NF-κB activation by the pre-T cell receptor serves as a selective survival signal in T lymphocyte development

Reinhard E. Voll, Eijiro Jimi, Roderick J. Phillips, Domingo F. Barber, Mercedes Rincon, Adrian C. Hayday, Richard A. Flavell, Sankar Ghosh

Research output: Contribution to journalArticle

229 Citations (Scopus)

Abstract

Activation of the transcription factor NF-κB and pre-T cell receptor (pre-TCR) expression is tightly correlated during thymocyte development. Inhibition of NF-κB in isolated thymocytes in vitro results in spontaneous apoptosis of cells expressing the pre-TCR, whereas inhibition of NF-κB in transgenic mice through expression of a mutated, superrepressor form of IκBα leads to a loss of β-selected thymocytes. In contrast, the forced activation of NF-κB through expression of a dominant-active I κB kinase allows differentiation to proceed to the CD4+CD8+ stage in a Rag1(-/-) mouse that cannot assemble the pre-TCR. Therefore, signals emanating from the pre-TCR are mediated at least in part by NF-κB, which provides a selective survival signal for developing thymocytes with productive chain rearrangements.

Original languageEnglish
Pages (from-to)677-689
Number of pages13
JournalImmunity
Volume13
Issue number5
DOIs
Publication statusPublished - Jan 1 2000

Fingerprint

Thymocytes
T-Cell Antigen Receptor
T-Lymphocytes
Transgenic Mice
Transcription Factors
Phosphotransferases
Apoptosis

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Cite this

NF-κB activation by the pre-T cell receptor serves as a selective survival signal in T lymphocyte development. / Voll, Reinhard E.; Jimi, Eijiro; Phillips, Roderick J.; Barber, Domingo F.; Rincon, Mercedes; Hayday, Adrian C.; Flavell, Richard A.; Ghosh, Sankar.

In: Immunity, Vol. 13, No. 5, 01.01.2000, p. 677-689.

Research output: Contribution to journalArticle

Voll, RE, Jimi, E, Phillips, RJ, Barber, DF, Rincon, M, Hayday, AC, Flavell, RA & Ghosh, S 2000, 'NF-κB activation by the pre-T cell receptor serves as a selective survival signal in T lymphocyte development', Immunity, vol. 13, no. 5, pp. 677-689. https://doi.org/10.1016/S1074-7613(00)00067-4
Voll, Reinhard E. ; Jimi, Eijiro ; Phillips, Roderick J. ; Barber, Domingo F. ; Rincon, Mercedes ; Hayday, Adrian C. ; Flavell, Richard A. ; Ghosh, Sankar. / NF-κB activation by the pre-T cell receptor serves as a selective survival signal in T lymphocyte development. In: Immunity. 2000 ; Vol. 13, No. 5. pp. 677-689.
@article{797735273b104ab79d53317f07aafda5,
title = "NF-κB activation by the pre-T cell receptor serves as a selective survival signal in T lymphocyte development",
abstract = "Activation of the transcription factor NF-κB and pre-T cell receptor (pre-TCR) expression is tightly correlated during thymocyte development. Inhibition of NF-κB in isolated thymocytes in vitro results in spontaneous apoptosis of cells expressing the pre-TCR, whereas inhibition of NF-κB in transgenic mice through expression of a mutated, superrepressor form of IκBα leads to a loss of β-selected thymocytes. In contrast, the forced activation of NF-κB through expression of a dominant-active I κB kinase allows differentiation to proceed to the CD4+CD8+ stage in a Rag1(-/-) mouse that cannot assemble the pre-TCR. Therefore, signals emanating from the pre-TCR are mediated at least in part by NF-κB, which provides a selective survival signal for developing thymocytes with productive chain rearrangements.",
author = "Voll, {Reinhard E.} and Eijiro Jimi and Phillips, {Roderick J.} and Barber, {Domingo F.} and Mercedes Rincon and Hayday, {Adrian C.} and Flavell, {Richard A.} and Sankar Ghosh",
year = "2000",
month = "1",
day = "1",
doi = "10.1016/S1074-7613(00)00067-4",
language = "English",
volume = "13",
pages = "677--689",
journal = "Immunity",
issn = "1074-7613",
publisher = "Cell Press",
number = "5",

}

TY - JOUR

T1 - NF-κB activation by the pre-T cell receptor serves as a selective survival signal in T lymphocyte development

AU - Voll, Reinhard E.

AU - Jimi, Eijiro

AU - Phillips, Roderick J.

AU - Barber, Domingo F.

AU - Rincon, Mercedes

AU - Hayday, Adrian C.

AU - Flavell, Richard A.

AU - Ghosh, Sankar

PY - 2000/1/1

Y1 - 2000/1/1

N2 - Activation of the transcription factor NF-κB and pre-T cell receptor (pre-TCR) expression is tightly correlated during thymocyte development. Inhibition of NF-κB in isolated thymocytes in vitro results in spontaneous apoptosis of cells expressing the pre-TCR, whereas inhibition of NF-κB in transgenic mice through expression of a mutated, superrepressor form of IκBα leads to a loss of β-selected thymocytes. In contrast, the forced activation of NF-κB through expression of a dominant-active I κB kinase allows differentiation to proceed to the CD4+CD8+ stage in a Rag1(-/-) mouse that cannot assemble the pre-TCR. Therefore, signals emanating from the pre-TCR are mediated at least in part by NF-κB, which provides a selective survival signal for developing thymocytes with productive chain rearrangements.

AB - Activation of the transcription factor NF-κB and pre-T cell receptor (pre-TCR) expression is tightly correlated during thymocyte development. Inhibition of NF-κB in isolated thymocytes in vitro results in spontaneous apoptosis of cells expressing the pre-TCR, whereas inhibition of NF-κB in transgenic mice through expression of a mutated, superrepressor form of IκBα leads to a loss of β-selected thymocytes. In contrast, the forced activation of NF-κB through expression of a dominant-active I κB kinase allows differentiation to proceed to the CD4+CD8+ stage in a Rag1(-/-) mouse that cannot assemble the pre-TCR. Therefore, signals emanating from the pre-TCR are mediated at least in part by NF-κB, which provides a selective survival signal for developing thymocytes with productive chain rearrangements.

UR - http://www.scopus.com/inward/record.url?scp=0033637216&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033637216&partnerID=8YFLogxK

U2 - 10.1016/S1074-7613(00)00067-4

DO - 10.1016/S1074-7613(00)00067-4

M3 - Article

C2 - 11114380

AN - SCOPUS:0033637216

VL - 13

SP - 677

EP - 689

JO - Immunity

JF - Immunity

SN - 1074-7613

IS - 5

ER -