Complement receptor 3 deficiency influences lesion progression during Leishmania major infection in BALB/c mice - Wikidata - awgldk - TriplyDB

Complement receptor 3 deficiency influences lesion progression during Leishmania major infection in BALB/c mice

Complement receptor 3 deficiency influences lesion progression during Leishmania major infection in BALB/c mice

http://www.wikidata.org/entity/Q37451138

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Innate immunity against Leishmania infections Suppression of LPS-induced inflammatory responses in macrophages infected with Leishmania Toll receptors type-2 and CR3 expression of canine monocytes and its correlation with immunohistochemistry and xenodiagnosis in visceral leishmaniasis A mathematical model of CR3/TLR2 crosstalk in the context of Francisella tularensis infection.The Role of Vitamin D and Vitamin D Receptor in Immunity to Leishmania major Infection Mechanisms of immune evasion in leishmaniasis Leishmania major inhibits IL-12 in macrophages by signalling through CR3 (CD11b/CD18) and down-regulation of ETS-mediated transcription.Innate immune activation and subversion of Mammalian functions by leishmania lipophosphoglycan.The circadian clock in immune cells controls the magnitude of Leishmania parasite infection.The Src kinases Hck, Fgr and Lyn activate Arg to facilitate IgG-mediated phagocytosis and Leishmania infection.Ecotin-like ISP of L. major promastigotes fine-tunes macrophage phagocytosis by limiting the pericellular release of bradykinin from surface-bound kininogens: a survival strategy based on the silencing of proinflammatory G-protein coupled kinin B2 a Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein During Francisella tularensis Phagocytosis by Human Mononuclear Phagocytes.

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Complement receptor 3 deficiency influences lesion progression during Leishmania major infection in BALB/c mice

http://www.wikidata.org/entity/Q37451138

description

article científic

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article scientifique

@fr

articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 21 September 2009

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Complement receptor 3 deficien ...... major infection in BALB/c mice

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Complement receptor 3 deficien ...... ajor infection in BALB/c mice.

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type

label

Complement receptor 3 deficien ...... major infection in BALB/c mice

@en

Complement receptor 3 deficien ...... ajor infection in BALB/c mice.

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prefLabel

Complement receptor 3 deficien ...... major infection in BALB/c mice

@en

Complement receptor 3 deficien ...... ajor infection in BALB/c mice.

@nl

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Infection and Immunity

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Complement receptor 3 deficien ...... major infection in BALB/c mice

@en

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Cristina R Carter

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James P Whitcomb

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Jessica A Campbell

http://www.w3.org/2001/XMLSchema#string

Mary Ann McDowell

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Rami M Mukbel

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P2860

Control of leukocyte rolling velocity in TNF-alpha-induced inflammation by LFA-1 and Mac-1.

Complement receptor type three (CD11b/CD18) of human polymorphonuclear leukocytes recognizes fibrinogen.

CR3: a general purpose adhesion-recognition receptor essential for innate immunity.

Activation of phosphotyrosine phosphatase activity attenuates mitogen-activated protein kinase signaling and inhibits c-FOS and nitric oxide synthase expression in macrophages infected with Leishmania donovani

The leishmaniases as emerging and reemerging zoonoses.

Parasitic adaptive mechanisms in infection by leishmania.

The levels and patterns of cytokines produced by CD4 T lymphocytes of BALB/c mice infected with Leishmania major by inoculation into the ear dermis depend on the infectiousness and size of the inoculum

The site of Leishmania major infection determines disease severity and immune responses.

CR3-dependent resistance to acute Toxoplasma gondii infection in mice.

Uptake of Leishmania major by dendritic cells is mediated by Fcgamma receptors and facilitates acquisition of protective immunity

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5668-5675

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scholarly article

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10.1128/IAI.00802-08

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12

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77

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2009-09-21T00:00:00Z

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26863462

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19797068

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2786468

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