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Wolf H. Fridman

Researcher at University of Paris

Publications -  551
Citations -  60835

Wolf H. Fridman is an academic researcher from University of Paris. The author has contributed to research in topics: Immune system & Receptor. The author has an hindex of 97, co-authored 525 publications receiving 48713 citations. Previous affiliations of Wolf H. Fridman include Queen Elizabeth Hospital Birmingham & Pasteur Institute.

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Proinflammatory and antitumor properties of interleukin-18 in the gastrointestinal tract.

TL;DR: The investigations on IL-18 synthesis in normal colonic mucosa, colonic cancer and Crohn's disease (CD) show clear patterns of action on Th1 cell differentiation, cell-mediated cytotoxicity and inflammation.
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Src Homology 2 Domain-containing Inositol 5-Phosphatase 1 Mediates Cell Cycle Arrest by FcγRIIB

TL;DR: The results demonstrate that FcγRIIB use SHIP1 to inhibit pathways shared by receptor tyrosine kinases and immunoreceptors to trigger cell proliferation and cell activation, respectively, but that, in the absence ofSHIP1, F cγR IIB can use other effectors that specifically inhibit cell proliferation.
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Impaired th1/tc1 cytokine production of tumor-infiltrating lymphocytes in a model of primary intraocular B-cell lymphoma.

TL;DR: The results suggest that T-cells from intraocular B-lymphomas are characterized by a Th1/Tc1-like profile that could be partially inhibited in vivo, and raise the possibility of a T-cell immunostimulation to reactivate the Th1-Tc 1-LYmphocytes and improve intraocular antitumoral immunity.
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Therapeutic Targeting of the Colorectal Tumor Stroma

TL;DR: The features of the colorectal tumor stroma that associate with outcomes of patients are reviewed and potential therapeutic agents that target these features are discussed.
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Binding Site of Human IgG Subclasses and Their Domains for Fc Receptors of Activated Murine T Cells

TL;DR: It was demonstrated that the three human IgG subclasses shown to be cytophilic share common or linked receptors, which were not associated with the H-2 alloantigens.