Nucleotide-binding oligomerization domain-1 and -2 play no role in controlling Brucella abortus infection in mice.
about
NOD2 is dispensable for ATG16L1 deficiency-mediated resistance to urinary tract infection.The Attenuated Brucella abortus Strain 19 Invades, Persists in, and Activates Human Dendritic Cells, and Induces the Secretion of IL-12p70 but Not IL-23What have we learned from brucellosis in the mouse model?TLR7 and TLR3 Sense Brucella abortus RNA to Induce Proinflammatory Cytokine Production but They Are Dispensable for Host Control of Infection.The role of innate immune signals in immunity to Brucella abortus.NOD1 and NOD2 Signaling in Infection and Inflammation.NLRP12 negatively regulates proinflammatory cytokine production and host defense against Brucella abortus.
P2860
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P2860
Nucleotide-binding oligomerization domain-1 and -2 play no role in controlling Brucella abortus infection in mice.
description
2011 nî lūn-bûn
@nan
2011年の論文
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2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
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2011年論文
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2011年论文
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2011年论文
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2011年论文
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name
Nucleotide-binding oligomeriza ...... lla abortus infection in mice.
@en
Nucleotide-binding oligomeriza ...... lla abortus infection in mice.
@nl
type
label
Nucleotide-binding oligomeriza ...... lla abortus infection in mice.
@en
Nucleotide-binding oligomeriza ...... lla abortus infection in mice.
@nl
prefLabel
Nucleotide-binding oligomeriza ...... lla abortus infection in mice.
@en
Nucleotide-binding oligomeriza ...... lla abortus infection in mice.
@nl
P2093
P2860
P356
P1476
Nucleotide-binding oligomeriza ...... lla abortus infection in mice.
@en
P2093
Fernanda S Oliveira
Natalia B Carvalho
Sergio C Oliveira
P2860
P304
P356
10.1155/2012/861426
P577
2011-11-30T00:00:00Z