CD4+ T cell-mediated tumor rejection involves inhibition of angiogenesis that is dependent on IFNγ receptor expression by nonhematopoietic cells
CD4+ T cell-mediated tumor rejection involves inhibition of angiogenesis that is dependent on IFNγ receptor expression by nonhematopoietic cells
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DOI：
10.1016/s1074-7613(00)80218-6
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发表时间：
2000-06-01
期刊：
影响因子：
32.4
通讯作者：
Blankenstein, T
中科院分区：
文献类型：
--
作者：
Qin, ZH;Blankenstein, T
针对MHC II类肿瘤的免疫可以通过效应期的CD4（+）T细胞通过未知的机制介导。我们表明，这是IFN γ依赖性的，但不需要IFN γ受体（IFN γ R）表达的肿瘤细胞，T细胞，或其他造血细胞和IFN γ R的表达是不必要的，在启动阶段。然而，肿瘤免疫需要在效应期的非造血细胞上表达IFN γ R，并涉及抑制肿瘤诱导的血管生成。这表明，有效的抗肿瘤反应涉及CD4（+）T细胞和非造血细胞之间的沟通，最有可能在肿瘤间质内，肿瘤免疫不能完全依赖于直接的肿瘤细胞杀伤。
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.