期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 136, 期 1, 页码 99-106出版社
ELSEVIER SCIENCE INC
DOI: 10.1038/JID.2015.383
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资金
- Japan Society for the Promotion of Science
- Federation of European Biochemical Societies Fellowship
- Wellcome Trust
- MRC
- MRC [MR/L022699/1, G1100073] Funding Source: UKRI
- Medical Research Council [G1100073, MR/L022699/1] Funding Source: researchfish
Mice lacking three epidermal barrier proteins-envoplakin, periplakin, and involucrin (EPI-/- mice)-have a defective cornified layer, reduced epidermal gamma delta T cells, and increased dermal CD4(+) T cells. They are also resistant to developing skin tumors. The tumor-protective mechanism involves signaling between Rae-1 expressing keratinocytes and the natural killer group 2D receptor on immune cells, which also plays a role in host defenses against infection. Given the emerging link between bacteria and cancer, we investigated whether EPI-/- mice have an altered skin microbiota. The bacterial phyla were similar in wild-type and EPI-/- skin. However, bacteria were threefold more abundant in EPI-/- skin and penetrated deeper into the epidermis. The major epithelial defense mechanism against bacteria is production of antimicrobial proteins (AMPs). EPI-/- skin exhibited enhanced expression of antimicrobial peptides. However, reducing the bacterial load by antibiotic treatment or breeding mice under specific pathogen-free conditions did not reduce AMP expression or alleviate the abnormalities in T-cell populations. We conclude that the atopic characteristics of EPI-/- skin are a consequence of the defective barrier rather than a response to the increased bacterial load. It is therefore unlikely that the increase in skin microbiota contributes directly to the observed cancer resistance.
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