Protective T cell response against intracellular pathogens in the absence of Toll-like receptor signaling via myeloid differentiation factor 88

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Protective T cell response against intracellular pathogens in the absence of Toll-like receptor signaling via myeloid differentiation factor 88. / Kursar, Mischo; Mittrücker, Hans-Willi; Koch, Markus; Köhler, Anne; Herma, Marion; Kaufmann, Stefan H E.

in: INT IMMUNOL, Jahrgang 16, Nr. 3, 01.03.2004, S. 415-21.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{c27aa2c0ae494fef8869851aac279bf2,
title = "Protective T cell response against intracellular pathogens in the absence of Toll-like receptor signaling via myeloid differentiation factor 88",
abstract = "Toll-like receptors (TLR) have been indicated as germline-encoded receptors for sensing a variety of pathogens. Although the role of TLR in innate immunity is beyond question, their function in acquired immunity, in particular in T cell immunity, is less clear. Here, we used experimental Listeria monocytogenes infection of mice to analyze requirements for TLR2, TLR4 and the central TLR adaptor protein myeloid differentiation factor 88 (MyD88) in the generation of specific T cell responses. We demonstrate that following L. monocytogenes infection, mice deficient in TLR2, TLR4 and MyD88 can generate Listeria-specific CD8+ and CD4+ Th1 responses. These T cell responses are sufficient to control secondary infection with a high dose of L. monocytogenes even in the absence of TLR signaling via MyD88. Thus, TLR2-, TLR4- and MyD88-dependent signals are not essential for the generation of CD4+ Th1 and CD8+ T cells, and T cells can protect mice against infection in the absence of these signals.",
keywords = "Adaptor Proteins, Signal Transducing, Ampicillin, Animals, Antigens, Differentiation, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cytokines, Disease Models, Animal, Immunity, Active, Listeria monocytogenes, Listeriosis, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Myeloid Differentiation Factor 88, Receptors, Cell Surface, Receptors, Immunologic, Signal Transduction, Toll-Like Receptor 2, Toll-Like Receptor 4, Toll-Like Receptors",
author = "Mischo Kursar and Hans-Willi Mittr{\"u}cker and Markus Koch and Anne K{\"o}hler and Marion Herma and Kaufmann, {Stefan H E}",
year = "2004",
month = mar,
day = "1",
language = "English",
volume = "16",
pages = "415--21",
journal = "INT IMMUNOL",
issn = "0953-8178",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Protective T cell response against intracellular pathogens in the absence of Toll-like receptor signaling via myeloid differentiation factor 88

AU - Kursar, Mischo

AU - Mittrücker, Hans-Willi

AU - Koch, Markus

AU - Köhler, Anne

AU - Herma, Marion

AU - Kaufmann, Stefan H E

PY - 2004/3/1

Y1 - 2004/3/1

N2 - Toll-like receptors (TLR) have been indicated as germline-encoded receptors for sensing a variety of pathogens. Although the role of TLR in innate immunity is beyond question, their function in acquired immunity, in particular in T cell immunity, is less clear. Here, we used experimental Listeria monocytogenes infection of mice to analyze requirements for TLR2, TLR4 and the central TLR adaptor protein myeloid differentiation factor 88 (MyD88) in the generation of specific T cell responses. We demonstrate that following L. monocytogenes infection, mice deficient in TLR2, TLR4 and MyD88 can generate Listeria-specific CD8+ and CD4+ Th1 responses. These T cell responses are sufficient to control secondary infection with a high dose of L. monocytogenes even in the absence of TLR signaling via MyD88. Thus, TLR2-, TLR4- and MyD88-dependent signals are not essential for the generation of CD4+ Th1 and CD8+ T cells, and T cells can protect mice against infection in the absence of these signals.

AB - Toll-like receptors (TLR) have been indicated as germline-encoded receptors for sensing a variety of pathogens. Although the role of TLR in innate immunity is beyond question, their function in acquired immunity, in particular in T cell immunity, is less clear. Here, we used experimental Listeria monocytogenes infection of mice to analyze requirements for TLR2, TLR4 and the central TLR adaptor protein myeloid differentiation factor 88 (MyD88) in the generation of specific T cell responses. We demonstrate that following L. monocytogenes infection, mice deficient in TLR2, TLR4 and MyD88 can generate Listeria-specific CD8+ and CD4+ Th1 responses. These T cell responses are sufficient to control secondary infection with a high dose of L. monocytogenes even in the absence of TLR signaling via MyD88. Thus, TLR2-, TLR4- and MyD88-dependent signals are not essential for the generation of CD4+ Th1 and CD8+ T cells, and T cells can protect mice against infection in the absence of these signals.

KW - Adaptor Proteins, Signal Transducing

KW - Ampicillin

KW - Animals

KW - Antigens, Differentiation

KW - CD4-Positive T-Lymphocytes

KW - CD8-Positive T-Lymphocytes

KW - Cytokines

KW - Disease Models, Animal

KW - Immunity, Active

KW - Listeria monocytogenes

KW - Listeriosis

KW - Membrane Glycoproteins

KW - Mice

KW - Mice, Inbred C57BL

KW - Myeloid Differentiation Factor 88

KW - Receptors, Cell Surface

KW - Receptors, Immunologic

KW - Signal Transduction

KW - Toll-Like Receptor 2

KW - Toll-Like Receptor 4

KW - Toll-Like Receptors

M3 - SCORING: Journal article

C2 - 14978015

VL - 16

SP - 415

EP - 421

JO - INT IMMUNOL

JF - INT IMMUNOL

SN - 0953-8178

IS - 3

ER -