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Responses of innate immune cells to group A Streptococcus.

Authors
  • Fieber, Christina
  • Kovarik, Pavel
Type
Published Article
Journal
Frontiers in Cellular and Infection Microbiology
Publisher
Frontiers Media SA
Publication Date
Jan 01, 2014
Volume
4
Pages
140–140
Identifiers
DOI: 10.3389/fcimb.2014.00140
PMID: 25325020
Source
Medline
Keywords
License
Unknown

Abstract

Group A Streptococcus (GAS), also called Streptococcus pyogenes, is a Gram-positive beta-hemolytic human pathogen which causes a wide range of mostly self-limiting but also several life-threatening diseases. Innate immune responses are fundamental for defense against GAS, yet their activation by pattern recognition receptors (PRRs) and GAS-derived pathogen-associated molecular patterns (PAMPs) is incompletely understood. In recent years, the use of animal models together with the powerful tools of human molecular genetics began shedding light onto the molecular mechanisms of innate immune defense against GAS. The signaling adaptor MyD88 was found to play a key role in launching the immune response against GAS in both humans and mice, suggesting that PRRs of the Toll-like receptor (TLR) family are involved in sensing this pathogen. The specific TLRs and their ligands have yet to be identified. Following GAS recognition, induction of cytokines such as TNF and type I interferons (IFNs), leukocyte recruitment, phagocytosis, and the formation of neutrophil extracellular traps (NETs) have been recognized as key events in host defense. A comprehensive knowledge of these mechanisms is needed in order to understand their frequent failure against GAS immune evasion strategies.

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