C
Cenk Sumen
Researcher at Harvard University
Publications - 15
Citations - 4781
Cenk Sumen is an academic researcher from Harvard University. The author has contributed to research in topics: T cell & Major histocompatibility complex. The author has an hindex of 10, co-authored 14 publications receiving 4625 citations. Previous affiliations of Cenk Sumen include Stanford University.
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Journal ArticleDOI
The Immunological Synapse: A Molecular Machine Controlling T Cell Activation
Arash Grakoui,Shannon K. Bromley,Cenk Sumen,Mark M. Davis,Andrey S. Shaw,Paul M. Allen,Michael L. Dustin +6 more
TL;DR: Immunological synapse formation is now shown to be an active and dynamic mechanism that allows T cells to distinguish potential antigenic ligands and was a determinative event for T cell proliferation.
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Continuous T cell receptor signaling required for synapse maintenance and full effector potential.
TL;DR: TCR signaling persists for hours, has a cumulative effect and is necessary for the maintenance of the immunological synapse.
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Agonist/endogenous peptide-MHC heterodimers drive T cell activation and sensitivity.
TL;DR: It is found that some specific combinations of these heterodimers can stimulate specific T cells in a CD4-dependent manner, and indicates that the basic unit of helper T cell activation is a heterodimer of agonist peptide– and endogenous peptide-MHC complexes, stabilized by CD4.
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Intravital Microscopy: Visualizing Immunity in Context
TL;DR: The current state of the field is discussed and how IVM can generate new discoveries and serve as a "reality check" for areas of research that were formerly the exclusive domain of in vitro experimentation are outlined.
Journal ArticleDOI
Costimulation and endogenous MHC ligands contribute to T cell recognition.
Christoph Wülfing,Christoph Wülfing,Cenk Sumen,Michael D. Sjaastad,Lawren C. Wu,Michael L. Dustin,Michael L. Dustin,Mark M. Davis +7 more
TL;DR: Low-affinity ligands can contribute to synapse formation and T cell signaling and, although it lacked major TCR contact residues, it could be driven into the synapse in a TCR-dependant manner.