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CD4+ T cells from IRF-1-deficient mice exhibit altered patterns of cytokine expression and cell subset homeostasis

Academic Article
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Overview

authors

  • McElligott, D. L.
  • Phillips, J. A.
  • Stillman, C. A.
  • Koch, R. J.
  • Mosier, Donald
  • Hobbs, M. V.

publication date

  • November 1997

journal

  • Journal of Immunology  Journal

abstract

  • Interferon regulatory factor-1 (IRF-1) is a member of a family of transcription factors that regulate an array of genes involved in cell growth, differentiation, and death. Analysis of cytokine expression by stimulated CD4+ cells from IRF-1(-/-) and IRF-1(+/+) mice revealed that IRF-1 deficiency resulted in an elevated production of Th2-related cytokines and a compensatory decrease in the expression of naive cell- and Th1-related cytokines. The altered cytokine profiles of IRF-1(-/-) cells could be explained, in part, by a shift in the representation of subsets of CD4+ cells; IRF-1(-/-) mice exhibited a decreased percentage of naive cells (a major source of IL-2) but increased numbers of memory or effector cells (the source of Th2-related cytokines). We analyzed purified, phenotypically matched memory/effector cells from IRF-1(-/-) and IRF-1(+/+) mice and found that the increased Th2:Th1 cytokine ratio was still evident in the IRF-1(-/-) group, thus suggesting that IRF-1 is involved in the polarization of the cytokine repertoire in CD4+ cells. Our data indicate that IRF-1 plays an important role in the maintenance of CD4+ cell subset homeostasis and in the expression of cytokines by naive and memory/effector cells.

subject areas

  • Animals
  • CD4-Positive T-Lymphocytes
  • Cytokines
  • DNA-Binding Proteins
  • Gene Expression Regulation
  • Interferon Regulatory Factor-1
  • Interferon-gamma
  • Mice
  • Mice, Inbred BALB C
  • Mice, Mutant Strains
  • Phosphoproteins
  • T-Lymphocyte Subsets
  • Transcription Factors
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 9379011
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Additional Document Info

start page

  • 4180

end page

  • 4186

volume

  • 159

issue

  • 9

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