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Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing.
Suárez-Fariñas, Mayte; Ungar, Benjamin; Noda, Shinji; Shroff, Anjali; Mansouri, Yasaman; Fuentes-Duculan, Judilyn; Czernik, Annette; Zheng, Xiuzhong; Estrada, Yeriel D; Xu, Hui; Peng, Xiangyu; Shemer, Avner; Krueger, James G; Lebwohl, Mark G; Guttman-Yassky, Emma.
Affiliation
  • Suárez-Fariñas M; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY; Department of Genetics and Genomics Science, Icahn School of Medicine at Mount Sinai, New York, NY; Icahn Insti
  • Ungar B; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY.
  • Noda S; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY.
  • Shroff A; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY.
  • Mansouri Y; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY.
  • Fuentes-Duculan J; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY.
  • Czernik A; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY.
  • Zheng X; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY.
  • Estrada YD; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY.
  • Xu H; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY.
  • Peng X; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY.
  • Shemer A; Department of Dermatology, Tel-Hashomer, Tel Aviv, Israel.
  • Krueger JG; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY.
  • Lebwohl MG; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY.
  • Guttman-Yassky E; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; Department of Genetics and Genomics Science, Icahn School of Medicine at Mount Sinai, New York, NY; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY; Department of Immunology, Icahn School
J Allergy Clin Immunol ; 136(5): 1277-87, 2015 Nov.
Article in En | MEDLINE | ID: mdl-26316095
BACKGROUND: Alopecia areata (AA) is a common T cell-mediated disorder with limited therapeutics. A molecular profile of cytokine pathways in AA tissues is lacking. Although studies have focused on TH1/IFN-γ responses, several observations support a shared genetic background between AA and atopy. OBJECTIVE: We sought to define the AA scalp transcriptome and associated biomarkers with comparisons with atopic dermatitis (AD) and psoriasis. METHODS: We performed microarray and RT-PCR profiling of 27 lesional and 17 nonlesional scalp samples from patients with AA for comparison with normal scalp samples (n = 6). AA gene expression was also compared with samples from patients with lesional or nonlesional AD and those with psoriasis. A fold change of greater than 1.5 and a false discovery rate of less than 0.05 were used for differentially expressed genes (DEGs). RESULTS: We established the AA transcriptomes (lesional vs nonlesional: 734 DEGs [297 upregulated and 437 downregulated]; lesional vs normal: 4230 DEGs [1980 upregulated and 2250 downregulated]), including many upregulated immune and downregulated hair keratin genes. Equally impressive as upregulation in TH1/interferon markers (IFNG and CXCL10/CXCL9) were those noted in TH2 (IL13, CCL18, CCL26, thymic stromal lymphopoietin, and periostin), TH9/IL-9, IL-23 (p40 and p19), and IL-16 mediators (all P < .05). There were no increases in TH17/TH22 markers. Hair keratin (KRT) expressions (ie, KRT86 and KRT85) were significantly suppressed in lesional skin. Greater scalp involvement (>25%) was associated with greater immune and keratin dysregulation and larger abnormalities in nonlesional scalp samples (ie, CXCL10 and KRT85). CONCLUSIONS: Our data associate the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting consideration of anti-TH2, anti-TH1, and anti-IL-23 targeting strategies. Similar to psoriasis and AD, clinical trials with selective antagonists are required to dissect key pathogenic pathways.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Psoriasis / Th2 Cells / Th1 Cells / Dermatitis, Atopic / Alopecia Areata Limits: Adult / Female / Humans / Male / Middle aged Language: En Journal: J Allergy Clin Immunol Year: 2015 Document type: Article Country of publication: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Psoriasis / Th2 Cells / Th1 Cells / Dermatitis, Atopic / Alopecia Areata Limits: Adult / Female / Humans / Male / Middle aged Language: En Journal: J Allergy Clin Immunol Year: 2015 Document type: Article Country of publication: United States