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Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells

Standard

Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells. / Lohoff, Michael; Mittrücker, Hans-Willi; Brüstle, Anne; Sommer, Frank; Casper, Bärbel; Huber, Magda; Ferrick, David A; Duncan, Gordon S; Mak, Tak W.

in: J EXP MED, Jahrgang 200, Nr. 2, 19.07.2004, S. 247-53.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Lohoff, M, Mittrücker, H-W, Brüstle, A, Sommer, F, Casper, B, Huber, M, Ferrick, DA, Duncan, GS & Mak, TW 2004, 'Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells', J EXP MED, Jg. 200, Nr. 2, S. 247-53. https://doi.org/10.1084/jem.20040182

APA

Lohoff, M., Mittrücker, H-W., Brüstle, A., Sommer, F., Casper, B., Huber, M., Ferrick, D. A., Duncan, G. S., & Mak, T. W. (2004). Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells. J EXP MED, 200(2), 247-53. https://doi.org/10.1084/jem.20040182

Vancouver

Lohoff M, Mittrücker H-W, Brüstle A, Sommer F, Casper B, Huber M et al. Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells. J EXP MED. 2004 Jul 19;200(2):247-53. https://doi.org/10.1084/jem.20040182

Bibtex

@article{46923dcaaa8e4a53a91f7cd7d358f327,
title = "Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells",
abstract = "Transcription factors of the interferon regulatory factor (IRF) family contribute to the regulation of cell proliferation and apoptosis. Here, we show that CD4(+) T helper (Th) cells lacking IRF4 (IRF4(-/-)) are highly sensitive to apoptosis. After infection of IRF4(-/-) mice with the protozoan parasite Leishmania major, the lesion-draining lymph nodes developed the prototypic lymphadenopathy of wild-type mice after 4 wk, but demonstrated almost total loss of cellularity and enhanced apoptosis after 7 wk. In vitro, activation of IRF4(-/-) CD4(+) Th cells led to greatly increased apoptosis compared with wild-type cells. Coculture of IRF4(-/-) and IRF4(+/+) CD4(+) cells did not increase survival of IRF4(-/-) CD4(+) cells, indicating that the enhanced rate of IRF4(-/-) Th cell apoptosis was neither transferable nor due to lack of a cytokine. Enhanced CD4(+) cell apoptosis was also observed after anti-CD95 mAb treatment, despite normal CD95 expression. Removal of endogenous cytokines, notably interleukin (IL)-4, led to increased and equally high levels of IRF4(-/-) and IRF4(+/+) cell apoptosis, whereas the protective activity of exogenous IL-4 was reduced in IRF4(-/-) CD4(+) cells despite normal expression of the IL-4 receptor. Therefore, IRF4 is central in protecting CD4(+) cells against proapoptotic stimuli.",
keywords = "Animals, Annexin A5, Antigens, CD4, Antigens, CD95, Apoptosis, CD4-Positive T-Lymphocytes, Cell Division, Coloring Agents, Cytokines, DNA-Binding Proteins, Flow Cytometry, In Situ Nick-End Labeling, Interferon Regulatory Factors, Leishmania major, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Receptors, Antigen, T-Cell, T-Lymphocytes, Helper-Inducer, Time Factors, Transcription Factors",
author = "Michael Lohoff and Hans-Willi Mittr{\"u}cker and Anne Br{\"u}stle and Frank Sommer and B{\"a}rbel Casper and Magda Huber and Ferrick, {David A} and Duncan, {Gordon S} and Mak, {Tak W}",
year = "2004",
month = jul,
day = "19",
doi = "10.1084/jem.20040182",
language = "English",
volume = "200",
pages = "247--53",
journal = "J EXP MED",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "2",

}

RIS

TY - JOUR

T1 - Enhanced TCR-induced apoptosis in interferon regulatory factor 4-deficient CD4(+) Th cells

AU - Lohoff, Michael

AU - Mittrücker, Hans-Willi

AU - Brüstle, Anne

AU - Sommer, Frank

AU - Casper, Bärbel

AU - Huber, Magda

AU - Ferrick, David A

AU - Duncan, Gordon S

AU - Mak, Tak W

PY - 2004/7/19

Y1 - 2004/7/19

N2 - Transcription factors of the interferon regulatory factor (IRF) family contribute to the regulation of cell proliferation and apoptosis. Here, we show that CD4(+) T helper (Th) cells lacking IRF4 (IRF4(-/-)) are highly sensitive to apoptosis. After infection of IRF4(-/-) mice with the protozoan parasite Leishmania major, the lesion-draining lymph nodes developed the prototypic lymphadenopathy of wild-type mice after 4 wk, but demonstrated almost total loss of cellularity and enhanced apoptosis after 7 wk. In vitro, activation of IRF4(-/-) CD4(+) Th cells led to greatly increased apoptosis compared with wild-type cells. Coculture of IRF4(-/-) and IRF4(+/+) CD4(+) cells did not increase survival of IRF4(-/-) CD4(+) cells, indicating that the enhanced rate of IRF4(-/-) Th cell apoptosis was neither transferable nor due to lack of a cytokine. Enhanced CD4(+) cell apoptosis was also observed after anti-CD95 mAb treatment, despite normal CD95 expression. Removal of endogenous cytokines, notably interleukin (IL)-4, led to increased and equally high levels of IRF4(-/-) and IRF4(+/+) cell apoptosis, whereas the protective activity of exogenous IL-4 was reduced in IRF4(-/-) CD4(+) cells despite normal expression of the IL-4 receptor. Therefore, IRF4 is central in protecting CD4(+) cells against proapoptotic stimuli.

AB - Transcription factors of the interferon regulatory factor (IRF) family contribute to the regulation of cell proliferation and apoptosis. Here, we show that CD4(+) T helper (Th) cells lacking IRF4 (IRF4(-/-)) are highly sensitive to apoptosis. After infection of IRF4(-/-) mice with the protozoan parasite Leishmania major, the lesion-draining lymph nodes developed the prototypic lymphadenopathy of wild-type mice after 4 wk, but demonstrated almost total loss of cellularity and enhanced apoptosis after 7 wk. In vitro, activation of IRF4(-/-) CD4(+) Th cells led to greatly increased apoptosis compared with wild-type cells. Coculture of IRF4(-/-) and IRF4(+/+) CD4(+) cells did not increase survival of IRF4(-/-) CD4(+) cells, indicating that the enhanced rate of IRF4(-/-) Th cell apoptosis was neither transferable nor due to lack of a cytokine. Enhanced CD4(+) cell apoptosis was also observed after anti-CD95 mAb treatment, despite normal CD95 expression. Removal of endogenous cytokines, notably interleukin (IL)-4, led to increased and equally high levels of IRF4(-/-) and IRF4(+/+) cell apoptosis, whereas the protective activity of exogenous IL-4 was reduced in IRF4(-/-) CD4(+) cells despite normal expression of the IL-4 receptor. Therefore, IRF4 is central in protecting CD4(+) cells against proapoptotic stimuli.

KW - Animals

KW - Annexin A5

KW - Antigens, CD4

KW - Antigens, CD95

KW - Apoptosis

KW - CD4-Positive T-Lymphocytes

KW - Cell Division

KW - Coloring Agents

KW - Cytokines

KW - DNA-Binding Proteins

KW - Flow Cytometry

KW - In Situ Nick-End Labeling

KW - Interferon Regulatory Factors

KW - Leishmania major

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Receptors, Antigen, T-Cell

KW - T-Lymphocytes, Helper-Inducer

KW - Time Factors

KW - Transcription Factors

U2 - 10.1084/jem.20040182

DO - 10.1084/jem.20040182

M3 - SCORING: Journal article

C2 - 15249594

VL - 200

SP - 247

EP - 253

JO - J EXP MED

JF - J EXP MED

SN - 0022-1007

IS - 2

ER -