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10. Regulatory T-cell dysfunction and cutaneous exposure to Staphylococcus aureus underlie eczema in DOCK8 deficiency

Author

Wilkie, Hazel, Das, Mrinmoy, Pelovitz, Tyler, Bainter, Wayne, Woods, Brian, Alasharee, Mohammed, Sobh, Ali, Baris, Safa, Eltan, Sevgi Bilgic, Al-Herz, Waleed, Barbouche, Mohamed-Ridha, Ben-Mustapha, Imen, Ben-Ali, Meriem, Sallam, Mohamed T.H., Awad, Amany, Lotfy, Sohilla, El Marsafy, Aisha, Ezzelarab, Moushira, Farrar, Michael, Schmidt, Brigitta A.R., NandyMazumdar, Monali, Guttman-Yassky, Emma, Sheets, Anthony, Vidic, Katie Maria, Murphy, George, Schlievert, Patrick M., Chou, Janet, Leyva-Castillo, Juan Manuel, Janssen, Erin, Timilshina, Maheshwor, and Geha, Raif S.

Published
2024
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13. Sclerotic-Type Cutaneous Chronic Graft-Versus-Host Disease Exhibits Activation of T Helper 1 and OX40 Cytokines

Author

Kim, Madeline, Renert-Yuval, Yael, Stepensky, Polina, Even-Or, Ehud, Zaidman, Irina, Fachler, Tahel, Neumark, Michal, Zamir, Mariana, NandyMazumdar, Monali, Gour, Digpal, Facheris, Paola, Carroll, Britta, Liu, Ying, Yu Ekey, Mitchelle L., Andrews, Elizabeth, Meariman, Marguerite, Angelov, Michael, Bose, Swaroop, Estrada, Yeriel D., Molho-Pessach, Vered, and Guttman-Yassky, Emma

Published
2024
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31. Long-Term Efficacy and Safety of Dupilumab in Adolescents with Moderate-to-Severe Atopic Dermatitis: Results Through Week 52 from a Phase III Open-Label Extension Trial (LIBERTY AD PED-OLE)

Author

Blauvelt, Andrew, Guttman-Yassky, Emma, Paller, Amy S., Simpson, Eric L., Cork, Michael J., Weisman, Jamie, Browning, John, Soong, Weily, Sun, Xian, Chen, Zhen, Kosloski, Matthew P., Kamal, Mohamed A., Delevry, Dimittri, Chuang, Chien-Chia, O’Malley, John T., and Bansal, Ashish

Published
2022
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35. Obesity alters pathology and treatment response in inflammatory disease

Author

Bapat, Sagar P., Whitty, Caroline, Mowery, Cody T., Liang, Yuqiong, Yoo, Arum, Jiang, Zewen, Peters, Michael C., Zhang, Ling-juan, Vogel, Ian, Zhou, Carmen, Nguyen, Vinh Q., Li, Zhongmei, Chang, Christina, Zhu, Wandi S., Hastie, Annette T., He, Helen, Ren, Xin, Qiu, Wenli, Gayer, Sarah G., Liu, Chang, Choi, Eun Jung, Fassett, Marlys, Cohen, Jarish N., Sturgill, Jamie L., Crotty Alexander, Laura E., Suh, Jae Myoung, Liddle, Christopher, Atkins, Annette R., Yu, Ruth T., Downes, Michael, Liu, Sihao, Nikolajczyk, Barbara S., Lee, In-Kyu, Guttman-Yassky, Emma, Ansel, K. Mark, Woodruff, Prescott G., Fahy, John V., Sheppard, Dean, Gallo, Richard L., Ye, Chun Jimmie, Evans, Ronald M., Zheng, Ye, and Marson, Alexander

Published
2022
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36. The role of OX40 ligand/OX40 axis signalling in atopic dermatitis.

Author

Guttman-Yassky, Emma, Croft, Michael, Geng, Bob, Rynkiewicz, Natalie, Lucchesi, Davide, Peakman, Mark, Krinks, Cassandra van, Valdecantos, Wendell, Xing, Heming, and Weidinger, Stephan

Subjects
*IMMUNE checkpoint proteins, *CELLULAR recognition, *IMMUNOLOGIC memory, *ATOPIC dermatitis, *T cells
Abstract

Atopic dermatitis (AD) is a heterogeneous inflammatory condition involving multiple immune pathways mediated by pathogenic T cells. OX40 ligand (OX40L) and OX40 are costimulatory immune checkpoint molecules that regulate effector and memory T-cell activity and promote sustained immune responses in multiple immunological pathways, including T helper (Th)2, Th1, Th17 and Th22. As such, OX40L/OX40 signalling between antigen-presenting cells (APCs) and activated T cells postantigen recognition promotes pathogenic T-cell proliferation and survival. Under inflammatory conditions, OX40L is upregulated on APCs, enhancing the magnitude of antigen-specific T-cell responses and secretion of proinflammatory cytokines. In AD, OX40L/OX40 signalling contributes to the amplification and chronic persistence of T-cell-mediated inflammation. Recent therapeutic success in clinical trials has highlighted the importance of the OX40L/OX40 axis as a promising target for the treatment of AD. Here, we discuss the many factors that are involved in the expression of OX40L and OX40, including the cytokine milieu, antigen presentation, the inflammatory environment in AD, and the therapeutic direction influenced by this costimulatory pathway. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Evolution of pathologic B‐cell subsets and serum environment‐specific sIgEs in patients with atopic dermatitis and controls, from infancy to adulthood.

Author

Czarnowicki, Tali, David, Eden, Yamamura, Kazuhiko, Han, Joseph, He, Helen, Pavel, Ana B., Glickman, Jacob, Erickson, Taylor, Estrada, Yeriel, Krueger, James G., Rangel, Stephanie M., Paller, Amy S., and Guttman‐Yassky, Emma

Subjects
PRINCIPAL components analysis, ATOPIC dermatitis, AGE groups, OLDER patients, FLOW cytometry
Abstract

Background: While B‐cells have historically been implicated in allergy development, a growing body of evidence supports their role in atopic dermatitis (AD). B‐cell differentiation across ages in AD, and its relation to disease severity scores, has not been well defined. Objective: To compare the frequency of B‐cell subsets in blood of 0–5, 6–11, 12–17, and ≥18 years old patients with AD versus age‐matched controls. Methods: Flow cytometry was used to measure B‐cell subset frequencies in the blood of 27 infants, 17 children, 11 adolescents, and 31 adults with moderate‐to‐severe AD and age‐matched controls. IgD/CD27 and CD24/CD38 core gating systems and an 11‐color flow cytometry panel were used to determine frequencies of circulating B‐cell subsets. Serum total and allergen‐specific IgE (sIgEs) levels were measured using ImmunoCAP®. Results: Adolescents with AD had lower frequencies of major B‐cells subsets (p <.03). CD23 expression increased with age and was higher in AD compared to controls across all age groups (p <.04). In AD patients, multiple positive correlations were observed between IL‐17‐producing T‐cells and B‐cell subsets, most significantly non‐switched memory (NSM) B‐cells (r =.41, p =.0005). AD severity positively correlated with a list of B‐cell subsets (p <.05). IL‐9 levels gradually increased during childhood, reaching a peak in adolescence, paralleling allergen sensitization, particularly in severe AD. Principal component analysis of the aggregated environmental sIgE data showed that while controls across all ages tightly clustered together, adolescents with AD demonstrated distinct clustering patterns relative to controls. Conclusions: Multiple correlations between B‐cells and T‐cells, as well as disease severity measures, suggest a complex interplay of immune pathways in AD. Unique B‐cell signature during adolescence, with concurrent allergen sensitization and IL‐9 surge, point to a potentially wider window of opportunity to implement interventions that may prevent the progression of the atopic march. [ABSTRACT FROM AUTHOR]

Published
2024
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38. Atopic dermatitis stratification: current and future perspective on skin and blood transcriptomic and proteomic profiling.

Author

Hawkins, Kelly, David, Eden, Glickman, Jacob W, Del Duca, Ester, Guttman-Yassky, Emma, and Krueger, James G

Subjects
IMMUNOGLOBULIN E, ATOPIC dermatitis, TRANSCRIPTOMES, BLOOD testing, DISEASE progression
Abstract

Atopic dermatitis (AD) is a common, chronic inflammatory skin disorder driven by an intricate interplay of genetic, environmental, and immunological factors. As a clinically heterogenous condition, AD may be stratified into subtypes based on factors including, chronicity, immunoglobulin E levels, severity, age, and ethnicity. Transcriptomic and proteomic analyses in skin and blood help elucidate the underlying molecular mechanisms of these AD subtypes, referred to as AD endotypes. Further characterizing AD endotypes using reliable biomarkers can facilitate the development of more effective and personalized therapeutics and improve our tools for monitoring disease progression and therapeutic response across a diverse subset of patients. Here, we aim to provide perspective on the latest research regarding AD stratification using skin and blood-based studies and insight into the implications of these findings on the future of AD research and clinical practice. The precise stratification of AD endotypes will allow for the development of reliable biomarkers and a more personalized medical treatment approach. Clinical practice and trials will eventually be able to bridge clinical with molecular data to optimize individualized treatments and more effectively monitor treatment response. [ABSTRACT FROM AUTHOR]

Published
2024
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39. Efficacy and safety of ritlecitinib in vitiligo patients across Fitzpatrick skin types with biomarker analyses.

Author

Peeva, Elena, Yamaguchi, Yuji, Ye, Zhan, King, Brett, Picardo, Mauro, Sloan, Abigail, Ezzedine, Khaled, Del Duca, Ester, Estrada, Yeriel, Hassan‐Zahraee, Mina, He, Wen, Hyde, Craig, Bar, Johnathan, Facheris, Paola, and Guttman‐Yassky, Emma

Subjects
KINASE inhibitors, VITILIGO, BIOMARKERS, PLACEBOS
Abstract

Efficacy and safety of ritlecitinib (an oral JAK3/TEC family kinase inhibitor) were evaluated in patients with nonsegmental vitiligo (NSV) across Fitzpatrick skin types (FSTs). Patients with FST I‐III ('light skin'; n = 247) and FST IV‐VI ('dark skin'; n = 117) received once‐daily ritlecitinib 50 mg (with/without 4‐week loading dose), low‐dose ritlecitinib or placebo for 24 weeks. At baseline, patients with light skin displayed higher CLM‐1 and NCR1 serum levels than patients with dark skin (p < 0.05). At 24 weeks, ritlecitinib 50 mg improved the extent of depigmentation measured by percent change from baseline in facial‐vitiligo area scoring index (placebo‐adjusted mean difference [90% CI]) in patients with light (−15.2 [−24.7, −5.8]; p = 0.004) and dark (−37.4 [−50.3, −24.4]; p < 0.0001) skin, with continuous re‐pigmentation through week 48. Treatment‐emergent adverse events were similar across FSTs. At weeks 4 and 24, ritlecitinib 50 mg reduced CXCL11 serum levels (p < 0.001) in patients with light skin, whereas patients with dark skin had increased levels at week 4 (p = 0.05) and no significant change at week 24. Ritlecitinib 50 mg decreased IL‐9 and IL‐22 expression levels in dark skin compared with light skin (qPCR; p < 0.05). These differences in immune dysregulations may explain why NSV patients with dark skin respond to therapy earlier than patients with light skin. [ABSTRACT FROM AUTHOR]

Published
2024
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40. Pharmacokinetics and pharmacodynamics of itepekimab in adults with moderate‐to‐severe atopic dermatitis: Results from two terminated phase II trials.

Author

Kosloski, Matthew P., Guttman‐Yassky, Emma, Cork, Michael J., Worm, Margitta, Nahm, Dong‐Ho, Zhu, Xiaoping, Ruddy, Marcella K., Harel, Sivan, Kamal, Mohamed A., Goulaouic, Hélène, Xu, Christine R., Avetisova, Elena, Davis, John D., Nivens, Michael C., Shabbir, Arsalan, and Radin, Allen

Subjects
*CHRONIC obstructive pulmonary disease, *EPITHELIUM, *ATOPIC dermatitis, *EPITHELIAL cells, *DUPILUMAB
Abstract

Interleukin‐33 (IL‐33) is a proinflammatory alarmin cytokine released by damaged epithelial tissue cells that initiates and amplifies both type 1 and type 2 inflammatory cascades. A role for IL‐33 in atopic dermatitis (AD; a chronic, relapsing type 2 inflammatory disease of the skin) has been proposed. Itepekimab is a novel human IgG4P monoclonal antibody against IL‐33, currently in clinical development for chronic obstructive pulmonary disease (COPD). Two global phase II studies—a dose‐ranging itepekimab monotherapy study (NCT03738423) and a proof‐of‐concept study of itepekimab alone and in combination with dupilumab (NCT03736967)—were conducted in patients with moderate‐to‐severe AD to assess safety, tolerability, pharmacokinetics, pharmacodynamics, and efficacy; both studies were terminated following an interim analysis of the proof‐of‐concept study, which failed to demonstrate the efficacy of itepekimab. In these two studies, itepekimab exhibited linear and dose‐proportional pharmacokinetics. Pharmacodynamics of total IL‐33 indicated that itepekimab saturated binding to the target in serum at 300 mg q2w and q4w doses, and decreased blood eosinophil counts. Concentration–time profiles of itepekimab and total IL‐33 were similar for itepekimab with or without dupilumab, and between East Asian and non‐East Asian subgroups. Itepekimab was generally well tolerated, both alone and in combination with dupilumab. The lack of clinical efficacy for itepekimab observed in these studies suggests that IL‐33 may not be a key pathogenic driver in moderate‐to‐severe AD. [ABSTRACT FROM AUTHOR]

Published
2024
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41. Cendakimab in Patients With Moderate to Severe Atopic Dermatitis: A Randomized Clinical Trial.

Author

Blauvelt, Andrew, Guttman-Yassky, Emma, Lynde, Charles, Khattri, Saakshi, Schlessinger, Joel, Imafuku, Shinichi, Tada, Yayoi, Morita, Akimichi, Wiseman, Marni, Kwiek, Bartlomiej, Machkova, Martina, Zhang, Peijin, Linaberry, Misti, Li, Jie, Zhang, Sandra, Franchin, Giovanni, Charles, Edgar D., De Oliveira, Claudia H.M.C., and Silverberg, Jonathan I.

Published
2024
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47. Baricitinib in patients with moderate-to-severe atopic dermatitis: Results from a randomized monotherapy phase 3 trial in the United States and Canada (BREEZE-AD5)

Author

Simpson, Eric L., Forman, Seth, Silverberg, Jonathan I., Zirwas, Matthew, Maverakis, Emanual, Han, George, Guttman-Yassky, Emma, Marnell, Daniel, Bissonnette, Robert, Waibel, Jill, Nunes, Fabio P., DeLozier, Amy M., Angle, Robinette, Gamalo, Margaret, Holzwarth, Katrin, Goldblum, Orin, Zhong, Jinglin, Janes, Jonathan, and Papp, Kim

Published
2021
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50. Dupilumab Improves Asthma and Sinonasal Outcomes in Adults with Moderate to Severe Atopic Dermatitis

Author

Boguniewicz, Mark, Beck, Lisa A., Sher, Lawrence, Guttman-Yassky, Emma, Thaçi, Diamant, Blauvelt, Andrew, Worm, Margitta, Corren, Jonathan, Soong, Weily, Lio, Peter, Rossi, Ana B., Lu, Yufang, Chao, Jingdong, Eckert, Laurent, Gadkari, Abhijit, Hultsch, Thomas, Ruddy, Marcella, Mannent, Leda P., Graham, Neil M.H., Pirozzi, Gianluca, Chen, Zhen, and Ardeleanu, Marius

Published
2021
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