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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >CD4+ T-cell-dependent tumour rejection in an immune-privileged environment requires macrophages.
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CD4+ T-cell-dependent tumour rejection in an immune-privileged environment requires macrophages.

机译：在免疫弱化的环境中，CD4 + T细胞依赖性肿瘤排斥反应需要巨噬细胞。

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Although intraocular tumours reside in an immune-privileged site, they can circumvent immune privilege and undergo rejection. Ocular tumour rejection typically follows one of two pathways. One pathway involves CD4+ T cells, delayed-type hypersensitivity (DTH), and culmination in ischemic necrosis of the tumour and phthisis (atrophy) of the eye. The second pathway is DTH-independent and does not inflict collateral injury to ocular tissues, and the eye is preserved. In this study, we used a well-characterized tumour, Ad5E1, to investigate the role of CD4+ T cells in the non-phthisical form of intraocular tumour rejection. It has been previously documented that CD4+ T cells and interferon (IFN)-gamma are necessary for rejection of these tumours in the eye. In this study, we demonstrate that CD4+ T cells can circumvent immune privilege and infiltrate intraocular Ad5E1 tumours. Following tumour rejection, CD4+ T cells from tumour rejector mice could be adoptively transferred to severe combined immunodeficiency (SCID) mice and protect them from intraocular Ad5E1 tumour growth. Tumour-specific CD4+ T cells produced IFN-gamma in response to Ad5E1 tumour antigens. Macrophages also contributed to rejection, as they were present in intraocular Ad5E1 tumours, and local depletion of macrophages resulted in progressive tumour growth. Ocular macrophages contributed to Ad5E1 tumour rejection, as Ad5E1 tumour rejection did not occur in macrophage-depleted SCID mice reconstituted with rejector CD4+ T cells. This demonstrates that macrophage and CD4+ T-cell co-operation is needed for non-phthisical rejection of intraocular tumours.
机译：尽管眼内肿瘤位于免疫特权部位，但它们可以绕开免疫特权并遭受排斥。眼部肿瘤排斥通常遵循两种途径之一。一种途径涉及CD4 + T细胞，迟发型超敏反应（DTH）以及肿瘤缺血性坏死和眼睛的睑板裂（萎缩）中的高潮。第二种途径是不依赖DTH的，不会对眼组织造成附带伤害，并且保留了眼睛。在这项研究中，我们使用了特征明确的肿瘤Ad5E1来研究CD4 + T细胞在非眼球形式的眼内肿瘤排斥中的作用。先前已有文献证明，CD4 + T细胞和干扰素（IFN）-γ对于排斥这些眼中的肿瘤是必需的。在这项研究中，我们证明了CD4 + T细胞可以规避免疫特权并浸润眼内Ad5E1肿瘤。肿瘤排斥后，可以将来自肿瘤排斥小鼠的CD4 + T细胞过继转移至严重的联合免疫缺陷（SCID）小鼠，并保护其免受眼内Ad5E1肿瘤生长的影响。肿瘤特异性CD4 + T细胞响应Ad5E1肿瘤抗原而产生IFN-γ。巨噬细胞也存在排斥反应，因为它们存在于眼内Ad5E1肿瘤中，并且巨噬细胞的局部耗竭导致肿瘤逐渐生长。眼巨噬细胞导致Ad5E1肿瘤排斥，因为在用排斥CD4 + T细胞重组的巨噬细胞贫化SCID小鼠中未发生Ad5E1肿瘤排斥。这表明巨噬细胞和CD4 + T细胞的合作是非物理性排斥眼内肿瘤所必需的。

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