Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-4-13
pubmed:abstractText
Th phenotype development is controlled not only by cytokines but also by other parameters including genetic background. One site of genetic variation between murine strains that has direct impact on Th development is the expression of the IL-12 receptor. T cells from B10.D2 and BALB/c mice show distinct control of IL-12 receptor expression. When activated by Ag, B10.D2 T cells express functional IL-12 receptors and maintain IL-12 responsiveness. In contrast, under the same conditions, BALB/c T cells fail to express IL-12 receptors and become unresponsive to IL-12, precluding any Th1-inducing effects if subsequently exposed to IL-12. Previously, we identified a locus, which we termed T cell phenotype modifier 1 (Tpm1), on murine chromosome 11 that controls this differential maintenance of IL-12 responsiveness. In this study, we have produced a higher resolution map around Tpm1. We produced and analyzed a series of recombinants from a first-generation backcross that significantly narrows the genetic boundaries of Tpm1. This allowed us to exclude from consideration certain previous candidates for Tpm1, including IFN-regulatory factor-1. Also, cellular analysis of F1(B10.D2 x BALB/c) T cells demonstrates that Tpm1 exerts its effect on IL-12 receptor expression in a cell-autonomous manner, rather than through influencing the extracellular milieu. This result strongly implies that despite the proximity of our locus to the IL-13/IL-4 gene cluster, these cytokines are not candidates for Tpm1.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
162
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1339-47
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9973388-Alleles, pubmed-meshheading:9973388-Animals, pubmed-meshheading:9973388-Base Sequence, pubmed-meshheading:9973388-CD4-Positive T-Lymphocytes, pubmed-meshheading:9973388-Chromosome Mapping, pubmed-meshheading:9973388-Crosses, Genetic, pubmed-meshheading:9973388-DNA Primers, pubmed-meshheading:9973388-Female, pubmed-meshheading:9973388-Genetic Linkage, pubmed-meshheading:9973388-Genetic Markers, pubmed-meshheading:9973388-Genotype, pubmed-meshheading:9973388-Interleukin-12, pubmed-meshheading:9973388-Male, pubmed-meshheading:9973388-Mice, pubmed-meshheading:9973388-Mice, Inbred BALB C, pubmed-meshheading:9973388-Mice, Transgenic, pubmed-meshheading:9973388-Phenotype, pubmed-meshheading:9973388-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:9973388-Receptors, Interleukin, pubmed-meshheading:9973388-Receptors, Interleukin-12, pubmed-meshheading:9973388-Recombination, Genetic, pubmed-meshheading:9973388-Sequence Tagged Sites
pubmed:year
1999
pubmed:articleTitle
Tpm1, a locus controlling IL-12 responsiveness, acts by a cell-autonomous mechanism.
pubmed:affiliation
Department of Pathology and Center for Immunology, Howard Hughes Medical Institute, Washington University School of Medicine, St. Louis, MO 63110, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't