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Lei Shi

Researcher at Georgia State University

Publications -  16
Citations -  649

Lei Shi is an academic researcher from Georgia State University. The author has contributed to research in topics: Myeloid-derived Suppressor Cell & Proinflammatory cytokine. The author has an hindex of 8, co-authored 16 publications receiving 461 citations. Previous affiliations of Lei Shi include Nanjing University.

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MicroRNA-17/20a/106a modulate macrophage inflammatory responses through targeting signal-regulatory protein α

TL;DR: The role of identified microRNAs in controlling SIRPα synthesis in leukocytes and leukocyte inflammatory responses was determined in this paper, showing that miR-17, miR20a, and miR106a specifically bound to the same seed sequence within the 3' untranslated region and correlated inversely with SIRpα protein levels in various cells.
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Cd47-Sirpα interaction and IL-10 constrain inflammation-induced macrophage phagocytosis of healthy self-cells

TL;DR: The present study reveals that macrophage phagocytosis toward healthy self-cells is controlled by a two-tier mechanism: a forefront activation mechanism requiring the inflammatory cytokine-stimulated protein kinase C (PKC)-spleen tyrosine kinase (Syk) pathway, and the subsequent self-target discrimination mechanism controlled by the CD47-signal regulatory protein α (SIRPα)–mediated inhibition.
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Loss of Cell Surface CD47 Clustering Formation and Binding Avidity to SIRPα Facilitate Apoptotic Cell Clearance by Macrophages

TL;DR: This study reveals that CD47 normally is clustered in lipid rafts on nonapoptotic cells but is diffused in the plasma membrane when apoptosis occurs; this transformation of CD47 greatly reduces the strength ofCD47–SIRPα engagement, resulting in the phagocytosis of apoptotic cells.
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Arginase-1 is neither constitutively expressed in nor required for myeloid-derived suppressor cell-mediated inhibition of T-cell proliferation.

TL;DR: Surprisingly, the study indicates that induction of arginase‐1 expression is not conducive to the critical MDSC‐mediated inhibition toward T cells, which is rather dependent on direct cell contacts undiminished by PD‐L1 blockade or SIRPα deficiency.