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Jenny E. Gumperz

Researcher at University of Wisconsin-Madison

Publications -  97
Citations -  9612

Jenny E. Gumperz is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Natural killer T cell & CD1D. The author has an hindex of 49, co-authored 90 publications receiving 9161 citations. Previous affiliations of Jenny E. Gumperz include Harvard University & Stanford University.

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Functionally Distinct Subsets of CD1d-restricted Natural Killer T Cells Revealed by CD1d Tetramer Staining

TL;DR: The results show that the various activities of CD1d-restricted T cells in tumor rejection, autoimmune disease, and microbial infections could result from activation of functionally distinct subsets, and that inflammatory and antigenic stimuli may influence different effector functions.
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Mechanism of CD1d-restricted natural killer T cell activation during microbial infection

TL;DR: This data support a model in which NKT cells use a unique activation mechanism not requiring their recognition of microbial antigens, and propose this mechanism of activation as a major pathway responsible for the rapid activation of N KT cells in different microbial infections.
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The Bw4 public epitope of HLA-B molecules confers reactivity with natural killer cell clones that express NKB1, a putative HLA receptor

TL;DR: The results show that the presence of the Bw4 epitope influences recognition of HLA-B molecules by NK cells that express NKB1, and suggest that the N KB1 molecule may act as a receptor for Bw 4+ H LA-B alleles.
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Murine CD1d-Restricted T Cell Recognition of Cellular Lipids

TL;DR: It is shown that after addition of a lipid extract from a tumor cell line, plate-bound mCD1d molecules stimulated an NKT cell hybridoma, which responded strongly to three purified phospholipids, but failed to recognize alpha-GalCer.
Journal Article

Direct Binding and Functional Transfer of NK Cell Inhibitory Receptors Reveal Novel Patterns of HLA-C Allotype Recognition

TL;DR: Results show that KIR2DL receptors are specific for HLA-C, but that recognition of H LA-C allotypes appears more permissive than indicated by previous functional experiments.