DESCRIPTION:

QTL associated with determination of interleukin 4 commitment 1. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (11616475)

LABEL:

QTL-Dice1-Mouse-Chr 16

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2020-05-06

SPECIES:

URI:

http://www.informatics.jax.org/searches/accession_report.cgi?id=MGI:2149367

AUTHORS:

Bix M, Wang ZE, Thiel B, Schork NJ, Locksley RM

TITLE:

Genetic regulation of commitment to interleukin 4 production by a CD4(+) T cell-intrinsic mechanism.

JOURNAL:

The Journal of experimental medicine Dec 1998, Vol 188, pp. 2289-99

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. PUBMED: 9858515
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