Research ExplorerPublicationsInterferon regulatory factor-1 is required for a T helper 1 ...

Interferon regulatory factor-1 is required for a T helper 1 immune response in vivo

Standard

Interferon regulatory factor-1 is required for a T helper 1 immune response in vivo. / Lohoff, M; Ferrick, D; Mittrucker, H W; Duncan, G S; Bischof, S; Rollinghoff, M; Mak, T W.

In: IMMUNITY, Vol. 6, No. 6, 01.06.1997, p. 681-9.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Lohoff, M, Ferrick, D, Mittrucker, HW, Duncan, GS, Bischof, S, Rollinghoff, M & Mak, TW 1997, 'Interferon regulatory factor-1 is required for a T helper 1 immune response in vivo', IMMUNITY, vol. 6, no. 6, pp. 681-9.

APA

Lohoff, M., Ferrick, D., Mittrucker, H. W., Duncan, G. S., Bischof, S., Rollinghoff, M., & Mak, T. W. (1997). Interferon regulatory factor-1 is required for a T helper 1 immune response in vivo. IMMUNITY, 6(6), 681-9.

Vancouver

Lohoff M, Ferrick D, Mittrucker HW, Duncan GS, Bischof S, Rollinghoff M et al. Interferon regulatory factor-1 is required for a T helper 1 immune response in vivo. IMMUNITY. 1997 Jun 1;6(6):681-9.

Bibtex

@article{290d6d077e7a480b811d03fcb6aef773,
title = "Interferon regulatory factor-1 is required for a T helper 1 immune response in vivo",
abstract = "The transcription factor interferon regulatory factor-1 (IRF-1) mediates the effects of IFN. No information exists on its role in lymphokine production. Protection against the intracellular pathogen Leishmania major depends on a Th1 response. Here, we show that CD4+ T cells from Leishmania-infected mice lacking one (+/-) or both (-/-) alleles of the IRF-1 gene developed a profound, gene dose-dependent decrease in IFNgamma production. IRF-1(-/-) mice showed dramatically exacerbated Leishmaniasis. They produced increased Leishmania-specific IgG1 and IgE, and their CD4+ T cells produced increased IL-4, characteristics of the non-protective Th2 response. In cell transfer experiments, IRF-1(-/-) CD4+ T cells mounted normal Th1 responses. However, the ability of IRF-1(-/-) mice to produce IL-12 was severely compromised. Thus, IRF-1 is a determining factor for Th1 responses.",
keywords = "Animals, CD4-Positive T-Lymphocytes, Cell Differentiation, Cytokines, DNA-Binding Proteins, Immunity, Cellular, Immunity, Innate, Interferon Regulatory Factor-1, Interleukin-12, Leishmania major, Leishmaniasis, Cutaneous, Lymph Nodes, Lymphocyte Cooperation, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Phosphoproteins, Th1 Cells, Th2 Cells",
author = "M Lohoff and D Ferrick and Mittrucker, {H W} and Duncan, {G S} and S Bischof and M Rollinghoff and Mak, {T W}",
year = "1997",
month = jun,
day = "1",
language = "English",
volume = "6",
pages = "681--9",
journal = "IMMUNITY",
issn = "1074-7613",
publisher = "Cell Press",
number = "6",

}

RIS

TY - JOUR

T1 - Interferon regulatory factor-1 is required for a T helper 1 immune response in vivo

AU - Lohoff, M

AU - Ferrick, D

AU - Mittrucker, H W

AU - Duncan, G S

AU - Bischof, S

AU - Rollinghoff, M

AU - Mak, T W

PY - 1997/6/1

Y1 - 1997/6/1

N2 - The transcription factor interferon regulatory factor-1 (IRF-1) mediates the effects of IFN. No information exists on its role in lymphokine production. Protection against the intracellular pathogen Leishmania major depends on a Th1 response. Here, we show that CD4+ T cells from Leishmania-infected mice lacking one (+/-) or both (-/-) alleles of the IRF-1 gene developed a profound, gene dose-dependent decrease in IFNgamma production. IRF-1(-/-) mice showed dramatically exacerbated Leishmaniasis. They produced increased Leishmania-specific IgG1 and IgE, and their CD4+ T cells produced increased IL-4, characteristics of the non-protective Th2 response. In cell transfer experiments, IRF-1(-/-) CD4+ T cells mounted normal Th1 responses. However, the ability of IRF-1(-/-) mice to produce IL-12 was severely compromised. Thus, IRF-1 is a determining factor for Th1 responses.

AB - The transcription factor interferon regulatory factor-1 (IRF-1) mediates the effects of IFN. No information exists on its role in lymphokine production. Protection against the intracellular pathogen Leishmania major depends on a Th1 response. Here, we show that CD4+ T cells from Leishmania-infected mice lacking one (+/-) or both (-/-) alleles of the IRF-1 gene developed a profound, gene dose-dependent decrease in IFNgamma production. IRF-1(-/-) mice showed dramatically exacerbated Leishmaniasis. They produced increased Leishmania-specific IgG1 and IgE, and their CD4+ T cells produced increased IL-4, characteristics of the non-protective Th2 response. In cell transfer experiments, IRF-1(-/-) CD4+ T cells mounted normal Th1 responses. However, the ability of IRF-1(-/-) mice to produce IL-12 was severely compromised. Thus, IRF-1 is a determining factor for Th1 responses.

KW - Animals

KW - CD4-Positive T-Lymphocytes

KW - Cell Differentiation

KW - Cytokines

KW - DNA-Binding Proteins

KW - Immunity, Cellular

KW - Immunity, Innate

KW - Interferon Regulatory Factor-1

KW - Interleukin-12

KW - Leishmania major

KW - Leishmaniasis, Cutaneous

KW - Lymph Nodes

KW - Lymphocyte Cooperation

KW - Mice

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Phosphoproteins

KW - Th1 Cells

KW - Th2 Cells

M3 - SCORING: Journal article

C2 - 9208841

VL - 6

SP - 681

EP - 689

JO - IMMUNITY

JF - IMMUNITY

SN - 1074-7613

IS - 6

ER -