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Daniel Lingwood

Researcher at Ragon Institute of MGH, MIT and Harvard

Publications -  66
Citations -  11494

Daniel Lingwood is an academic researcher from Ragon Institute of MGH, MIT and Harvard. The author has contributed to research in topics: Antibody & Antigen. The author has an hindex of 27, co-authored 55 publications receiving 9015 citations. Previous affiliations of Daniel Lingwood include Harvard University & University of Guelph.

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Defining and Manipulating B Cell Immunodominance Hierarchies to Elicit Broadly Neutralizing Antibody Responses against Influenza Virus.

TL;DR: A computational model of affinity maturation is developed to map the patterns of immunodominance that evolve upon immunization with natural and engineered displays of hemagglutinin (HA), the influenza vaccine antigen and demonstrates that complex patterns in antibody immunogenicity can be rationally defined and then manipulated to elicit engineered immunity.
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Generation of Cubic Membranes by Controlled Homotypic Interaction of Membrane Proteins in the Endoplasmic Reticulum

TL;DR: In this paper, the authors used controlled dimerization of artificial membrane proteins in mammalian tissue culture cells to induce an expansion of the endoplasmic reticulum (ER) with cubic symmetry.
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The Loss of Bcl-6 Expressing T Follicular Helper Cells and the Absence of Germinal Centers in COVID-19

TL;DR: Analysis of postmortem thoracic lymph nodes and spleens in acute SARS-CoV-2 infection identifies defective Bcl-6+TFH cell generation and dysregulated humoral immune induction early in COVID-19 disease, providing a mechanistic explanation for the limited durability of antibody responses in coronavirus infections and suggest that achieving herd immunity through natural infection may be difficult.
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The persistence of interleukin-6 is regulated by a blood buffer system derived from dendritic cells.

TL;DR: In this article, the authors found that conventional dendritic cells (cDCs), defined in mice via expression of the transcription factor Zbtb46, were a major source of circulating sIL-6R and thus regulated IL-6 signaling.