Type I interferons in host defence and inflammatory diseases

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 mic...

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Published inLupus science & medicine Vol. 6; no. 1; p. e000336
Main Authors Crow, Mary K., Ronnblom, Lars
Format Journal Article
LanguageEnglish
Published England Lupus Foundation of America 01.01.2019
BMJ Publishing Group LTD
BMJ Publishing Group
Subjects
Antigens
Apoptosis
Arthritis
Autoimmune diseases
Cytokines
Dendritic cells
Deoxyribonucleic acid
Disease
DNA
Inflammatory diseases
Interferon
Kinases
Lupus
Lymphocytes
Mitochondrial DNA
Pathogenesis
Patients
Review
Sensors
systemic lupus erythematosus
Tumor necrosis factor-TNF
Viral infections
autoimmune diseases
interferon
systemic lupus erythematosus
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Abstract 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.
AbstractList 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.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.
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.
Author Ronnblom, Lars
Crow, Mary K.
AuthorAffiliation 2 Section of Rheumatology, Science for Life Laboratory, Department of Medical Sciences , Uppsala University , Uppsala , Sweden
1 Mary Kirkland Center for Lupus Research , Hospital for Special Surgery, Weill Cornell Medical College , New York City , New York , USA
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Issue 1
Keywords autoimmune diseases
interferon
systemic lupus erythematosus
Language English
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OpenAccessLink http://dx.doi.org/10.1136/lupus-2019-000336
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  day: 01
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PublicationTitle Lupus science & medicine
PublicationTitleAbbrev Lupus Sci Med
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Publisher Lupus Foundation of America
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Aman (2024111101252129000_6.1.e000336.137) 1996; 87
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Li (2024111101252129000_6.1.e000336.119) 2014; 10
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Carmona (2024111101252129000_6.1.e000336.97) 2013; 8
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Nabet (2024111101252129000_6.1.e000336.126) 2017; 170
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2024111101252129000_6.1.e000336.11
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Snippet 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...
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StartPage e000336
SubjectTerms Antigens
Apoptosis
Arthritis
Autoimmune diseases
Cytokines
Dendritic cells
Deoxyribonucleic acid
Disease
DNA
Inflammatory diseases
Interferon
Kinases
Lupus
Lymphocytes
Mitochondrial DNA
Pathogenesis
Patients
Review
Sensors
systemic lupus erythematosus
Tumor necrosis factor-TNF
Viral infections
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Title Type I interferons in host defence and inflammatory diseases
URI https://lupus.bmj.com/content/6/1/e000336.full
https://www.ncbi.nlm.nih.gov/pubmed/31205729
https://www.proquest.com/docview/2231784852
https://www.proquest.com/docview/2242187558
https://pubmed.ncbi.nlm.nih.gov/PMC6541752
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-390013
https://doaj.org/article/5d8ac73f37c14d5581ef6414db4cbe6b
Volume 6
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