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See Liang Ng

Researcher at Nanyang Technological University

Publications -  5
Citations -  194

See Liang Ng is an academic researcher from Nanyang Technological University. The author has contributed to research in topics: Immune system & CD8. The author has an hindex of 4, co-authored 5 publications receiving 141 citations.

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Transient ablation of alveolar macrophages leads to massive pathology of influenza infection without affecting cellular adaptive immunity

TL;DR: AM‐ablated mice, infected with a normally sublethal dose of PR8 influenza virus, showed dramatically increased virus load in the lungs, severe airway inflammation, pulmonary edema and vascular leakage, which caused the death of the infected animals.
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A Discrete Subset of Monocyte-Derived Cells among Typical Conventional Type 2 Dendritic Cells Can Efficiently Cross-Present

TL;DR: It is reported that classically defined cDC2s contain a discrete population of monocyte-derived migratory antigen-presenting cells with Mϕ phenotype but functional DC features, including cross-presentation.
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Type 1 Conventional CD103+ Dendritic Cells Control Effector CD8+ T Cell Migration, Survival, and Memory Responses During Influenza Infection.

TL;DR: A previously unappreciated and multifaceted role of CD103+ DCs in controlling pulmonary T cell-mediated immune responses is demonstrated, suggesting that cDC1 are not only involved in primary T cell activation, but also in supporting the development of effective memory CD8+ T cell precursors.
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Role and contribution of pulmonary CD103+ dendritic cells in the adaptive immune response to Mycobacterium tuberculosis

TL;DR: A previously unidentified role for pulmonary CD103+ DCs is supported in the rapid mobilization of mycobacteria from the lungs to the draining LN soon after exposure to M. tuberculosis, which is a critical step for the development of the host adaptive immune response.
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Renal CD169++ resident macrophages are crucial for protection against acute systemic candidiasis.

TL;DR: In this article, the authors describe a unique CD169++ TRM subset that controls Candida growth and inflammation during acute systemic candidiasis, without being actively involved in direct fungal clearance, increase host resistance by promoting IFNγ release and neutrophil ROS activity.