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Cited by 160T-cell and B-cell Immunologyinterferon and immune responsesCytokine Signaling Pathways and Interactions

Interferon (IFN) Consensus Sequence-binding Protein, a Transcription Factor of the IFN Regulatory Factor Family, Regulates Immune Responses In Vivo through Control of Interleukin 12 Expression

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Giese, Nathalia A., Gabriele, Lucia, Doherty, T. Mark, Klinman, Dennis M., Tadesse-Heath, Lekidelu, Contursi, Christina, Epstein, Suzanne L., Morse, Herbert C.·1997·The Journal of Experimental Medicine
DOI 10.1084/jem.186.9.1535PMC PMC2199114
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Abstract

Mice with a null mutation of the gene encoding interferon consensus sequence-binding protein (ICSBP) develop a chronic myelogenous leukemia-like syndrome and mount impaired responses to certain viral and bacterial infections. To gain a mechanistic understanding of the contributions of ICSBP to humoral and cellular immunity, we characterized the responses of control and ICSBP−/− mice to infection with influenza A (flu) and Leishmania major (L. major). Mice of both genotypes survived infections with flu, but differed markedly in the isotype distribution of antiflu antibodies. In sera of normal mice, immunoglobulin (Ig)G2a antibodies were dominant over IgG1 antibodies, a pattern indicative of a T helper cell type 1 (Th1)-driven response. In sera of ICSBP−/− mice, however, IgG1 antibodies dominated over IgG2a antibodies, a pattern indicative of a Th2-driven response. The dominance of IgG1 and IgE over IgG2a was detected in the sera of uninfected mice as well. A seeming Th2 bias of ICSBP-deficient mice was also uncovered in their inability to control infection with L. major, where resistance is known to be dependent on IL-12 and IFN-γ as components of a Th1 response. Infected ICSBP-deficient mice developed fulminant, disseminated leishmaniasis as a result of failure to mount a Th1-mediated curative response, although T cells remained capable of secreting IFN-γ and macrophages of producing nitric oxide. Compromised Th1 differentiation in ICSBP−/− mice could not be attributed to hyporesponsiveness of CD4+ T cells to interleukin (IL)-12; however, the ability of uninfected and infected ICSBP-deficient mice to produce IL-12 was markedly impaired. This indicates that ICSBP is a deciding factor in Th responses governing humoral and cellular immunity through its role in regulating IL-12 expression.

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  • ICSBP-/- mice are immunodeficient and susceptible to various pathogens.

    “ICSBP 2 / 2 mice are immunodeficient and susceptible to various pathogens.”

    From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [40]

  • ICSBP-/- mice have defects in macrophage function, including the ability to induce IL-12 p40 and some IFN-γ-responsible genes.

    “They have defects in the macrophage function, including the ability to induce interleukin-12 (IL-12) p40 and some IFNg -responsible genes.”

    From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [40]

  • ICSBP-/- macrophages or cells from draining lymph nodes are severely impaired in both basal and induced expression of the IL-12 p40 gene after infection, and a similar impairment occurs in peritoneal macrophages in response to various in vitro stimuli.

    “Strikingly, ICSBP 2 / 2 macrophages or cells from draining lymph nodes were severely impaired in both basal and induced expression of the IL-12 p40 gene after infection. (40,41)”

    From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [40]

  • ICSBP-/- mice are deficient in producing IL-12 and IFN-γ and are unable to mount a Th1-mediated response.

    “ICSBP 2 / 2 mice were shown to be deficient in producing IL-12 and IFNg and were unable to mount a Th1-mediated response. (37,40,41)”

    From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [40]

  • Splenocytes or purified CD4+ T cells from ICSBP-/- mice could produce IFN-γ in vitro in response to ConA, IL-12, or anti-CD3 plus anti-CD28 antibodies.

    “On the other hand, splenocytes or purified CD4 1 T cells from ICSBP 2 / 2 mice could produce IFNg in vitro in response to concanavalin A (ConA), IL-12, or anti-CD3 plus anti-CD28 antibodies. (40,41,44)”

    From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [40]

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Authors
Giese, N. A., Gabriele, L., Doherty, T. M., Klinman, D. M., Tadesse-Heath, L., Contursi, C., Epstein, S. L., & Morse, H. C.
Affiliations
  • National Institutes of Health (US)
  • From the *Laboratory of Immunopathology and ‡Laboratory of Parisitology, National Institute of Allergy and Infectious Diseases; §Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892-0760; and ¶Division of Virology and ‖Division of Cell and Gene Therapies, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20852-1448
ORCID
Venue
The Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
1997-11-03
Volume
186
Issue
9
Pages
1535-1546
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
DOI
10.1084/jem.186.9.1535
PMC
PMC2199114
OpenAlex
W2006786538
Cited by
160
References
73
Citations by year
2025: 3 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 5 · 2015: 5 · 2014: 11 · 2013: 9 · 2012: 4
FWCI
4.07
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (MD 20892)
  • National Institute of Allergy and Infectious Diseases
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
Keywords
IRF8, IL-12, Th1/Th2 balance, Th1 differentiation, influenza A virus, Leishmania major, disseminated leishmaniasis, humoral immunity, cell-mediated immunity, interferon-gamma, nitric oxide, CD4+ T cells
MeSH terms
Interferon Regulatory Factor-8, Animals, Carrier Proteins, Cell Differentiation, Disease Susceptibility, Interferons, Mice, Inbred C57BL, Orthomyxoviridae Infections, Influenza A virus, Repressor Proteins, Transcription Factors, Consensus Sequence, Leishmaniasis, Cutaneous, Leishmania major, Mice, Knockout, Th1 Cells, Th2 Cells, Interleukin-12, Interferon Regulatory Factors, Mice

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