期刊
CANCER LETTERS
卷 452, 期 -, 页码 244-253出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2019.03.040
关键词
CCL22; IL-8; Macrophage; Malignant pleural effusion; Immunosuppressive tumor microenvironment
类别
资金
- National Natural Science Foundation of China [81771781, 81602024, 81872410]
- States Key Project of Research and Development Plan [2016YFC1303501]
- International Research Cooperation Grant from Science and Technology Department of Henan Province [162102410059]
- Ministry of Public Health [201501004]
Immune dysfunction often occurs in malignant pleural effusion (MPE). In our previous study, TGF-beta derived predominantly from macrophages plays an important role in impairing T cell cytotoxicity in MPE. Therefore, we aimed to investigate whether other immunoregulatory cells and factors mediated TGF-beta secretion from macrophages, involved in the immunosuppressive microenvironment of MPE, and to provide clues for potential immune therapy for MPE as well. We found that CCL22 level in MPE was significantly higher than that in nonmalignant pleural effusion. The high level of CCL22 was closely associated with poor survival in MPE patients with lung cancer. CCL22 was dominantly produced by tumor-associated macrophages (TAMs) in MPE. Meanwhile, TAM-derived TGF-beta, mediated CCL22 expression in TAMs via c-Fos. CCL22 promoted the recruitment of regulatory T cells (Tregs) in MPE. Lastly, Treg-secreted high level of IL-8 further induced TGF-beta production from TAMs, and promoted the immunosuppressive tumor microenvironment in MPE. Our results indicate that macrophage-derived CCL22 plays an important role in the immunosuppressive tumor microenvironment via IL-8 in MPE.
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