Ma YH, Cheng WZ, Gong F, Ma AL, Yu QW, Zhang JY, Hu CY, Chen XH, Zhang DQ. Active chinese mistletoe lectin-55 enhances colon cancer surveillance through regulating innate and adaptive immune responses. World J Gastroenterol 2008; 14(34): 5274-5281 [PMID: 18785279 DOI: 10.3748/wjg.14.5274]
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Dong-Qing Zhang, Shanghai Institute of Immunology,Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. email@example.com
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Yan-Hui Ma, Wei-Zhi Cheng, Fang Gong, An-Lun Ma, Qi-Wen Yu, Ji-Ying Zhang, Chao-Ying Hu, Shanghai Jiao Tong University School of Medicine, Shanghai Institute of Immunology, Shanghai 200025, China
Xue-Hua Chen, Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai 200025, China
An-Lun Ma, Centre de recherche du CHUM, Hôpital Notre-Dame, Université de Montréal, Montréal, Québec H2L 4M1, Canada
Author contributions: Ma YH and Cheng WZ contributed equally to this work; Zhang DQ, Ma YH and Cheng WZ designed research; Ma YH, Cheng WZ, Gong F, Ma AL, Yu QW, Zhang JY, Hu CY and Chen XH performed research; Chen XH contributed new reagents/analytic tools; Ma YH, Cheng WZ and Zhang DQ wrote the paper.
Supported by The National Natural Science Foundation of China, No. 30471593 and No. 30670939; the Shanghai Leading Academic Discipline Project, No. T0206; the Shanghai Commission of Science and Technology, No. 07JC14033; the Shanghai Institute of Immunology Project, No. 07-A02
Correspondence to: Dong-Qing Zhang, Shanghai Institute of Immunology,Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. firstname.lastname@example.org
Telephone: +86-21-64453049 Fax: +86-21-64453049
Received: May 26, 2008 Revised: July 17, 2008 Accepted: July 24, 2008 Published online: September 14, 2008
AIM: To investigate the potential role of Active Chinese mistletoe lectin-55 (ACML-55) in tumor immune surveillance.
METHODS: In this study, an experimental model was established by hypodermic inoculating the colon cancer cell line CT26 (5 × 105 cells) into BALB/c mice. The experimental treatment was orally administered with ACML-55 or PBS, followed by the inoculation of colon cancer cell line CT26. Intracellular cytokine staining was used to detect IFN-γ production by tumor antigen speciﬁc CD8+ T cells. FACS analysis was employed to profile composition and activation of CD4+, CD8+, γδ T and NK cells.
RESULTS: Our results showed, compared to PBS treated mice, ACML-55 treatment significantly delayed colon cancer development in colon cancer -bearing Balb/c mice in vivo. Treatment with ACML-55 enhanced both Ag specific activation and proliferation of CD4+ and CD8+ T cells, and increased the number of tumor Ag specific CD8+ T cells. It was more important to increase the frequency of tumor Ag specific IFN-γ producing-CD8+ T cells. Interestingly, ACML-55 treatment also showed increased cell number of NK, and γδT cells, indicating the role of ACML-55 in activation of innate lymphocytes.
CONCLUSION: Our results demonstrate that ACML-55 therapy can enhance function in immune surveillance in colon cancer-bearing mice through regulating both innate and adaptive immune responses.