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胸腺基质淋巴细胞生成素是乳腺癌进展的关键介质。

Thymic stromal lymphopoietin is a key mediator of breast cancer progression.

机构信息

Immunotherapeutics Unit, Laboratory of Molecular Biology and Immunology, National Institute on Aging, Baltimore, MD 21224, USA.

出版信息

J Immunol. 2011 May 15;186(10):5656-62. doi: 10.4049/jimmunol.1100463. Epub 2011 Apr 13.

DOI:10.4049/jimmunol.1100463
PMID:21490155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3401482/
Abstract

Inflammation is a double-edged sword that can promote or suppress cancer progression. In this study, we report that thymic stromal lymphopoietin (TSLP), an IL-7-like type 1 inflammatory cytokine that is often associated with the induction of Th2-type allergic responses in the lungs, is also expressed in human and murine cancers. Our studies with murine cancer cells indicate that TSLP plays an essential role in cancer escape, as its inactivation in cancer cells alone was sufficient to almost completely abrogate cancer progression and lung metastasis. The cancer-promoting activity of TSLP primarily required signaling through the TSLP receptor on CD4(+) T cells, promoting Th2-skewed immune responses and production of immunosuppressive factors such as IL-10 and IL-13. Expression of TSLP therefore may be a useful prognostic marker, and its targeting could have therapeutic potential.

摘要

炎症是一把双刃剑,既能促进也能抑制癌症的进展。在这项研究中,我们报告称,胸腺基质淋巴细胞生成素(TSLP)是一种 IL-7 样的 1 型炎症细胞因子,通常与肺部诱导 Th2 型过敏反应有关,它也在人类和鼠类癌症中表达。我们对鼠类癌细胞的研究表明,TSLP 在癌症逃逸中起着至关重要的作用,因为单独在癌细胞中失活 TSLP 就足以几乎完全阻止癌症的进展和肺转移。TSLP 的促癌活性主要需要通过 TSLP 受体在 CD4(+) T 细胞上信号传导来实现,促进 Th2 偏向性免疫反应,并产生免疫抑制因子,如 IL-10 和 IL-13。因此,TSLP 的表达可能是一个有用的预后标志物,其靶向治疗可能具有潜在的治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/791bea26393b/nihms389948f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/0a204f502101/nihms389948f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/0d46dcb2cccc/nihms389948f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/51301b8d9f8c/nihms389948f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/4bff564fbb64/nihms389948f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/7bb6077708f9/nihms389948f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/791bea26393b/nihms389948f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/0a204f502101/nihms389948f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/0d46dcb2cccc/nihms389948f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/51301b8d9f8c/nihms389948f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/4bff564fbb64/nihms389948f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/7bb6077708f9/nihms389948f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de73/3401482/791bea26393b/nihms389948f6.jpg

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Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19455-60. doi: 10.1073/pnas.1008271107. Epub 2010 Oct 25.
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Cancer Res. 2009 Jul 15;69(14):5996-6004. doi: 10.1158/0008-5472.CAN-08-4619. Epub 2009 Jun 30.
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TSLP conditions the lung immune environment for the generation of pathogenic innate and antigen-specific adaptive immune responses.
J Immunol. 2025 Feb 24;214(3):399-412. doi: 10.1093/jimmun/vkae021.
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Metabolic reprogramming and therapeutic resistance in primary and metastatic breast cancer.原发性和转移性乳腺癌中的代谢重编程和治疗抵抗。
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