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Plasmonic Nanoparticles for Cancer Bioimaging, Diagnostics and Therapy
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Bridget Crawford, Tuan Vo-Dinh
Our group has demonstrated a novel cancer therapy, synergistic immune photo nanotherapy (SYMPHONY) on bladder cancer with mice animal model [195]. The SYMPHONY therapy combines GNS-mediated PTT and immune checkpoint inhibitor [196]. In recent years, immunotherapy with specific immune checkpoint inhibitor has provided a promising way to break tumor immunosuppressive environment. PD-L1, a protein overexpressed on cancer cell membrane, contributes to the suppression of the immune system. To modulate T cell function, PDL1 binds to its receptor, PD-1, found on activated T cells, B cells and myeloid cells. The therapeutic anti-PD-L1 antibody is designed to block the PD-L1/PD-1 interaction and reverse tumor-mediated immunosuppression. Blocking the PD-L1/PD-1 axis has been shown to be highly beneficial in many human tumors [197]. However, only modest clinical response to single-agent activity of PD-L1 and PD-1 antibodies is achieved in patients [198].
Anti-Cancer and Anti-Angiogenic Properties of Nano-Diamino-Tetrac, A Thyroid Hormone Derivative
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Paul J. Davis, Shaker A. Mousa
There is substantial current interest in the programmed death-1 (PD-1)/PD-ligand 1 (PD-L1) checkpoint that regulates T cell-cancer cell interactions [95, 96] and defends cancer cells against immune destruction. Produced by cancer cells, PD-L1 binds to PD-1 expressed by T lymphocytes, suppressing activated T cell engagement of tumor cells and also inducing T cell apoptosis. Antibodies to PD-L1 have been shown to have clinical anti-cancer activity in subpopulations of cancer patients [95, 97], but also have induced undesirable autoimmune responses in previously healthy organs.
Anti-Cancer and Anti-Angiogenic Properties of Nano-Diamino-Tetrac, A Thyroid Hormone Derivative
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2019
Paul J. Davis, Shaker A. Mousa
There is substantial current interest in the programmed death-1 (PD-1)/PD-ligand 1 (PD-L1) checkpoint that regulates T cell-cancer cell interactions [95, 96] and defends cancer cells against immune destruction. Produced by cancer cells, PD-L1 binds to PD-1 expressed by T lymphocytes, suppressing activated T cell engagement of tumor cells and also inducing T cell apoptosis. Antibodies to PD-L1 have been shown to have clinical anti-cancer activity in subpopulations of cancer patients [95, 97], but also have induced undesirable autoimmune responses in previously healthy organs.
Expression of a recombinant anti-programed cell death 1 antibody in the mammary gland of transgenic mice
Published in Preparative Biochemistry & Biotechnology, 2021
Guihua Gong, Wei Zhang, Liping Xie, Lei Xu, Shu Han, Youjia Hu
Programed cell death 1(PD-1) is an inhibitory co-stimulatory receptor expressed on the surface of activated T cells and B cells.[10] The ligand of PD-1, PD-L1, is found to have a high expression level in many human tumors, including melanoma, lung cancer, and kidney. The interaction of PD-1 with PD-L1 limits effector T-cell activity, and therefore downregulates immune responses and autoimmunity. The PD-1/PD-L1 pathway was thought to play a vital role in maintaining an immunosuppressive tumor microenvironment.[11] The blockade of such pathway has been developed as a therapy for a variety types of cancer in clinical use.[12] Nivolumab (Opdivo) is the first approved anti-PD-1 antibody by FDA in 2014 for the treatment of melanoma. As a new targeted immunotherapy, Nivolumab has become one of the most promising approaches for patients with a variety of tumor types.
Nanobodies targeting the interaction interface of programmed death receptor 1 (PD-1)/PD-1 ligand 1 (PD-1/PD-L1)
Published in Preparative Biochemistry & Biotechnology, 2020
Biyan Wen, Lin Zhao, Yuchu Wang, Chuangnan Qiu, Zhimin Xu, Kunling Huang, He Zhu, Zemin Li, Huangjin Li
Programmed cell death protein (PD-1) is a member of the CD28 receptor family expressed on the surface of T cells, T regulatory cells (Tregs) and B cells.[1–3] PD-1 has two major ligands, termed programmed death-ligand 1 (PD-L1) and programmed death-ligand 2 (PD-L2). The binding of PD-1 to its ligand inhibits the proliferation and activation of T cells and the secretion of related cytokines. Under normal conditions, PD-1 combined with PD-L1 or PD-L2 inhibits the activation and function of T cells, which in turn upregulates Tregs[4,5] leading to a loss of autoimmunity and enhanced self-tolerance.[6–9] PD-L1 is expressed in normal human tissues and organs but is overexpressed on the surface of various tumor cells. PD-L2 is also been detected in a small number of B-cell lymphomas9.[10] In the normal immune system, the primary role of PD-1/PD-L1 signaling is to maintain the balance of protective immunity and immune tolerance. In the tumor microenvironment, PD-1/PD-L1 signaling prevents effector T cells from identifying and killing tumor cells, resulting in immune cell escape.[1–3]
Modelling tumour–immune dynamics, disease progression and treatment
Published in Letters in Biomathematics, 2018
Amina Eladdadi, Lisette de Pillis, Peter Kim
The use of immune checkpoint inhibitors is becoming more commonplace in clinical trials across the nation. Two important factors in the tumour–immune response are the checkpoint protein programmed death-1 (PD-1) and its ligand PD-L1. Also, the effects of intermittent and continuous treatments on tumour–immune dynamics is of great importance to both experimental and quantitative researchers alike. In the paper, ‘Tumour-immune dynamics with an immune checkpoint inhibitor’ by Elpiniki Nikolopoulou, Lauren R. Johnson, Duane Harris, John D. Nagy, Edward C. Stites and Yang Kuang, the authors derive a mathematical model using a system of ordinary differential equations to study the tumour–immune dynamics with and without the use of anti-PD-1. They consider the system without the anti-PD-1 drug to determine the stability of the tumour-free and tumorous equilibria. Through simulations, they find that a normally functioning immune system might control the tumour. Treatment with anti-PD-1 alone, however, may not be sufficient to eradicate tumour cells. Therefore, it might be beneficial to combine single agent treatments with additional therapies to obtain a better anti-tumour response.