driven lung inflammation, late phase cutaneous anaphylaxis, and collagen-induced arthritis were aggravated, in contrast to experimental autoimmune encephalomyelitis and immediate anaphylaxis. Our results provide in vivo evidence that hyperactive mast cells can exacerbate inflammatory disorders and define diseases that might benefit from therapeutic intervention with mast cell function.