Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii.

Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii. Research Abstract Details 

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Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii. Abstract Text:

Debierre-Grockiego,Marco A Campos,Nahid Azzouz, Schmidt,Ulrike Bieker,Marianne Garcia Resende,Daniel Santos Mansur,Ralf Weingart,Richard R Schmidt,Douglas T Golenbock,Ricardo T Gazzinelli,Ralph T Schwarz,

GPIs isolated from Toxoplasma gondii, as well as a chemically synthesized GPI lacking the lipid moiety, activated a reporter gene in Chinese hamster ovary cells expressing TLR4, while the core glycan and lipid moieties cleaved from the GPIs activated both TLR4- and TLR2-expressing cells. MyD88, but not TLR2, TLR4, or CD14, is absolutely needed to trigger TNF-alpha production by macrophages exposed to T. gondii GPIs. Importantly, TNF-alpha response to GPIs was completely abrogated in macrophages from TLR2/4-double-deficient mice. MyD88(-/-) mice were more susceptible to death than wild-type (WT), TLR2(-/-), TLR4(-/-), TLR2/4(-/-), and CD14(-/-) mice infected with the ME-49 strain of T. gondii. The cyst number was higher in the brain of TLR2/4(-/-), but not TLR2(-/-), TLR4(-/-), and CD14(-/-), mice, as compared with WT mice. Upon infection with the ME-49 strain of T. gondii, we observed no decrease of IL-12 and IFN-gamma production in TLR2-, TLR4-, or CD14-deficient mice. Indeed, splenocytes from T. gondii-infected TLR2(-/-) and TLR2/4(-/-) mice produced more IFN-gamma than cells from WT mice in response to in vitro stimulation with parasite extracts enriched in GPI-linked surface proteins. Together, our results suggest that both TLR2 and TLR4 receptors may participate in the host defense against T. gondii infection through their activation by the GPIs and could work together with other MyD88-dependent receptors, like other TLRs or even IL-18R or IL-1R, to obtain an effective host response against T. gondii infection.

Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii. Publishing Authors By Initials

F Debierre-Grockiego,MA Campos,N Azzouz,J Schmidt,U Bieker,MG Resende,DS Mansur,R Weingart,RR Schmidt,DT Golenbock,RT Gazzinelli,RT Schwarz,

For similar parasitic diseases: parasitic diseases, animal: protozoan infections, animal: toxoplasmosis, animal research abstracts see: parasitic diseases: parasitic diseases, animal: protozoan infections, animal: toxoplasmosis, animal research

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Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 179

Page Numbers: 1129-37

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 15

MONTH: Jul

YEAR: 2007

Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii. Keywords Mesh Terms:

KEYWORDS: Toxoplasmosis, Animal

MESH TERMS: immunology

Chemical & Substance for Abstract: Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii. Information

Substance Name: Toll-Like Receptor 4

Registry Number: 0

Grant and Affiliation Information for Activation of TLR2 and TLR4 by glycosylphosphatidylinositols derived from Toxoplasma gondii.

AFFILIATION: Institut für Virologie, AG Parasitologie, Philipps University, Marburg, Germany. debierre@staff.uni-marburg.de

Country: United States

AGENCY: United States NIAID

GRANT: 1R01AI071319-01

ACRONYM: AI

MEDLINETA: J Immunol

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