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Hong-Erh Liang

Researcher at University of California, San Francisco

Publications -  42
Citations -  10281

Hong-Erh Liang is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Innate lymphoid cell & Immune system. The author has an hindex of 28, co-authored 38 publications receiving 8525 citations.

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Journal ArticleDOI

Tissue signals imprint ILC2 identity with anticipatory function.

TL;DR: Tissue-specific imprinting dictates the activating receptors ILC2s express, even in germ-free mice, and it is shown that endogenous, tissue-derived signals drive the maturation of I LC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific perturbations occurring later in life.
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A Metabolite-Triggered Tuft Cell-ILC2 Circuit Drives Small Intestinal Remodeling

TL;DR: A metabolic sensing circuit that may have evolved to facilitate mutualistic responses to luminal pathosymbionts is described that impairs infestation by new helminths, consistent with the phenomenon of concomitant immunity.
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Genetic analysis of basophil function in vivo

TL;DR: The contribution of basophils to allergic and helminth immunity remains unclear as discussed by the authors, and Locksley et al. used reporter strains and two-photon microscopy to demonstrate that basophilia does not mediate T helper type 2 priming in vivo.
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Homeostasis and effector function of lymphopenia-induced "memory-like" T cells in constitutively T cell-depleted mice.

TL;DR: Infection with the helminth Nippostrongylus brasiliensis resulted in diminished effector cell recruitment and impaired worm expulsion, demonstrating that TML cells are not sufficient to mediate an effective immune response.
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Chitin activates parallel immune modules that direct distinct inflammatory responses via innate lymphoid type 2 and γδ T cells.

TL;DR: Inhaled chitin elicited patterns of innate cytokines that targeted distinct populations of resident lymphoid cells, revealing divergent but interacting pathways underlying the tissue accumulation of specific types of inflammatory myeloid cells.