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Psoriasis: HELP
Articles by Benjamin Ungar
Based on 4 articles published since 2008
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Between 2008 and 2019, Benjamin Ungar wrote the following 4 articles about Psoriasis.
 
+ Citations + Abstracts
1 Article Molecular signatures order the potency of topically applied anti-inflammatory drugs in patients with atopic dermatitis. 2017

Guttman-Yassky, Emma / Ungar, Benjamin / Malik, Kunal / Dickstein, Daniel / Suprun, Maria / Estrada, Yeriel D / Xu, Hui / Peng, Xiangyu / Oliva, Margeaux / Todd, Dan / Labuda, Tord / Suarez-Farinas, Mayte / Bissonnette, Robert. ·Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY; Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY. Electronic address: Emma.Guttman@mountsinai.org. · 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. · LEO Pharma A/S, Ballerup, Denmark. · 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 Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY. · Innovaderm Research, Montreal, Quebec, Canada. ·J Allergy Clin Immunol · Pubmed #28238742.

ABSTRACT: BACKGROUND: Atopic dermatitis (AD) presents a large unmet need for treatments with better safety and efficacy. To facilitate development of topical therapeutics, we need an efficient model for assessing different formulations and concentrations. The "plaque model" has been successfully implemented in patients with psoriasis, another common inflammatory disease, to assess the efficacy of topical treatments. This model has not been validated for AD, which has higher placebo responses and less stable lesions than psoriasis. OBJECTIVE: We aimed to assess changes in molecular signatures of intrapatient target lesions treated with topical therapeutics. METHODS: We enrolled 30 patients with mild-to-moderate AD in a randomized, double-blind, intraindividual comparison of 3 approved agents applied blindly at the investigator site daily for 14 days: pimecrolimus, betamethasone dipropionate, clobetasol propionate, and a vehicle/emollient control. Changes in total sign scores (TSSs), transepidermal water loss, and tissue biomarkers (determined by using RT-PCR and immunohistochemistry) were evaluated. RESULTS: TSSs showed improvements of 30%, 40%, 68%, and 76% at 2 weeks with vehicle, pimecrolimus, betamethasone, and clobetasol, respectively, with parallel changes in transepidermal water loss (P < .05). Significant differences versus vehicle values were limited to steroids (P < .0001). Steroids (particularly clobetasol) restored epidermal hyperplasia and terminal differentiation versus minimal changes with vehicle or pimecrolimus (P < .001). Levels of cellular infiltrates and cytokines (IL-13, IL-22, and S100As) were similarly reduced only by steroids (P < .001). TSS improvement correlated with changes in hyperplasia, infiltrates, and differentiation markers. CONCLUSION: We detected significant clinical and tissue differences between agents, providing a novel approach to study the differential effects of topical formulations using a limited sample size.

2 Article An IL-17-dominant immune profile is shared across the major orphan forms of ichthyosis. 2017

Paller, Amy S / Renert-Yuval, Yael / Suprun, Maria / Esaki, Hitokazu / Oliva, Margeaux / Huynh, Thy Nhat / Ungar, Benjamin / Kunjravia, Norma / Friedland, Rivka / Peng, Xiangyu / Zheng, Xiuzhong / Estrada, Yeriel D / Krueger, James G / Choate, Keith A / Suárez-Fariñas, Mayte / Guttman-Yassky, Emma. ·Departments of Dermatology and Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Ill. Electronic address: apaller@northwestern.edu. · 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 Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY. · Departments of Dermatology and Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, Ill. · Laboratory for Investigative Dermatology, Rockefeller University, New York, NY. · Department of Dermatology, Yale University School of Medicine, New Haven, Conn. · 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; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY; Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY. ·J Allergy Clin Immunol · Pubmed #27554821.

ABSTRACT: BACKGROUND: The ichthyoses are rare genetic disorders associated with generalized scaling, erythema, and epidermal barrier impairment. Pathogenesis-based therapy is largely lacking because the underlying molecular basis is poorly understood. OBJECTIVE: We sought to characterize molecularly cutaneous inflammation and its correlation with clinical and barrier characteristics. METHODS: We analyzed biopsy specimens from 21 genotyped patients with ichthyosis (congenital ichthyosiform erythroderma, n = 6; lamellar ichthyosis, n = 7; epidermolytic ichthyosis, n = 5; and Netherton syndrome, n = 3) using immunohistochemistry and RT-PCR and compared them with specimens from healthy control subjects, patients with atopic dermatitis (AD), and patients with psoriasis. Clinical measures included the Ichthyosis Area Severity Index (IASI), which integrates erythema (IASI-E) and scaling (IASI-S); transepidermal water loss; and pruritus. RESULTS: Ichthyosis samples showed increased epidermal hyperplasia (increased thickness and keratin 16 expression) and T-cell and dendritic cell infiltrates. Increases of general inflammatory (IL-2), innate (IL-1β), and some T CONCLUSION: Our data associate a shared T

3 Article The Asian atopic dermatitis phenotype combines features of atopic dermatitis and psoriasis with increased TH17 polarization. 2015

Noda, Shinji / Suárez-Fariñas, Mayte / Ungar, Benjamin / Kim, Soo Jung / de Guzman Strong, Cristina / Xu, Hui / Peng, Xiangyu / Estrada, Yeriel D / Nakajima, Saeko / Honda, Tetsuya / Shin, Jung U / Lee, Hemin / Krueger, James G / Lee, Kwang-Hoon / Kabashima, Kenji / Guttman-Yassky, Emma. ·Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY. · Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY; 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 Institute for Genomics and Multiscale Biology, New York, NY. · Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY. · Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY. · Division of Biology and Biomedical Sciences, Washington University, St Louis, Mo. · Department of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. · Department of Dermatology & Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea. · Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY; Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY. Electronic address: Emma.Guttman@mountsinai.org. ·J Allergy Clin Immunol · Pubmed #26428954.

ABSTRACT: BACKGROUND: Atopic dermatitis (AD) shows very high prevalence in Asia, with a large unmet need for effective therapeutics. Direct comparisons between European American (EA) and Asian patients with AD are unavailable, but earlier blood studies detected increased IL-17(+)-producing cell counts in Asian patients with AD. OBJECTIVE: We sought to characterize the Asian AD skin phenotype and compare it with the EA AD skin phenotype. METHODS: We performed genomic profiling (real-time PCR) and immunohistochemistry on lesional and nonlesional biopsy specimens from 52 patients with AD (25 EAs and 27 Asians), 10 patients with psoriasis (all EAs), and 27 healthy subjects (12 EAs and 15 Asians). RESULTS: Although disease severity/SCORAD scores were similar between the AD groups (58.0 vs 56.7, P = .77), greater acanthosis, higher Ki67 counts, and frequent parakeratosis were characteristics of lesional epidermis from Asian patients with AD (P < .05). Most (24/27) Asian patients had high IgE levels. A principal component analysis using real-time PCR data clustered the Asian AD phenotype between the EA AD and psoriasis phenotypes. TH2 skewing characterized both Asian and EA patients with AD but not patients with psoriasis. Significantly higher TH17 and TH22 (IL17A, IL19, and S100A12 in lesional and IL-22 in nonlesional skin; P < .05) and lower TH1/interferon (CXCL9, CXCL10, MX1, and IFNG in nonlesional skin; P < .05) gene induction typified AD skin in Asian patients. CONCLUSION: The Asian AD phenotype presents (even in the presence of increased IgE levels) a blended phenotype between that of EA patients with AD and those with psoriasis, including increased hyperplasia, parakeratosis, higher TH17 activation, and a strong TH2 component. The relative pathogenic contributions of the TH17 and TH2 axes in creating the Asian AD phenotype need to be tested in future clinical trials with appropriate targeted therapeutics.

4 Article Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing. 2015

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. ·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 Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY. · Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY; Laboratory for Investigative Dermatology, Rockefeller University, New York, NY. · Laboratory for Investigative Dermatology, Rockefeller University, New York, NY. · Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY. · Department of Dermatology, Tel-Hashomer, Tel Aviv, Israel. · 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 of Medicine at Mount Sinai, New York, NY. Electronic address: Emma.Guttman@mountsinai.org. ·J Allergy Clin Immunol · Pubmed #26316095.

ABSTRACT: 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.