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    <identifier>10.57760/sciencedb.j00217.10894</identifier>
    <datestamp>2025-12-11T10:17:28Z</datestamp>
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  <dc:date>2025-12-11</dc:date>
  <dc:title>Study on the Protective Effect and Mechanism of ERMAP in OXZ-Induced Atopic Dermatitis</dc:title>
  <dc:identifier>doi:10.57760/sciencedb.j00217.10894</dc:identifier>
  <dc:language>en</dc:language>
  <dc:description>Objective The impact of ERMAP (erythrocyte membrane-associated protein) gene deletion on the pathological development of oxazolone (OXA)-induced atopic dermatitis (AD) and its possible mechanism.Methods ERMAP⁻/⁻ mice were generated to establish an OXA-induced AD model and were compared to wild-type mice. Skin lesions were assessed using EASI scores and HE staining; protein levels of Claudin-1, Gata3, CD4, and others were measured by immunofluorescence; mRNA levels of IL-17A, TSLP, and other markers were determined through qRT-PCR; and splenic T cell cytokines and macrophage subpopulations were analyzed via flow cytometry.Results ERMAP deletion significantly increased TSLP in the skin, leading to Th2/Th17 inflammation, worsening immune cell infiltration and skin barrier disruption, and boosting the activation of pro-inflammatory T cells and M2 macrophages in the spleen. This broadly exacerbates both local and systemic inflammation in AD.Conclusion ERMAP is an essential protective factor against OXA-induced AD, and its removal worsens the disease through a TSLP-mediated immune pathway, suggesting that ERMAP could be a new potential target for AD therapy.</dc:description>
  <dc:subject>Atopic dermatitis; Oxazolone; Inflammation; Skin barrier; ERMAP knockout mice</dc:subject>
  <dc:creator>QuXunru</dc:creator>
  <dc:creator>Wang Jiayao</dc:creator>
  <dc:creator>An Yajun</dc:creator>
  <dc:creator>wangzuli</dc:creator>
  <dc:creator>Hu Rong</dc:creator>
  <dc:creator>Su Min</dc:creator>
  <dc:rights>PUBLIC</dc:rights>
  <dc:rights>https://creativecommons.org/publicdomain/zero/1.0/</dc:rights>
  <dc:type>dataset</dc:type>
  <dc:publisher>Science Data Bank</dc:publisher>
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