Rezeptoren und Signalproteine des angeborenen Immunsystems als neue Zielstrukturen der Sepsistherapie. Reprogrammierung der Immunantwort

B. Holzmann; H. Weighardt; C. D. Heidecke

doi:10.1007/s00104-002-0592-4

Rezeptoren und Signalproteine des angeborenen Immunsystems als neue Zielstrukturen der Sepsistherapie. Reprogrammierung der Immunantwort

Translated title of the contribution: Receptors and signal proteins of the innate immune system as new targets in sepsis therapy. Reprogramming of the immune response

B. Holzmann
, H. Weighardt
, C. D. Heidecke

Department of Surgery

Technical University of Munich
Ernst-Moritz-Arndt Universität Greifswald

Research output: Contribution to journal › Review article › peer-review

1 Scopus citations

Abstract

During polymicrobial sepsis, microbial pathogens and their products activate the innate immune system through signaling receptors of the Toll-like receptor (TLR) family, resulting in hyperinflammation and organ injury. The analysis of preclinical mouse models has shown that inactivation of the common TLR signaling adaptor protein MyD88 prevents the hyperinflammatory response and improves survival. Importantly, MyD88 deficiency does not impair antibacterial defense mechanisms. Thus, TLRs and proteins involved in TLR signaling may represent interesting targets for the development of new drugs for reprogramming pathophysiological immune responses during sepsis.

Translated title of the contribution	Receptors and signal proteins of the innate immune system as new targets in sepsis therapy. Reprogramming of the immune response
Original language	German
Pages (from-to)	61-64
Number of pages	4
Journal	Chirurg
Volume	74
Issue number	1
DOIs	https://doi.org/10.1007/s00104-002-0592-4
State	Published - Jan 2003

Access to Document

10.1007/s00104-002-0592-4

Cite this

@article{d35a5cb8c54a42ae80e3c5da34193e07,

title = "Rezeptoren und Signalproteine des angeborenen Immunsystems als neue Zielstrukturen der Sepsistherapie. Reprogrammierung der Immunantwort",

abstract = "During polymicrobial sepsis, microbial pathogens and their products activate the innate immune system through signaling receptors of the Toll-like receptor (TLR) family, resulting in hyperinflammation and organ injury. The analysis of preclinical mouse models has shown that inactivation of the common TLR signaling adaptor protein MyD88 prevents the hyperinflammatory response and improves survival. Importantly, MyD88 deficiency does not impair antibacterial defense mechanisms. Thus, TLRs and proteins involved in TLR signaling may represent interesting targets for the development of new drugs for reprogramming pathophysiological immune responses during sepsis.",

keywords = "Cytokines, Innate immunity, Sepsis, Toll-like receptors",

author = "B. Holzmann and H. Weighardt and Heidecke, \{C. D.\}",

year = "2003",

month = jan,

doi = "10.1007/s00104-002-0592-4",

language = "Deutsch",

volume = "74",

pages = "61--64",

journal = "Chirurg",

issn = "0009-4722",

publisher = "Springer Medizin",

number = "1",

}

TY - JOUR

T1 - Rezeptoren und Signalproteine des angeborenen Immunsystems als neue Zielstrukturen der Sepsistherapie. Reprogrammierung der Immunantwort

AU - Holzmann, B.

AU - Weighardt, H.

AU - Heidecke, C. D.

PY - 2003/1

Y1 - 2003/1

N2 - During polymicrobial sepsis, microbial pathogens and their products activate the innate immune system through signaling receptors of the Toll-like receptor (TLR) family, resulting in hyperinflammation and organ injury. The analysis of preclinical mouse models has shown that inactivation of the common TLR signaling adaptor protein MyD88 prevents the hyperinflammatory response and improves survival. Importantly, MyD88 deficiency does not impair antibacterial defense mechanisms. Thus, TLRs and proteins involved in TLR signaling may represent interesting targets for the development of new drugs for reprogramming pathophysiological immune responses during sepsis.

AB - During polymicrobial sepsis, microbial pathogens and their products activate the innate immune system through signaling receptors of the Toll-like receptor (TLR) family, resulting in hyperinflammation and organ injury. The analysis of preclinical mouse models has shown that inactivation of the common TLR signaling adaptor protein MyD88 prevents the hyperinflammatory response and improves survival. Importantly, MyD88 deficiency does not impair antibacterial defense mechanisms. Thus, TLRs and proteins involved in TLR signaling may represent interesting targets for the development of new drugs for reprogramming pathophysiological immune responses during sepsis.

KW - Cytokines

KW - Innate immunity

KW - Sepsis

KW - Toll-like receptors

UR - https://www.scopus.com/pages/publications/0037672878

U2 - 10.1007/s00104-002-0592-4

DO - 10.1007/s00104-002-0592-4

M3 - Übersichtsartikel

C2 - 12552407

AN - SCOPUS:0037672878

SN - 0009-4722

VL - 74

SP - 61

EP - 64

JO - Chirurg

JF - Chirurg

IS - 1

ER -

Rezeptoren und Signalproteine des angeborenen Immunsystems als neue Zielstrukturen der Sepsistherapie. Reprogrammierung der Immunantwort

Abstract

Access to Document

Other files and links

Fingerprint

Cite this