AI Chat Paper
Note: Please note that the following content is generated by AMiner AI. SciOpen does not take any responsibility related to this content.
{{lang === 'zh_CN' ? '文章概述' : 'Summary'}}
{{lang === 'en_US' ? '中' : 'Eng'}}
Chat more with AI
Powered by AMiner. Clicking this button will take you away from SciOpen.
Home Nano Biomedicine and Engineering Article
PDF (1.3 MB)
Cite
EndNote(RIS) BibTeX
Collect
Submit Manuscript AI Chat Paper
Show Outline
Outline
Show full outline
Hide outline
Outline
Show full outline
Hide outline
Research Article | Open Access

Clinical Trial Analysis of Different Stages of HBV Patients Treated with Human CIK Cells

Fangfang Xia1, Ruihua Song2, Jingjing Zhang1, Yang Zhu2, Yao Yang1, Ling He1, Yun Cao1, Chenlu Li1, Zheng Wang1, Shangli Cheng1, Jian Ni1, Lijun Ma3( ), Ding Li2( ), Daxiang Cui1( )
Institute of Nano Biomedicine and Engineering, Shanghai Engineering Research Center for Intelligent Diagnosis and Therapy Instrument, Department of Instrument Science and Engineering, School of Electronic Information and Electrical Engineering; National Center for Translational Medicine, Collaborative Innovational Center for System Biology, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai 200240, P. R. China
Center for Biotechnological Diagnosis and Therapy, The 261 Hospital of PLA, Beijing 100094, China
Department of Oncology, Shanghai Tongren Hospital, Shanghai JiaoTong University School of Medicine, 1111 Xianxia Road, Shanghai 200336, P. R. China
Show Author Information

Abstract

Cellular immunotherapy has become a potential therapeutic method for different diseases. Herein, we reported clinical trial results of Cytokine-induced killer (CIK) cells used for patients with hepatitis B, cirrhosis and liver cancers from 2000 to 2015. Results showed CIK cell therapeutic effects were closely positively associated with CIK cell numbers, treated times and HBV genotypes. Different stages of HBV patients treated with > 1010 CIK cells per time for more than ten times exhibited remarkable decrease of HBV DNA numbers (P < 0.01), ALT and AST gradually recovered to normal scope, cytokine factors such as IFN-γ, IL-1b, IL-2, IL-4, IL-6, IL-10, IL-22 and IL-27 exhibited obvious increase, lifespan of patients with cirrhosis and hepatocellular carcinoma were extended, and that all the patients felt better in sleep, diet and pain during the period of CIK therapy. In conclusion, CIK cell therapy is a good alternative therapeutic method and can be effectively used for treatment of different stages of HBV patients.

Keywords

Cell therapyHepatocellular carcinomaCirrhosisHepatitis B virusCytokine-induced killer cellsCytokine factors

References

[1]

P. Marcellin, et al., Regression of cirrhosis during treatment with tenofovir disoproxil fumarate for chronic hepatitis B: A 5-year open-label follow-up study. The Lancet, 2013, 381(9865): 468-475.
Crossref Google Scholar
[2]

J. Lamontagne, J.C. Mell and M.J. Bouchard, Transcriptome-wide analysis of hepatitis B virus-mediated changes to normal hepatocyte gene expression. PLoS Pathog, 2016. 12(2): e1005438.
Crossref Google Scholar
[3]

T. Hosaka, et al., Long-term entecavir treatment reduces hepatocellular carcinoma incidence in patients with hepatitis B virus infection. Hepatology, 2013. 58(1): 98-107.
Crossref Google Scholar
[4]

C.L. Lai, M.F. Yuen, Prevention of hepatitis B virus–related hepatocellular carcinoma with antiviral therapy. Hepatology, 2013. 57(1): 399-408.
Crossref Google Scholar
[5]
G. Fattovich, Natural history and prognosis of hepatitis B. In Seminars in Liver Disease. Thieme Medical Publishers, Inc., 2003.
Crossref
[6]

E.A.F.T.S.O.T. Liver, EASL clinical practice guidelines: Management of chronic hepatitis B virus infection. Journal of hepatology, 2012. 57(1): 167-185.
Crossref Google Scholar
[7]

G. Raimondo, G. Cacciamo and C. Saitta, Hepatitis B virus and hepatitis C virus co-infection: additive players in chronic liver disease. Ann Hepatol, 2005. 4(2): 100-106.
Crossref Google Scholar
[8]

W.D. Carey, The prevalence and natural history of hepatitis B in the 21st century. Cleveland Clinic Journal of Medicine, 2009. 76: S2-5.
Crossref Google Scholar
[9]

J. Lucifora, et al., Specific and nonhepatotoxic degradation of nuclear hepatitis B virus cccDNA. Science, 2014. 343(6176): 1221-1228.
Crossref Google Scholar
[10]

C.J. Wooddell, et al., Hepatocyte-targeted RNAi therapeutics for the treatment of chronic hepatitis B virus infection. Molecular Therapy, 2013. 21(5): 973-985.
Crossref Google Scholar
[11]

S.C. Gordon, et al., Antiviral therapy for chronic hepatitis B virus infection and development of hepatocellular carcinoma in a US population. Clinical Gastroenterology and Hepatology, 2014. 12(5): 885-893.
Crossref Google Scholar
[12]

R.E. Lanford, et al., GS-9620, an oral agonist of Toll-like receptor-7, induces prolonged suppression of hepatitis B virus in chronically infected chimpanzees. Gastroenterology, 2013. 144(7): 1508-1517.
Crossref Google Scholar
[13]

B. Rehermann, A. Bertoletti, Immunological aspects of antiviral therapy of chronic hepatitis B virus and hepatitis C virus infections. Hepatology, 2015. 61(2): 712-721.
Crossref Google Scholar
[14]

C. Trépo, H.L. Chan and A. Lok, Hepatitis B virus infection. The Lancet, 2014. 384(9959): 2053-2063.
Crossref Google Scholar
[15]

G. Schmidt-Wolf, R. Negrin, and I. Schmidt-Wolf, Activated T cells and cytokine-induced CD3+ CD56+ killer cells. Annals of Hematology, 1997. 74(2): 51-56.
Crossref Google Scholar
[16]

S.A. Rosenberg, J.C. Yang, and N.P. Restifo, Cancer immunotherapy: moving beyond current vaccines. Nature Medicine, 2004. 10(9): 909-915.
Crossref Google Scholar
[17]

K. Palucka, J. Banchereau, Cancer immunotherapy via dendritic cells. Nature Reviews Cancer, 2012. 12(4): 265-277.
Crossref Google Scholar
[18]

I. Schmidt-Wolf, et al., Phenotypic characterization and identification of effector cells involved in tumor cell recognition of cytokine-induced killer cells. Experimental Hematology, 1993. 21(13): 1673-1679.
Google Scholar
[19]

R. Nen, P. Lu, Novel population of expanded human CD3, CD56 cells derived from T cells with potent in vivo antitumor activity in micewith severe combined immun0deficiency. J Immunol, 2004. 153(4): 1687-1696.
Crossref Google Scholar
[20]

A. Sasaki, et al., Preferential localization of human adherent lymphokine-activated killer cells in tumor microcirculation. Journal of the National Cancer Institute, 1991. 83(6): 433-437.
Crossref Google Scholar
[21]

I. Schmidt-Wolf, et al., Use of a SCID mouse/human lymphoma model to evaluate cytokine-induced killer cells with potent antitumor cell activity. The Journal of Experimental Medicine, 1991. 174(1): 139-149.
Crossref Google Scholar
[22]

R. Nishimura, et al., In vivo trafficking and survival of cytokine-induced killer cells resulting in minimal GVHD with retention of antitumor activity. Blood, 2008. 112(6): 2563-2574.
Crossref Google Scholar
[23]

A.A. Hombach, G. Rappl and H. Abken, Arming cytokine-induced killer cells with chimeric antigen receptors: CD28 outperforms combined CD28–OX40 “super-stimulation”. Molecular Therapy, 2013. 21(12): 2268-2277.
Crossref Google Scholar
[24]

J. Zhang, et al., Human CIK cells loaded with gold nanoprisms as theranostic platform for targeted photoacoustic imaging and enhanced immuno-photothermal combined therapy. Nano Biomed. Eng, 2016. 8(3): 109-124.
Crossref Google Scholar
[25]

Y. Yang, et al., Human CIK cells loaded with Au nanorods as a theranostic platform for targeted photoacoustic imaging and enhanced immunotherapy and photothermal therapy. Nanoscale Research Letters, 2016. 11(1): 1-13.
Crossref Google Scholar
[26]

G. Mesiano, et al., Cytokine-induced killer (CIK) cells as feasible and effective adoptive immunotherapy for the treatment of solid tumors. Expert Opinion on Biological Therapy, 2012, 12(6): 673-684
Crossref Google Scholar
[27]

D. Sangiolo, Cytokine induced killer cells as promising immunotherapy for solid tumors. J Cancer, 2011, 2(1): 363-368.
Crossref Google Scholar
[28]

G. Bonanno, et al., Thymoglobulin, interferon-γ and interleukin-2 efficiently expand cytokine-induced killer (CIK) cells in clinical-grade cultures. Journal of Translational Medicine, 2010. 8(1): 1.
Crossref Google Scholar
[29]

A. Pievani, et al., Dual-functional capability of CD3+ CD56+ CIK cells, a T-cell subset that acquires NK function and retains TCR-mediated specific cytotoxicity. Blood, 2011. 118(12): 3301-3310.
Crossref Google Scholar
[30]

C.-S. Wang, et al., Smoking and alanine aminotransferase levels in hepatitis C virus infection: implications for prevention of hepatitis C virus progression. Archives of Internal Medicine, 2002. 162(7): 811-815.
Crossref Google Scholar
[31]

C.K. Hyeon, et al., Normal serum aminotransferase concentration and risk of mortality from liver diseases: prospective cohort study. BMJ, 2004. 328(7446): 983.
Crossref Google Scholar
[32]

C.-J. Chen, et al., Risk of hepatocellular carcinoma across a biological gradient of serum hepatitis B virus DNA level. Jama, 2006. 295(1): 65-73.
Crossref Google Scholar
Nano Biomedicine and Engineering
Volume 8 Issue 3,
September 2016
Pages 203-211
DOI: 10.5101/nbe.v8i3.p203-211
Cite this article:
Xia F, Song R, Zhang J, et al. Clinical Trial Analysis of Different Stages of HBV Patients Treated with Human CIK Cells. Nano Biomedicine and Engineering, 2016, 8(3): 203-211. https://doi.org/10.5101/nbe.v8i3.p203-211

382

Views

9

Downloads

0

Crossref

0

Scopus

Altmetrics
Received: 21 September 2016
Accepted: 28 September 2016
Published: 29 September 2016
© 2016 Fangfang Xia, Ruihua Song, Jingjing Zhang, Yang Zhu, Yao Yang, Ling He, Yun Cao, Chenlu Li, Zheng Wang, Shangli Cheng, Jian Ni, Lijun Ma, Ding Li and Daxiang Cui.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Return