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Jonathan S. Maltzman

Researcher at Stanford University

Publications -  82
Citations -  3469

Jonathan S. Maltzman is an academic researcher from Stanford University. The author has contributed to research in topics: Cytotoxic T cell & T-cell receptor. The author has an hindex of 23, co-authored 67 publications receiving 3072 citations. Previous affiliations of Jonathan S. Maltzman include University of Pennsylvania & VA Palo Alto Healthcare System.

Papers
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T cell receptor signal strength in Treg and iNKT cell development demonstrated by a novel fluorescent reporter mouse

TL;DR: Generation of a Nur77 reporter mouse is used to demonstrate TCR signal strength during thymic selection and peripheral maintenance of conventional and nonconventional T cell subsets and presents a novel tool for studying antigen receptor activation in vivo.
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Platelets regulate lymphatic vascular development through CLEC-2–SLP-76 signaling

TL;DR: It is demonstrated that platelets regulate lymphatic vascular development by directly interacting with lymphatic endothelial cells through C-type lectin-like receptor 2 (CLEC-2) receptors, identifying platelets as the cell type in which SLP-76 signaling is required to regulate lymphatics vascular development.
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Azathioprine: old drug, new actions

TL;DR: A knowledge of the biochemical loci of action of 6-MP in the inhibition of nucleic acid synthesis is not sufficient to explain the effects of the thiopurines on the immune system.
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Enhanced T cell responses due to diacylglycerol kinase ζ deficiency

TL;DR: It is shown that DGKζ-deficient T cells are hyperresponsive to TCR stimulation both ex vivo and in vivo, and these results demonstrate the importance of DGK ζ as a physiological negative regulator of TCR signaling and T cell activation.
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An obligate cell-intrinsic function for CD28 in Tregs

TL;DR: Clear postmaturational roles for CD28 are demonstrated in FOXP3+ Tregs and mechanisms which are believed to be novel to explain how interruption of CD28-ligand interactions may enhance immune responses independent of effects on thymic development or on other cell types are provided.