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The Role of Cutaneous Type I IFNs in Autoimmune and Autoinflammatory Diseases

Jessica L. Turnier and J. Michelle Kahlenberg
J Immunol December 1, 2020, 205 (11) 2941-2950; DOI: https://doi.org/10.4049/jimmunol.2000596
Jessica L. Turnier
*Department of Pediatrics, Division of Rheumatology, University of Michigan, Ann Arbor, MI 48109; and
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J. Michelle Kahlenberg
†Department of Internal Medicine, Division of Rheumatology, University of Michigan, Ann Arbor, MI 48109
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Abstract

IFNs are well known as mediators of the antimicrobial response but also serve as important immunomodulatory cytokines in autoimmune and autoinflammatory diseases. An increasingly critical role for IFNs in evolution of skin inflammation in these patients has been recognized. IFNs are produced not only by infiltrating immune but also resident skin cells, with increased baseline IFN production priming for inflammatory cell activation, immune response amplification, and development of skin lesions. The IFN response differs by cell type and host factors and may be modified by other inflammatory pathway activation specific to individual diseases, leading to differing clinical phenotypes. Understanding the contribution of IFNs to skin and systemic disease pathogenesis is key to development of new therapeutics and improved patient outcomes. In this review, we summarize the immunomodulatory role of IFNs in skin, with a focus on type I, and provide insight into IFN dysregulation in autoimmune and autoinflammatory diseases.

Footnotes

  • This work was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health Award R01-AR071384 (to J.M.K.), the A. Alfred Taubman Medical Research Institute (to J.M.K.), the Parfet Emerging Scholar Award (to J.M.K.), the Rheumatology Research Foundation (to J.M.K.), and the Doris Duke Charitable Foundation through a Physician Scientist Development award (to J.M.K.). J.L.T. was supported by a Eunice Kennedy Shriver National Institute of Child Health and Human Development K12 Child Health Research Center Career Development Award (K12 HD028820-28), a Michigan Institute for Clinical and Health Research Pathway to First Grant Award, and a Cure JM Foundation Research Grant. J.M.K. has received grant support from Celgene/Bristol Myers Squibb and Q32 Bio.

  • Abbreviations used in this article:

    AGS
    Aicardi–Goutières syndrome
    CANDLE
    chronic atypical neutrophilic dermatosis with lipodystrophy and elevated temperature
    cGAS
    cyclic GMP–AMP synthase
    CLASI
    Cutaneous Lupus Erythematosus Disease Area and Severity Index
    CLE
    cutaneous lupus erythematosus
    DAMP
    damage-associated molecular pattern
    DM
    dermatomyositis
    IFNAR
    IFN-α/βR
    IRF
    IFN regulatory factor
    ISG
    IFN-stimulated gene
    JDM
    juvenile DM
    LSc
    localized scleroderma
    MxA
    myxovirus resistance gene A
    PAMP
    pathogen-associated molecular pattern
    pDC
    plasmacytoid dendritic cell
    poly(I:C)
    polyinosinic–polycytidylic acid
    PRR
    pattern recognition receptor
    SAVI
    STING-associated vasculopathy with onset in infancy
    SLE
    systemic lupus erythematosus
    SS
    Sjögren syndrome
    SSc
    systemic sclerosis
    STING
    stimulator of IFN genes
    TYK2
    tyrosine kinase 2.

  • Received May 21, 2020.
  • Accepted August 18, 2020.
  • Copyright © 2020 by The American Association of Immunologists, Inc.
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The Journal of Immunology: 205 (11)
The Journal of Immunology
Vol. 205, Issue 11
1 Dec 2020
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The Role of Cutaneous Type I IFNs in Autoimmune and Autoinflammatory Diseases
Jessica L. Turnier, J. Michelle Kahlenberg
The Journal of Immunology December 1, 2020, 205 (11) 2941-2950; DOI: 10.4049/jimmunol.2000596

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The Role of Cutaneous Type I IFNs in Autoimmune and Autoinflammatory Diseases
Jessica L. Turnier, J. Michelle Kahlenberg
The Journal of Immunology December 1, 2020, 205 (11) 2941-2950; DOI: 10.4049/jimmunol.2000596
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