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Courtney A. Becker

Researcher at Cedars-Sinai Medical Center

Publications -  13
Citations -  2733

Courtney A. Becker is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Staphylococcus aureus & Pattern recognition receptor. The author has an hindex of 10, co-authored 12 publications receiving 2324 citations.

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Interactions Between Commensal Fungi and the C-Type Lectin Receptor Dectin-1 Influence Colitis

TL;DR: It is shown that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1, which substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.
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Activation of the innate immune receptor Dectin-1 upon formation of a /`phagocytic synapse/'

TL;DR: The ‘phagocytic synapse’ now provides a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance, thereby initiating direct cellular antimicrobial responses only when they are required.
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Hexokinase Is an Innate Immune Receptor for the Detection of Bacterial Peptidoglycan

TL;DR: This study shows that a metabolic enzyme can act as a pattern recognition receptor and is caused by release of N-acetylglucosamine that is detected in the cytosol by the glycolytic enzyme hexokinase.
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Staphylococcus aureus Evades Lysozyme-Based Peptidoglycan Digestion that Links Phagocytosis, Inflammasome Activation, and IL-1β Secretion

TL;DR: It is demonstrated that phagocytosis and lysozyme-based cell wall degradation of S. aureus are functionally coupled to inflammasome activation and IL-1beta secretion and a case whereby a bacterium specifically subverts IL- 1beta secretion through chemical modification of its cell wall PGN is illustrated.
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Dectin-1-triggered recruitment of light chain 3 protein to phagosomes facilitates major histocompatibility complex class II presentation of fungal-derived antigens

TL;DR: Dectin-1 signaling in macrophages and bone marrow-derived dendritic cells triggers formation of LC3II, a major component of the autophagy machinery that facilitates recruitment of MHC class II molecules to phagosomes and promotes presentation of fungal-derived antigens to CD4 T cells.