(Q46154582)

20 December 2017

title

Blocking IL-1α but not IL-1β increases susceptibility to chronic Mycobacterium tuberculosis infection in mice (English)

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20 December 2017

Mycobacterium tuberculosis

main subject

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6

Martin F Bachmann

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20 December 2017

author name string

Reto Guler

1

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20 December 2017

Suraj P Parihar

2

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20 December 2017

Gunther Spohn

3

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20 December 2017

Pål Johansen

4

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20 December 2017

Frank Brombacher

5

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20 December 2017

language of work or name

English

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publication date

18 November 2010

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20 December 2017

published in

Vaccine

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20 December 2017

volume

29

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20 December 2017

issue

6

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20 December 2017

page(s)

1339-1346

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20 December 2017

The balance between IL-1 and IL-1Ra in disease

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1 reference

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IL-1 receptor-mediated signal is an essential component of MyD88-dependent innate response to Mycobacterium tuberculosis infection

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Production of mice deficient in genes for interleukin (IL)-1alpha, IL-1beta, IL-1alpha/beta, and IL-1 receptor antagonist shows that IL-1beta is crucial in turpentine-induced fever development and glucocorticoid secretion

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Gene expression during preimplantation mouse development

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Fate of Mycobacterium tuberculosis in mouse tissues as determined by the microbial enumeration technique. I. The persistence of drug-susceptible tubercle bacilli in the tissues despite prolonged antimicrobial therapy

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A virus-like particle-based vaccine selectively targeting soluble TNF-alpha protects from arthritis without inducing reactivation of latent tuberculosis

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Caspase-1 independent IL-1beta production is critical for host resistance to mycobacterium tuberculosis and does not require TLR signaling in vivo

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IL-1-induced inflammation promotes development of leishmaniasis in susceptible BALB/c mice

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Endogenous Interleukin (IL)–1α and IL‐1β Are Crucial for Host Defense against Disseminated Candidiasis

7 January 2021

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Reduced inflammatory response in cigarette smoke exposed Mrp1/Mdr1a/1b deficient mice

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Normal human alveolar macrophages have more ability than blood monocytes to produce cell-associated interleukin-1-alpha

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7 January 2021

Identifiers

DOI

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20 December 2017

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20 December 2017