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Publication : CD4+ T cell--mediated tumor rejection involves inhibition of angiogenesis that is dependent on IFN gamma receptor expression by nonhematopoietic cells.

First Author  Qin Z Year  2000
Journal  Immunity Volume  12
Issue  6 Pages  677-86
PubMed ID  10894167 Mgi Jnum  J:63089
Mgi Id  MGI:1860414 Doi  10.1016/s1074-7613(00)80218-6
Citation  Qin Z, et al. (2000) CD4+ T cell--mediated tumor rejection involves inhibition of angiogenesis that is dependent on IFN gamma receptor expression by nonhematopoietic cells. Immunity 12(6):677-86
abstractText  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 IFN gamma dependent but does not require IFN gamma receptor (IFN gamma R) 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.
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