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Genetic regulation of commitment to interleukin 4 production by a cd4(+) t cell-intrinsic mechanism

Academic Article
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Overview

authors

  • Bix, M.
  • Wang, Z. E.
  • Thiel, B.
  • Schork, Nicholas
  • Locksley, R. M.

publication date

  • December 1998

journal

  • Journal of Experimental Medicine  Journal

abstract

  • The dysregulated expression of interleukin 4 (IL-4) can have deleterious effects on the outcome of infectious and allergic diseases. Despite this, the mechanisms by which naive T cells commit to IL-4 expression during differentiation into mature effector cells remain incompletely defined. As compared to cells from most strains of mice, activated CD4(+) T cells from BALB mice show a bias towards IL-4 production and T helper 2 commitment in vitro and in vivo. Here, we show that this bias arises not from an increase in the amount of IL-4 produced per cell, but rather from an increase in the proportion of CD4(+) T cells that commit to IL-4 expression. This strain-specific difference in commitment was independent of signals mediated via the IL-4 receptor and hence occurred upstream of potential autoregulatory effects of IL-4. Segregation analysis of the phenotype in an experimental backcross cohort implicated a polymorphic locus on chromosome 16. Consistent with a role in differentiation, expression of the phenotype was CD4(+) T cell intrinsic and was evident as early as 16 h after the activation of naive T cells. Probabilistic gene activation is proposed as a T cell-intrinsic mechanism capable of modulating the proportion of naive T cells that commit to IL-4 production.

subject areas

  • Animals
  • CD4-Positive T-Lymphocytes
  • Cell Differentiation
  • Chimera
  • Crosses, Genetic
  • Genetic Linkage
  • Hematopoietic Stem Cells
  • Interleukin-4
  • Interleukins
  • L-Selectin
  • Liver
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred Strains
  • Phenotype
  • Polymorphism, Genetic
  • RNA, Messenger
  • Receptors, Interleukin-4
  • Signal Transduction
  • Spleen
  • Th2 Cells
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Research

keywords

  • BALB/c mice
  • T helper 2
  • cytokine expression
  • genetic analysis
  • interleukin 4
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Identity

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.188.12.2289

PubMed ID

  • 9858515
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Additional Document Info

start page

  • 2289

end page

  • 2299

volume

  • 188

issue

  • 12

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