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William C. Fanslow

Researcher at Amgen

Publications -  102
Citations -  13667

William C. Fanslow is an academic researcher from Amgen. The author has contributed to research in topics: CD40 & Antibody. The author has an hindex of 51, co-authored 101 publications receiving 13312 citations. Previous affiliations of William C. Fanslow include Science Applications International Corporation.

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Journal ArticleDOI

ULBPs, Novel MHC Class I–Related Molecules, Bind to CMV Glycoprotein UL16 and Stimulate NK Cytotoxicity through the NKG2D Receptor

TL;DR: Masking of NK cell recognition of ULBP or MIC antigens by UL16 provides a potential mechanism by which human cytomegalovirus-infected cells might evade attack by the immune system.
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Molecular and biological characterization of a murine ligand for CD40

TL;DR: The cloning of a ligand for CD40 that is expressed on the cell surface of activated T cells and mediates B-cell proliferation in the absence of co-stimulus, as well as IgE production in the presence of interIeukin-4 is reported.
Journal Article

Human IL-17: a novel cytokine derived from T cells.

TL;DR: A cDNA encoding human IL-17 (hIL-17) was cloned from a CD4+ T cell library and contains an N-terminal signal peptide and exhibits 72% amino acid identity with HVS13, an open reading frame from a T-lymphotropic Herpesvirus saimiri, and 63% with murine CTLA8.
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Herpesvirus saimiri encodes a new cytokine, IL-17, which binds to a novel cytokine receptor.

TL;DR: Herpesvirus Saimiri gene 13 (HVS13) exhibits 57% identity with the predicted sequence of a T cell-derived molecule termed CTLA8, which is defined as novel cytokines that bind to a novel cytokine receptor and proposed to call these molecules IL- 17, vIL-17, and IL-17R.
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CD40 ligand gene defects responsible for X-linked hyper-IgM syndrome

TL;DR: Abnormalities in the CD40L gene were associated with an X-linked immunodeficiency in humans [hyper-IgM (immunoglobulin M) syndrome], characterized by elevated concentrations of serum IgM and decreased amounts of all other isotypes.