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Cited by 47Multiple Sclerosis Research Studiesinterferon and immune responsesPsoriasis: Treatment and Pathogenesis

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Janus‐like effects of type I interferon in autoimmune diseases

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Axtell, Robert C., Raman, Chander·2012·Immunological Reviews
DOI 10.1111/j.1600-065x.2012.01131.xPMC PMC3383665
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Abstract

Summary: In multiple sclerosis, type I interferon (IFN) is considered immune‐modulatory, and recombinant forms of IFN‐β are the most prescribed treatment for this disease. This is in contrast to most other autoimmune disorders, because type I IFN contributes to the pathologies. Even within the relapsing‐remitting multiple sclerosis (RRMS) population, 30–50% of MS patients are non‐responsive to this treatment, and it consistently worsens neuromyelitis optica, a disease similar to RRMS. In this article, we discuss the recent advances in the field of autoimmunity and introduce the theory explain how type I IFNs can be pro‐inflammatory in disease that is predominantly driven by a Th17 response and are therapeutic when disease is predominantly Th1.

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  • The long-term persistence of (re-)activatable autoantigen-specific ThEx cells in patients in remission may well explain the less-than-perfect treatment efficacy of steroid-sparing agents, depletion of CD19/CD20 memory B cells, as well as exacerbation of disease by b-IFN.

    “In any case, the long-term persistence of (re-)activatable autoantigen-specific ThEx cells in patients in remission may well explain the less-than-perfect treatment efficacy of steroid-sparing agents, 64-67 depletion of CD19/CD20 memory B cells, 68,69 as well as exacerbation of disease by b -IFN. 27,70”

    From Autoantigen-specific CD4+ T cells acquire an exhausted phenotype and persist in human antigen-specific autoimmune diseases (2024) · cites this paper as [70]

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Metadata

Authors
Axtell, R. C., & Raman, C.
Affiliations
  • Stanford University (US)
  • University of Alabama at Birmingham (US)
Corresponding author
Axtell, Robert C.
ORCID
Venue
Immunological Reviews
Publisher
Wiley
Published
2012-06-21
Volume
248
Issue
1
Pages
23-35
ISSN
  • 0105-2896 (ISSN-L)
  • 1600-065X
DOI
10.1111/j.1600-065x.2012.01131.x
PMC
PMC3383665
OpenAlex
W2101777577
Cited by
47
References
3
Citations by year
2025: 1 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 5 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 7 · 2014: 9 · 2013: 7 · 2012: 3
FWCI
1.22
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Immunological Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Allergy and Infectious Diseases (R01AI076562, T32AI007051)
  • National Institute of Neurological Disorders and Stroke (K99NS075099)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
type I interferon, multiple sclerosis, neuromyelitis optica, relapsing-remitting multiple sclerosis, Th17 response, Th1 response, interferon-beta, autoimmunity, pro-inflammatory effects, treatment resistance
MeSH terms
Animals, Autoimmune Diseases, Disease Models, Animal, Encephalomyelitis, Humans, Interferon Type I, Interferon-beta, Th1 Cells, Multiple Sclerosis, Relapsing-Remitting, Th17 Cells

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