دورية أكاديمية
أعرض في EDS

IL-23 induces CLEC5A + IL-17A + neutrophils and elicit skin inflammation associated with psoriatic arthritis.

التفاصيل البيبلوغرافية
العنوان: IL-23 induces CLEC5A + IL-17A + neutrophils and elicit skin inflammation associated with psoriatic arthritis.
المؤلفون: Furuya H; Department of Rheumatology and Clinical Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA., Nguyen CT; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, USA., Chan T; Department of Computer Science, University of California, Davis, CA, USA; Genome Center, University of California, Davis, CA, USA., Marusina AI; Department of Dermatology, University of California, Davis, Sacramento, USA., Merleev AA; Department of Dermatology, University of California, Davis, Sacramento, USA., Garcia-Hernandez ML; Division of Allergy, Immunology & Rheumatology, University of Rochester Medical School, NY, USA., Hsieh SL; Genomics Research Center, Academia Sinica, Nankang, Taipei, Taiwan., Tsokos GC; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, USA., Ritchlin CT; Division of Allergy, Immunology & Rheumatology, University of Rochester Medical School, NY, USA., Tagkopoulos I; Department of Computer Science, University of California, Davis, CA, USA; Process Integration and Predictive Analytics, PIPA LLC, CA, USA., Maverakis E; Department of Dermatology, University of California, Davis, Sacramento, USA., Adamopoulos IE; Department of Rheumatology and Clinical Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, USA. Electronic address: Iadamopo@bidmc.harvard.edu.
المصدر: Journal of autoimmunity [J Autoimmun] 2024 Feb; Vol. 143, pp. 103167. Date of Electronic Publication: 2024 Feb 01.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Academic Press Country of Publication: England NLM ID: 8812164 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1095-9157 (Electronic) Linking ISSN: 08968411 NLM ISO Abbreviation: J Autoimmun Subsets: MEDLINE
أسماء مطبوعة: Publication: London : Academic Press
Original Publication: London ; San Diego : Academic Press, c1988-
مواضيع طبية MeSH: Arthritis, Psoriatic*/pathology , Psoriasis* , Dermatitis*/pathology, Humans ; Interleukin-17/genetics ; Interleukin-17/metabolism ; Neutrophils/metabolism ; Skin/pathology ; Inflammation ; Interleukin-23/genetics ; Interleukin-23/metabolism ; Receptors, Cell Surface/metabolism ; Lectins, C-Type/genetics
مستخلص: IL-23-activation of IL-17 producing T cells is involved in many rheumatic diseases. Herein, we investigate the role of IL-23 in the activation of myeloid cell subsets that contribute to skin inflammation in mice and man. IL-23 gene transfer in WT, IL-23R GFP reporter mice and subsequent analysis with spectral cytometry show that IL-23 regulates early innate immune events by inducing the expansion of a myeloid MDL1 + CD11b + Ly6G + population that dictates epidermal hyperplasia, acanthosis, and parakeratosis; hallmark pathologic features of psoriasis. Genetic ablation of MDL-1, a major PU.1 transcriptional target during myeloid differentiation exclusively expressed in myeloid cells, completely prevents IL-23-pathology. Moreover, we show that IL-23-induced myeloid subsets are also capable of producing IL-17A and IL-23R + MDL1 + cells are present in the involved skin of psoriasis patients and gene expression correlations between IL-23 and MDL-1 have been validated in multiple patient cohorts. Collectively, our data demonstrate a novel role of IL-23 in MDL-1-myelopoiesis that is responsible for skin inflammation and related pathologies. Our data open a new avenue of investigations regarding the role of IL-23 in the activation of myeloid immunoreceptors and their role in autoimmunity.
Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
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معلومات مُعتمدة: R01 AR062173 United States AR NIAMS NIH HHS
فهرسة مساهمة: Keywords: Arthritis; Autoimmune diseases; Autoimmunity; Inflammation; Psoriatic
المشرفين على المادة: 0 (Interleukin-17)
0 (Interleukin-23)
0 (CLEC5A protein, human)
0 (Receptors, Cell Surface)
0 (Lectins, C-Type)
تواريخ الأحداث: Date Created: 20240201 Date Completed: 20240401 Latest Revision: 20240506
رمز التحديث: 20240506
مُعرف محوري في PubMed: PMC10981569
DOI: 10.1016/j.jaut.2024.103167
PMID: 38301504
قاعدة البيانات: MEDLINE
الوصف
تدمد:1095-9157
DOI:10.1016/j.jaut.2024.103167