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Klaas P. J. M. van Gisbergen

Researcher at University of Amsterdam

Publications -  59
Citations -  4191

Klaas P. J. M. van Gisbergen is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Cytotoxic T cell & CD8. The author has an hindex of 29, co-authored 49 publications receiving 3241 citations. Previous affiliations of Klaas P. J. M. van Gisbergen include Walter and Eliza Hall Institute of Medical Research & VU University Amsterdam.

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Neutrophils mediate immune modulation of dendritic cells through glycosylation-dependent interactions between Mac-1 and DC-SIGN

TL;DR: In this article, the authors demonstrate that neutrophils strongly cluster with immature dendritic cells (DCs) and that activated, not resting, neutrophILS induce maturation of DCs that enables these DCs to trigger strong T cell proliferation and T helper type 1 polarization of T cells.
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Timing and tuning of CD27–CD70 interactions: the impact of signal strength in setting the balance between adaptive responses and immunopathology

TL;DR: It is concluded that optimal tuning of CD27–CD70 interaction is crucial for the regulation of the cellular immune response and that these receptors do not have a unique function per se but that rather the timing, context, and intensity of these costimulatory signals determine the functional consequence of their activity.
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Tissue-resident memory T cells at the center of immunity to solid tumors.

TL;DR: What defines TRM cells as a separate lineage and how these cells are generated are described and discussed, as well as implications for the treatment of patients with cancer.
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Dendritic cells recognize tumor-specific glycosylation of carcinoembryonic antigen on colorectal cancer cells through dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin.

TL;DR: Dendritic cells may recognize colorectal cancer cells through binding of DC-SIGN to tumor-specific glycosylation on CEA, similar to pathogens that target DC-sign to escape immunosurveillance, tumor cells may interact with DC- SIGN to suppress dendritic cell functions.