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Cited by 330Blood disorders and treatmentsinterferon and immune responsesHematological disorders and diagnostics

Interferon is a mediator of hematopoietic suppression in aplastic anemia in vitro and possibly in vivo

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Zoumbos, N C, Gascon, P, Djeu, J Y, Young, N S·1985·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.82.1.188PMC PMC396997
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Abstract

We have investigated interferon as a mediator of hematopoietic suppression in bone marrow failure. Interferon production by stimulated peripheral blood mononuclear cells from patients with aplastic anemia was significantly higher than that observed in controls; spontaneous interferon production by these cells was also high for more than half of aplastic anemia patients. Circulating interferon, not detectable in normal individuals, was detected in 10 of 24 patients. Interferon is a potent inhibitor of hematopoietic cell proliferation and, therefore, may be the mediator of suppression in many in vitro models employing patients' cells and sera. The possible pathogenic importance of interferon in aplastic anemia was suggested by an increase in hematopoietic colony formation in vitro after exposure of bone marrow cells to antiinterferon antisera (277 +/- 71% increase for patients compared to 1.6 +/- 1.6% for normal individuals). Interferon levels in the bone marrow sera of aplastic anemia patients were high (mean = 203 international units (IU)/ml, n = 8), even in comparison to circulating levels in the same patients. Normal bone marrow sera also contained measurable interferon but at lower levels (41 IU/ml, n = 16), indicating that interferon may be a normal bone marrow product. High concentration of bone marrow interferon, possibly due to abnormal immunologic activity or a reaction to virus infection of the bone marrow, may mediate hematopoietic suppression in aplastic anemia patients.

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  • Type I IFNs are involved in the development of AA.

    “Although the pathogenesis is still not entirely understood, type I IFNs have been identified to be involved in the development of AA. 55”

    From Inflammatory bone marrow microenvironment (2019) · cites this paper as [55]

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Authors
Zoumbos, N. C., Gascon, P., Djeu, J. Y., & Young, N. S.
ORCID
Young, N S
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1985-01
Volume
82
Issue
1
Pages
188-192
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.82.1.188
PMC
PMC396997
OpenAlex
W2064632541
Cited by
330
References
35
Citations by year
2026: 4 · 2025: 3 · 2024: 4 · 2023: 5 · 2022: 6 · 2021: 9 · 2020: 5 · 2019: 5 · 2018: 10 · 2017: 7 · 2016: 2 · 2015: 6 · 2014: 4 · 2013: 7 · 2012: 6
FWCI
11.83
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Health Sciences › Medicine › Emergency Medicine › Hematological disorders and diagnostics
Keywords
interferon, aplastic anemia, hematopoietic suppression, bone marrow failure, peripheral blood mononuclear cells, hematopoietic colony formation, immunological activity
MeSH terms
Anemia, Aplastic, Bone Marrow Cells, Hematopoiesis, Humans, Interferon-gamma, Isoantibodies, Monocytes

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