Induction of experimental cerebral malaria is independent of TLR2/4/9.

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Induction of experimental cerebral malaria is independent of TLR2/4/9. / Lepenies, Bernd; Cramer, Jakob; Burchard, Gerd-Dieter; Wagner, Hermann; Kirschning, Carsten J; Jacobs, Thomas.

in: MED MICROBIOL IMMUN, Jahrgang 197, Nr. 1, 1, 2008, S. 39-44.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Lepenies, B, Cramer, J, Burchard, G-D, Wagner, H, Kirschning, CJ & Jacobs, T 2008, 'Induction of experimental cerebral malaria is independent of TLR2/4/9.', MED MICROBIOL IMMUN, Jg. 197, Nr. 1, 1, S. 39-44. <http://www.ncbi.nlm.nih.gov/pubmed/17668237?dopt=Citation>

APA

Lepenies, B., Cramer, J., Burchard, G-D., Wagner, H., Kirschning, C. J., & Jacobs, T. (2008). Induction of experimental cerebral malaria is independent of TLR2/4/9. MED MICROBIOL IMMUN, 197(1), 39-44. [1]. http://www.ncbi.nlm.nih.gov/pubmed/17668237?dopt=Citation

Vancouver

Lepenies B, Cramer J, Burchard G-D, Wagner H, Kirschning CJ, Jacobs T. Induction of experimental cerebral malaria is independent of TLR2/4/9. MED MICROBIOL IMMUN. 2008;197(1):39-44. 1.

Bibtex

@article{b4aed129b0fb4ab9855378b7dfae0c5c,
title = "Induction of experimental cerebral malaria is independent of TLR2/4/9.",
abstract = "The contribution of the Toll-like receptor (TLR) cascade to the pathogenesis of cerebral malaria (CM) is controversially discussed. TLR2 and TLR9 were reported to be involved in the induction of CM in a study while recently TLR signaling was shown to be dispensable for the development of CM. Using Plasmodium berghei ANKA (PbA) infection of mice as a model of CM, we demonstrate here that the induction of CM is independent of TLR2, 4 and 9. Using triple TLR2/4/9-deficient mice, we exclude synergistic effects between the single TLRs that have been previously implicated with malaria pathology. In conclusion, this study shows that the activation of the innate immune response and the development of CM is not dependent on the engagement of TLR2/4/9.",
author = "Bernd Lepenies and Jakob Cramer and Gerd-Dieter Burchard and Hermann Wagner and Kirschning, {Carsten J} and Thomas Jacobs",
year = "2008",
language = "Deutsch",
volume = "197",
pages = "39--44",
journal = "MED MICROBIOL IMMUN",
issn = "0300-8584",
publisher = "Springer",
number = "1",

}

RIS

TY - JOUR

T1 - Induction of experimental cerebral malaria is independent of TLR2/4/9.

AU - Lepenies, Bernd

AU - Cramer, Jakob

AU - Burchard, Gerd-Dieter

AU - Wagner, Hermann

AU - Kirschning, Carsten J

AU - Jacobs, Thomas

PY - 2008

Y1 - 2008

N2 - The contribution of the Toll-like receptor (TLR) cascade to the pathogenesis of cerebral malaria (CM) is controversially discussed. TLR2 and TLR9 were reported to be involved in the induction of CM in a study while recently TLR signaling was shown to be dispensable for the development of CM. Using Plasmodium berghei ANKA (PbA) infection of mice as a model of CM, we demonstrate here that the induction of CM is independent of TLR2, 4 and 9. Using triple TLR2/4/9-deficient mice, we exclude synergistic effects between the single TLRs that have been previously implicated with malaria pathology. In conclusion, this study shows that the activation of the innate immune response and the development of CM is not dependent on the engagement of TLR2/4/9.

AB - The contribution of the Toll-like receptor (TLR) cascade to the pathogenesis of cerebral malaria (CM) is controversially discussed. TLR2 and TLR9 were reported to be involved in the induction of CM in a study while recently TLR signaling was shown to be dispensable for the development of CM. Using Plasmodium berghei ANKA (PbA) infection of mice as a model of CM, we demonstrate here that the induction of CM is independent of TLR2, 4 and 9. Using triple TLR2/4/9-deficient mice, we exclude synergistic effects between the single TLRs that have been previously implicated with malaria pathology. In conclusion, this study shows that the activation of the innate immune response and the development of CM is not dependent on the engagement of TLR2/4/9.

M3 - SCORING: Zeitschriftenaufsatz

VL - 197

SP - 39

EP - 44

JO - MED MICROBIOL IMMUN

JF - MED MICROBIOL IMMUN

SN - 0300-8584

IS - 1

M1 - 1

ER -