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CD4+ T cell-mediated tumor rejection involves inhibition of angiogenesis that is dependent on IFNgamma receptor expression by nonhematopoietic cells

PubMed:View item in PubMed
Creators Name:Qin, Z.H. and Blankenstein, T.
Journal Title:Immunity
Journal Abbreviation:Immunity
Volume:12
Number:6
Page Range:677-686
Date:1 June 2000
Keywords:Angiogenesis Inhibitors, CD4-Positive T-Lymphocytes, Cell-Free System, Cultured Tumor Cells, Experimental Neoplasms, Graft Rejection, Growth Inhibitors, Hematopoietic Stem Cells, Interferon Receptors, Knockout Mice, Lymphocyte Activation, Lymphocyte Depletion, Neoplasm Transplantation, Nude Mice, T-Lymphocyte Subsets, Animals, Mice
Abstract:Immunity against MHC class II- tumors can be mediated by CD4+ T cells in the effector phase through an unknown mechanism. We show that this is IFNγ dependent but does not require IFN{gamma} receptor (IFNγR) expression on tumor cells, T cells, or other hematopoietic cells and that IFN{gamma}R expression is not necessary in the priming phase. However, tumor immunity requires IFN{gamma}R expression on nonhematopoietic cells in the effector phase and involves inhibition of tumor-induced angiogenesis. This shows that an effective anti-tumor response involves communication between CD4+ T cells and nonhematopoietic cells, most likely within the tumor stroma, and that tumor immunity must not entirely rely on direct tumor cell killing.
ISSN:1074-7613
Publisher:Cell Press (U.S.A.)
Item Type:Article

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