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Type I interferons in host defence and inflammatory diseases
Weill Cornell Med Coll, Hosp Special Surg Weill, Mary Kirkland Ctr Lupus Res, New York, NY 10065 USA.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Rheumatology. Uppsala University, Science for Life Laboratory, SciLifeLab.
2019 (English)In: Lupus Science and Medicine, ISSN 2053-8790, E-ISSN 1625-9823, Vol. 6, no 1, article id e000336Article, review/survey (Refereed) Published
Abstract [en]

Type I interferons (IFN) can have dual and opposing roles in immunity, with effects that are beneficial or detrimental to the individual depending on whether IFN pathway activation is transient or sustained. Determinants of IFN production and its functional consequences include the nature of the microbial or nucleic acid stimulus, the type of nucleic acid sensor involved in inducing IFN, the predominant subtype of type I IFN produced and the immune ecology of the tissue at the time of IFN expression. When dysregulated, the type I IFN system drives many autoimmune and non-autoimmune inflammatory diseases, including SLE and the tissue inflammation associated with chronic infection. The type I IFN system may also contribute to outcomes for patients affected by solid cancers or myocardial infarction. Significantly more research is needed to discern the mechanisms of induction and response to type I IFNs across these diseases, and patient endophenotyping may help determine whether the cytokine is acting as 'friend' or 'foe', within a particular patient, and at the time of treatment. This review summarises key concepts and discussions from the second International Summit on Interferons in Inflammatory Diseases, during which expert clinicians and scientists evaluated the evidence for the role of type I IFNs in autoimmune and other inflammatory diseases.

Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2019. Vol. 6, no 1, article id e000336
National Category
Rheumatology and Autoimmunity
Identifiers
URN: urn:nbn:se:uu:diva-390013DOI: 10.1136/lupus-2019-000336ISI: 000471929000016PubMedID: 31205729OAI: oai:DiVA.org:uu-390013DiVA, id: diva2:1340221
Funder
AstraZenecaAvailable from: 2019-08-02 Created: 2019-08-02 Last updated: 2019-08-02Bibliographically approved

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