Journal
IMMUNITY
Volume 34, Issue 6, Pages 973-984Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2011.03.028
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Funding
- German Research Council (DFG) [Ro2133/2, Ro2133/3, Ro2133/4, 1394, CRC/SFB832, A14, Du1172/1, Du1172/2, 1468]
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A prominent feature of sensitizing environmental compounds that cause allergic contact dermatitis is the rapid induction of an innate inflammatory response that seems to provide danger signals for efficient T cell priming. We generated mouse models of mast cell deficiency, mast cell-specific gene inactivation, and mast cell reporter mice for intravital imaging and showed that these adjuvant effects of contact allergens are mediated by mast cells and histamine. Mast cell deficiency resulted in impaired emigration of skin DCs to the lymph node and contact hypersensitivity was dramatically reduced in the absence of mast cells. In addition, mast cell-specific inactivation of the II10 gene did not reveal any role for mast cell-derived IL-10 in the regulation of contact allergy. Collectively, we demonstrate that mast cells are essential promoters of contact hypersensitivity, thereby highlighting their potential to promote immune responses to antigens entering via the skin.
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