Journal
CARCINOGENESIS
Volume 32, Issue 3, Pages 296-304Publisher
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgq265
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Funding
- 863 Program of China [2006AA02Z158]
- Important National Science and Technology Specific Projects [2009ZX09301-014]
- Chinese Department of Education [20070487103]
- National Natural Science Foundation of China [30671970, 30901341]
- Medicine Science Foundation of Guangdong Province, China [A2009390]
- Basic Medicine School of Southern Medical University [B1100363, B1000344]
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CC chemokine ligand 21 (CCL21) is a known attractant for CCR7-positive (CCR7+) cells, but its additional role in the immunogenicity of CCR7+ cells remains poorly understood. This study explored the effects of CCL21-CCR7 ligation on cancer immunogenicity and related antitumor immune response, in the presence and absence of mitomycin C (MMC) treatment. CCL21-CCR7 binding upregulated human leukocyte antigen class I-restricted tumor antigen presentation with increased expression of human leukocyte antigen class I and transporter associated with antigen processing-1. In addition, CCL21 restrained the tumor-derived immunosuppressive factors FasL and transforming growth factor-beta. Consequently, CCL21 facilitated cancer-educated lymphocytes reaction in vitro. In the tumor-bearing mouse, CCL21 inhibited tumor growth and prolonged mouse survival via lymphocytes, especially in CCR7+ cancer cells. Furthermore, Toll-like receptor 2 activation of lymphocytes assisted the tumor-suppression functions of CCL21, in vitro and in vivo. This study implies that CCL21 improved the immunogenicity of the CCR7+ breast cancer cell line even with MMC treatment and triggered antitumor response by lymphocytes. These findings provide a new insight into the research and application of CCL21-associated antitumor response.
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