Journal
SCIENCE
Volume 334, Issue 6060, Pages 1293-1297Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1211250
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Funding
- Wellcome Trust
- National Institute of Health Research cBRC
- Croatian Ministry of Science, Education and Sports [062-0621261-1271]
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Epithelial cells respond to physicochemical damage with up-regulation of major histocompatibility complex-like ligands that can activate the cytolytic potential of neighboring intraepithelial T cells by binding the activating receptor, NKG2D. The systemic implications of this lymphoid stress-surveillance response, however, are unknown. We found that antigens encountered at the same time as cutaneous epithelial stress induced strong primary and secondary systemic, T helper 2 (T(H)2)-associated atopic responses in mice. These responses required NKG2D-dependent communication between dysregulated epithelial cells and tissue-associated lymphoid cells. These data are germane to uncertainty over the afferent induction of T(H)2 responses and provide a molecular framework for considering atopy as an important component of the response to tissue damage and carcinogenesis.
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