Chronic pneumonia despite adaptive immune response to Mycobacterium bovis BCG in MyD88-deficient mice (Q80350100)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:15258598%20AND%20SRC:MED&resulttype=core&format=json

30 December 2019

title

Chronic pneumonia despite adaptive immune response to Mycobacterium bovis BCG in MyD88-deficient mice (English)

1 reference

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30 December 2019

Mycobacterium bovis

1 reference

Delphine M Nicolle

1

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30 December 2019

Xavier Pichon

2

1 reference

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30 December 2019

André Bouchot

3

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30 December 2019

Isabelle Maillet

4

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30 December 2019

François Erard

5

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30 December 2019

Shizuo Akira

6

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30 December 2019

Bernhard Ryffel

7

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30 December 2019

Valérie F J Quesniaux

8

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30 December 2019

publication date

1 October 2004

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30 December 2019

published in

Laboratory Investigation

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30 December 2019

volume

84

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30 December 2019

issue

10

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30 December 2019

page(s)

1305-1321

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https://scigraph.springernature.com/pub.10.1038/labinvest.3700149

30 December 2019

exact match

0 references

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The role of Toll-like receptors in immunity against mycobacterial infection

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Maturation of human dendritic cells by cell wall skeleton of Mycobacterium bovis bacillus Calmette-Guérin: involvement of toll-like receptors

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Induction of direct antimicrobial activity through mammalian toll-like receptors

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Control of Mycobacterium bovis BCG infection with increased inflammation in TLR4-deficient mice

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Toll-like receptor 2-deficient mice succumb to Mycobacterium tuberculosis infection

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Toll-like receptor 4 expression is required to control chronic Mycobacterium tuberculosis infection in mice.

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Toll-like receptor 4 plays a protective role in pulmonary tuberculosis in mice

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Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway

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TICAM-1, an adaptor molecule that participates in Toll-like receptor 3-mediated interferon-beta induction

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The Toll-IL-1 receptor adaptor family grows to five members.

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MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways

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Cellular responses to bacterial cell wall components are mediated through MyD88-dependent signaling cascades

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Endotoxin-induced maturation of MyD88-deficient dendritic cells

1 reference

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Lipopolysaccharide stimulates the MyD88-independent pathway and results in activation of IFN-regulatory factor 3 and the expression of a subset of lipopolysaccharide-inducible genes

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Unresponsiveness of MyD88-deficient mice to endotoxin

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Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function

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Cutting edge: myeloid differentiation factor 88 deficiency improves resistance against sepsis caused by polymicrobial infection

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Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection

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Cutting edge: MyD88 is required for resistance to Toxoplasma gondii infection and regulates parasite-induced IL-12 production by dendritic cells.

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Mice lacking myeloid differentiation factor 88 display profound defects in host resistance and immune responses to Mycobacterium avium infection not exhibited by Toll-like receptor 2 (TLR2)- and TLR4-deficient animals

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An advanced culture method for generating large quantities of highly pure dendritic cells from mouse bone marrow

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Extended freeze-dried Mycobacterium bovis Bacillus Calmette-Guérin induces the release of interleukin-12 but not tumour necrosis factor-alpha by alveolar macrophages, both in vitro and in vivo

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Comparative analysis of T lymphocytes recovered from the lungs of mice genetically susceptible, resistant, and hyperresistant to Mycobacterium tuberculosis-triggered disease.

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Reactivation of latent tuberculosis infection in TNF-deficient mice

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Acylation state of the phosphatidylinositol hexamannosides from Mycobacterium bovis bacillus Calmette Guerin and mycobacterium tuberculosis H37Rv and its implication in Toll-like receptor response

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Toll-like receptors control activation of adaptive immune responses

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Fatal Mycobacterium bovis BCG infection in TNF-LT-alpha-deficient mice.

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MyD88 primes macrophages for full-scale activation by interferon-gamma yet mediates few responses to Mycobacterium tuberculosis

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