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Marina Cella

Researcher at Washington University in St. Louis

Publications -  177
Citations -  41569

Marina Cella is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Receptor & T cell. The author has an hindex of 90, co-authored 164 publications receiving 37300 citations. Previous affiliations of Marina Cella include Hoffmann-La Roche & Basel Institute for Immunology.

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Dendritic cells use macropinocytosis and the mannose receptor to concentrate macromolecules in the major histocompatibility complex class II compartment: downregulation by cytokines and bacterial products.

TL;DR: The capacity of DCs to capture and process antigen could be modulated by exogenous stimuli was investigated and it was found that DCs respond to tumor necrosis factor alpha, CD40 ligand, IL-1, and lipopolysaccharide with a coordinate series of changes that include downregulation of macropinocytosis and Fc receptors, disappearance of the class II compartment, and upregulation of adhesion and costimulatory molecules.
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Ligation of CD40 on dendritic cells triggers production of high levels of interleukin-12 and enhances T cell stimulatory capacity: T-T help via APC activation.

TL;DR: It is found that ligation of CD40 by CD40L triggers the production of extremely high levels of bioactive IL-12, which is the most potent stimulus in upregulating the expression of ICAM-1, CD80, and CD86 molecules on DCs.
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Plasmacytoid monocytes migrate to inflamed lymph nodes and produce large amounts of type I interferon.

TL;DR: Results, with the distinct cell phenotype, indicate that plasmacytoid monocytes represent a specialized cell lineage that enters inflamed lymph nodes at high endothelial venules, where it produces type I interferon.
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Origin, maturation and antigen presenting function of dendritic cells

TL;DR: Dendritic cells represent the natural adjuvants for T cell responses and their therapeutic exploitation in the near future is foreseen.
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Serial triggering of many T-cell receptors by a few peptide–MHC complexes

TL;DR: It is shown that a small number of peptide–MHC complexes can achieve a high TCR occupancy, because a single complex can serially engage and trigger up to ∼200 TCRs.