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, Vol. 16, No. 3, 01.03.2004, p. 415-21.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -