THE CTLA-4 AND PD-1 BLOCKADE PATHWAY IN CANCER IMMUNOTHERAPY

Trần Thị Thanh Hương

THE CTLA-4 AND PD-1 BLOCKADE PATHWAY IN CANCER IMMUNOTHERAPY

About this article

Received: 14/11/19 Revised: 12/06/20 Published: 22/06/20

Authors

Tran Thi Thanh Huong , TNU - University of Information and Communication Technology

Abstract

Cancer is one of the top ten causes of death worldwide. With the goal of searching new methods of cancer treatment, we have approached cancer immunotherapy. In recent years, cancer immunotherapy has been a "breakthrough" in the treatment of cancer, in particular, the method of inhibiting the immune checkpoint is a promising direction. Checkpoints are surface receptors that regulate cell signals and inhibit the immune activity of T lymphocytes, but they can be exploited by tumors to create an immunosuppressive state for allow tumors to grow. When we using the method of inhibit immune checkpoint CTLA-4 and PD-1 then tumors reduce their growth significantly. That has opened up a potential new direction for clinicians in choosing new, effective cancer treatments in specific cases.

Keywords

Cancer; immunity; PD1; CTLA-4; ligand.

Full Text:

PDF (Tiếng Việt)

References

[1]. E. I. Buchbinder, and A. Desai, “CTLA-4 and PD-1 Pathways: Similarities, Differences, and Implications of Their Inhibition,” Am. J. Clin. Oncol., vol. 39, no. 1, pp. 98-106, 2016.

[2]. J. G. Egen, M. S. Kuhns, and J. P. Allison, “CTLA-4: new insights into its biological function and use in tumor immunotherapy,” Nat Immunol, vol. 3, pp. 611-618, 2002.

[3]. R. V. Parry et al., “CTLA-4 and PD-1 receptors inhibit T-cell activation by distinct mechanisms,” Mol Cell Biol, vol. 25, pp. 9543-9553, 2005.

[4]. F. Fallarino, P. E. Fields, and T. F.Gajewski, “B7–1 engagement of cytotoxic T lymphocyte antigen 4 inhibits T cell activation in the absence of CD28,” J. Exp. Med., vol. 188, pp. 205-210, 1998.

[5]. I. P. Oschke, D. Mougiakakos, and R. Kiessling, “Camouflage and sabotage: tumor escape from the immune system,” Cancer Immunol Immunother, vol. 60, pp. 1161-1711, 2011.

[6]. C. A. Chambers et al., “CTLA-4-mediated inhibition in regulation of T cell responses: mechanisms and manipulation in tumor immunotherapy,” Annu. Rev. Immunol, vol. 19, pp. 565-594, 2001.

[7]. P. S. Linsley et al., “Intracellular trafficking of CTLA-4 and focal localization towards sites of TCR engagement,” Immunity, vol. 4, pp. 535-543, 1996.

[8]. M. E. Keir et al., “PD-1 and its ligands in tolerance and immunity,” Annu Rev Immunol, vol. 26, pp. 677-704, 2008.

[9]. B. T. Fife, and J. A. Bluestone, “Control of peripheral T-cell tolerance and autoimmunity via the CTLA-4 and PD-1 pathways,” Immunol Rev., vol. 224, pp. 166-182, 2008.

[10]. E. N. Rozali et al., “Programmed death ligand 2 in cancer-induced immune suppression,” Clin. Dev. Immunol, vol. 2012, pp. 320-328, 2012.

[11]. L. Wang et al., “Programmed death 1 ligand signaling regulates the generation of adaptive Foxp3+CD4+ regulatory T cells,” Proc. Natl. Acad. Sci., vol. 105, pp. 9331-9336, 2008.

[12]. Bristol-Myers Squibb Company Yervoy (Ipilimumab) [package insert], Princeton, NJ: Bristol-Myers Squibb Company, 2013.

[13]. Bristol-Myers Squibb Company. Opdivo (Nivolumab) [package insert], Princeton, NJ: Bristol-Myers Squibb Company; 2015.

[14]. J. S. Weber et al., “Nivolumab versus chemotherapy in patients with advanced melanoma who progressed after anti-CTLA-4 treatment (CheckMate 037): a randomised, controlled, open-label, phase 3 trial,” Lancet Oncol., vol. 16, pp. 375-384, 2015.

[15]. M. A. Postow et al., “Nivolumab and ipilimumab versus ipilimumab in untreated melanoma,” N. Engl. J. Med., vol. 372, pp. 2006-2017, 2015.

[16]. S. J. Antonia et al., “Phase I/II study of nivolumab with or without ipilimumab for treatment of recurrent small cell lung cancer (SCLC): CA209-032,” J. Clin. Oncol., vol. 33, p. 7503, 2015.

[17]. E. L. Masteller et al., “Structural analysis of CTLA-4 function in vivo,” J. Immunol, vol. 164, pp. 5319-5327, 2000.

[18]. Merck & Co Inc. Keytruda (Pembrolizumab) [package insert], Whitehouse Station, NJ: Merck & Co Inc; 2015.

Refbacks

There are currently no refbacks.



Remember me