T cytotoxic 17 cells suppress the inflammatory
reaction by regulating chemokines in colonic cancer
Submission date: 2013-06-25
Final revision date: 2013-08-15
Acceptance date: 2013-10-09
Publication date: 2013-12-30
Cent Eur J Immunol 2013;38(4):443-448
KEYWORDS
ABSTRACT
Objective: The aim of this study was to detect the level of T cytotoxic 17 (Tc17) cells in patients with colonic cancer and explore the relationship between Tc17 cells and colonic cancer cells.
Material and methods: The numbers of Tc17 cells in both colon cancer tissue and co-culture system with SW620 were evaluated by FACS sorting. The expression of the CCL2, CXCL12, G-CSF, M-CSF and GM-CSF in SW620 was detected by qPCR after being co-cultured with Tc17 cells.
Results: Compared to the normal colon tissue, the number of Tc17 cells was significantly increased in the cancer tissue. And this number was remarkably increased after being co-cultured with SW620. Co-cultured Tc17 cells could also enhance the expression of CCL2, CXCL12 and GM-CSF.
Conclusions: Colonic cancer cells can recruit Tc17 cells to cancer tissue. These recruited Tc17 cells can promote the expression of inflammatory suppression chemokines in order to induce the immune suppression in cancer development.
Material and methods: The numbers of Tc17 cells in both colon cancer tissue and co-culture system with SW620 were evaluated by FACS sorting. The expression of the CCL2, CXCL12, G-CSF, M-CSF and GM-CSF in SW620 was detected by qPCR after being co-cultured with Tc17 cells.
Results: Compared to the normal colon tissue, the number of Tc17 cells was significantly increased in the cancer tissue. And this number was remarkably increased after being co-cultured with SW620. Co-cultured Tc17 cells could also enhance the expression of CCL2, CXCL12 and GM-CSF.
Conclusions: Colonic cancer cells can recruit Tc17 cells to cancer tissue. These recruited Tc17 cells can promote the expression of inflammatory suppression chemokines in order to induce the immune suppression in cancer development.
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| eISSN: | 1644-4124 |
| ISSN: | 1426-3912 |
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