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Mechanical injury by tape stripping causes Th2 responses in mice
Author(s) -
Oyoshi Michiko K,
Geha Raif S
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.670.4
Subject(s) - immunology , scratching , cytokine , sensitization , medicine , secretion , cd11c , t cell , immune system , chemistry , endocrinology , materials science , phenotype , biochemistry , composite material , gene
Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental allergens. In AD, skin injury caused by scratching and subsequent entry of antigen in the skin is critical to disease development. We hypothesize that DCs that emigrate from mechanically injured skin polarize the T cell response towards Th2. We used the hapten FITC as a marker to isolate DCs that have recently migrated from skin to draining lymph node (DLN). FITC was applied to shaved and tape‐stripped mouse skin, a surrogate for scratching, or to shaved skin without tape stripping. After 24 hrs, CD11cFITC hi cells were enumerated in DLN, and examined for their capacity to cause proliferation and cytokine secretion in T cells. In each of the two groups CD11c + FITC + constituted ~10% of DCs in DLNs and supported comparable proliferation of naïve DO11.10 CD4 + T cells to OVA 323–339 peptide. In contrast, FITC + DCs from DLN of shaved/stripped skin induced significantly greater secretion of the Th2 cytokines IL‐4, IL‐5, IL‐13 and IL‐10, and less production of the Th1 cytokine IFN‐γ. IL‐10 is released in skin following mechanical injury. FITC + DCs from DLN of IL‐10 −/− mice were impaired in their ability to support Th2 cytokine secretion, consistent with our previous finding that the Th2 response to EC sensitization was impaired in these mice J Clin Invest. 114:399–407, 2004). The results demonstrate that mechanical skin injury polarizes skin DCs to support Th2 differentiation of naïve T cells; this is in part dependent on IL‐10.