Evasion of alternative complement pathway by Trypanosoma cruzi results from inefficient binding of factor B. - Wikidata - awgldk - TriplyDB

Evasion of alternative complement pathway by Trypanosoma cruzi results from inefficient binding of factor B.

Evasion of alternative complement pathway by Trypanosoma cruzi results from inefficient binding of factor B.

http://www.wikidata.org/entity/Q37397900

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Evasion and Immuno-Endocrine Regulation in Parasite Infection: Two Sides of the Same Coin in Chagas Disease?Immune Evasion Strategies of Trypanosoma cruzi Siglecs and immune regulation Monitoring of the Parasite Load in the Digestive Tract of Rhodnius prolixus by Combined qPCR Analysis and Imaging Techniques Provides New Insights into the Trypanosome Life Cycle Infectious diseases associated with complement deficiencies.Inefficient complement system clearance of Trypanosoma cruzi metacyclic trypomastigotes enables resistant strains to invade eukaryotic cells Complement control protein factor H: the good, the bad, and the inadequate.Human mannose-binding protein activates the alternative complement pathway and enhances serum bactericidal activity on a mannose-rich isolate of Salmonella.Complement component C1q enhances invasion of human mononuclear phagocytes and fibroblasts by Trypanosoma cruzi trypomastigotes.Discovery and verification of osteopontin and Beta-2-microglobulin as promising markers for staging human African trypanosomiasis Inhibitory effects of Trypanosoma cruzi sialoglycoproteins on CD4+ T cells are associated with increased susceptibility to infection Chagas' disease.Three-dimensional structures in the design of therapeutics targeting parasitic protozoa: reflections on the past, present and future.Amastigotes of Trypanosoma cruzi escape destruction by the terminal complement components.Developmentally regulated expression by Trypanosoma cruzi of molecules that accelerate the decay of complement C3 convertases.The Role of Sialic Acid-Binding Receptors (Siglecs) in the Immunomodulatory Effects of Trypanosoma cruzi Sialoglycoproteins on the Protective Immunity of the Host.The Complement System: A Prey of Trypanosoma cruzi.Developmentally-regulated virulence factors of Trypanosoma cruzi and their relationship to evasion of host defences.Identification of C3 acceptors responsible for complement activation in Crithidia fasciculata.The emerging role of complement lectin pathway in trypanosomatids: molecular bases in activation, genetic deficiencies, susceptibility to infection, and complement system-based therapeutics.

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P2860

Evasion of alternative complement pathway by Trypanosoma cruzi results from inefficient binding of factor B.

http://www.wikidata.org/entity/Q37397900

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on September 1986

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Evasion of alternative complem ...... efficient binding of factor B.

@en

Evasion of alternative complem ...... efficient binding of factor B.

@nl

type

label

Evasion of alternative complem ...... efficient binding of factor B.

@en

Evasion of alternative complem ...... efficient binding of factor B.

@nl

prefLabel

Evasion of alternative complem ...... efficient binding of factor B.

@en

Evasion of alternative complem ...... efficient binding of factor B.

@nl

P1433

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P356

PNAS.83.17.6593

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Proceedings of the National Academy of Sciences of the United States of America

P1476

Evasion of alternative complem ...... efficient binding of factor B.

@en

P2093

Gaither T

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Hammer C

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Joiner K

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Sher A

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P2860

Isolation of a human erythrocyte membrane glycoprotein with decay-accelerating activity for C3 convertases of the complement system

Complement receptor is an inhibitor of the complement cascade

Control of the amplification convertase of complement by the plasma protein beta1H

Interaction between the third complement protein and cell surface macromolecules

Regulation of the amplification C3 convertase of human complement by an inhibitory protein isolated from human erythrocyte membrane

Inhibition of complement activation on the surface of cells after incorporation of decay-accelerating factor (DAF) into their membranes

Formation of the initial C3 convertase of the alternative complement pathway. Acquisition of C3b-like activities by spontaneous hydrolysis of the putative thioester in native C3

Growth cycle-dependent generation of complement-resistant Leishmania promastigotes.

Enzymatic treatment transforms trypomastigotes of Trypanosoma cruzi into activators of alternative complement pathway and potentiates their uptake by macrophages

Studies on the mechanism of bacterial resistance to complement-mediated killing. II. C8 and C9 release C5b67 from the surface of Salmonella minnesota S218 because the terminal complex does not insert into the bacterial outer membrane.

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6593-6597

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scholarly article

P356

10.1073/PNAS.83.17.6593

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17

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83

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1986-09-01T00:00:00Z

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20212371

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P698

2944112

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P921

Trypanosoma cruzi

P932

386550

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