Interferon‐alpha induced psoriasis in a teenager

Mendieta, Karen L.; Irfan, Mahwish; Faith, Esteban Fernández

doi:10.1111/pde.13418

Cited by 12 publications

(6 citation statements)

References 5 publications

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“…While much less common, other syndromes have also been observed in patients treated with IFNα, including (but not limited to) hypoparathyroidism [89, 90], celiac disease [91–93], myasthenia gravis [94, 95], Guillain-Barré syndrome [94], polymyositis [94], acute and chronic demyelinating polyneuropathy [94], psoriasis [96], vitiligo [97], both psoriasis and vitiligo [98], porphyria cutanea tarda [99], autoimmune hemolysis [100, 101], myositis and polymyositis [102], sarcoidosis [103] and retinal hemorrhage [104].…”

Section: Ifnα In Other Autoimmune Disordersmentioning

confidence: 99%

Interferon alpha: The key trigger of type 1 diabetes

Lombardi

Tsomos

Hammerstad

et al. 2018

Journal of Autoimmunity

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IFNα is a cytokine essential to a vast array of immunologic processes. Its induction early in the innate immune response provides a priming mechanism that orchestrates numerous subsequent pathways in innate and adaptive immunity. Despite its beneficial effects in viral infections IFNα has been reported to be associated with several autoimmune diseases including autoimmune thyroid disease, systemic lupus erythematosus, rheumatoid arthritis, primary biliary cholangitis, and recently emerged as a major cytokine that triggers Type 1 Diabetes. In this review, we dissect the role of IFNα in T1D, focusing on the potential pathophysiological mechanisms involved. Evidence from human and mouse studies indicates that IFNα plays a key role in enhancing islet expression of HLA-I in patients with T1D, thereby increasing autoantigen presentation and beta cell activation of autoreactive cytotoxic CD8 T-lymphocytes. The binding of IFNα to its receptor induces the secretion of chemokines, attracting monocytes, T lymphocytes, and NK cells to the infected tissue triggering autoimmunity in susceptible individuals. Furthermore, IFNα impairs insulin production through the induction of endoplasmic reticulum stress as well as by impairing mitochondrial function. Due to its central role in the early phases of beta cell death, targeting IFNα and its pathways in genetically predisposed individuals may represent a potential novel therapeutic strategy in the very early stages of T1D.

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Section: Ifnα In Other Autoimmune Disordersmentioning

confidence: 99%

Interferon alpha: The key trigger of type 1 diabetes

Lombardi

Tsomos

Hammerstad

et al. 2018

Journal of Autoimmunity

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“…The factors that provoke psoriasis development and worsen its clinical course include lymphoid periopharyngeal ring streptococcal infection, psychological stress, smoking, excessive alcohol consumption, use of certain medications (β-adrenergic blocking agents, α-interferon, aminoquinolines, etc.) [10][11][12].…”

Section: Underlying Risk For Disease Developmentmentioning

confidence: 99%

New aspects of the pathogenesis of psoriasis

Жуков¹,

Патрушев²,

Хайрутдинов³

et al. 2022

Vestnik dermatologii i venerologii

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Psoriasis is a chronic multi-factorial immune-mediated inflammatory disease of skin and joints. The variety of clinical forms of dermatosis is consistent with various pathogenetic features of the disease progress which have been significantly supplemented and reviewed recently. Knowledge of these mechanisms will improve and personalize the prescribed therapy. This study places the emphasis on modern ideas about the formation of T cell memory, the role of melanocytes and innate lymphoid cells. Development mechanisms of guttate and paradoxical psoriasis with important distinguishing characteristics are described separately. Today, knowledge of the molecular basis of the disease progression has led to the creation and introduction of a number of highly effective targeted drugs into clinical practice. Further developments related to the inhibition of resident memory cells, innate lymphoid cells, as well as the study of guttate psoriasis perpetuation and the occurrence of paradoxical psoriasis will significantly increase the effectiveness of the therapy.

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“…These findings indicate that the innate immune system driven by pDC-derived type I IFN may play a crucial role in paradoxical psoriasis. IFN-α therapy for hepatitis C can also induce an exacerbation of preexisting psoriasis or the development of new-onset psoriasis, but this can be resolved by the discontinuation of therapy 61 , 67 , 68 . Psoriatic lesions can also be induced by the application of topical imiquimod and may be related to the overexpression of IFN-α 69 .…”

Section: Type I Ifn Signature and Psoriasismentioning

confidence: 99%

Role of interferon regulatory factor-mediated signaling in psoriasis

2021

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Psoriasis is a chronic inflammatory disease that involves both the innate and adaptive immune systems. Type I interferons (IFNs), the production of which is partially regulated by toll-like receptors (TLRs), play an important role in the pathogenesis of psoriasis, especially psoriasis caused by skin trauma, known as the Koebner phenomenon. IFN regulatory factors (IRFs) function in both innate and adaptive immune responses, and their effect is associated with the regulation of type I IFNs. In this review, we focus on recent advances in understanding the expression of TLRs, IRFs, and type I IFNs in psoriasis. We also highlight the interplay among TLRs, IRFs, and type I IFNs.

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Interferon‐alpha induced psoriasis in a teenager

Cited by 12 publications

References 5 publications

Interferon alpha: The key trigger of type 1 diabetes

Interferon alpha: The key trigger of type 1 diabetes

New aspects of the pathogenesis of psoriasis

Role of interferon regulatory factor-mediated signaling in psoriasis

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