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Recent Advances of Nanotechnologies for Cancer Immunotherapy Treatment
Published in Loutfy H. Madkour, Nanoparticle-Based Drug Delivery in Cancer Treatment, 2022
Besides these, many other immune checkpoint molecules are being investigated, including LAG3 (lymphocyte activation gene 3), TIM-3 (T-cell immunoglobulin domain and Mucin domain 3), KIR (killer-cell immunoglobulin-like receptor), B7-H3 (CD276), VISTA (V-domain Ig suppressor of T-cell activation), and so on. Recently, TIGIT (T-cell Ig and ITIM domain) was exploited that it can function as an immune checkpoint that mainly expressed on NK cell and T cells. When it binds to its ligand CD155 on APCs or target cells, the immune responses initiated by NK cells were significantly suppressed. The research demonstrated that blockade of TIGIT could restore the activity of tumor-infiltrating NK cells and enhance antitumor therapeutic effects. Furthermore, it can be incorporated with other ICB, such as PD-1 or PD-L1 to provide promising antitumor immunotherapy in future [231].
Genome Editing and Gene Therapies: Complex and Expensive Drugs
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
CAR-T cell activity may be impaired via immunosuppressive mechanisms in the tumor microenvironment (TME) mediated by programmed cell death protein 1 (PD1) or lymphocyte activation gene 3 protein (LAG3). Rupp et al. (2017) first demonstrated that PD-1 expression in human K562 myelogenous leukemia cells impairs anti-CD19 CAR T cell activity in vitro and tumor clearance in a xenograft model (in vivo). Then they developed a CRISPR/ Cas9-mediated procedure of PD-1 disruption protocol to generate PD-1 deficient anti-CD19 CAR T cells. For this purpose, electroporation of Cas9 ribonucleoproteins loaded with crRNA:tracrRNA duplex targeting Pdcdl (programmed cell death 1) exon 1, and subsequent transduction with alentiviral vector encoding the anti-CD19 CAR was performed. As a result, all mice injected before subcutaneously with CD19+ PD-L1+ K562 cells and tumors were able to clear tumors after receiving PD-1 edited CAR T cells.
Gender-specific associations between polymorphisms in the Toll-like receptor (TLR) genes and lung function among workers in swine operations
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Zhiwei Gao, James A. Dosman, Donna C. Rennie, David A. Schwartz, Ivana V. Yang, Jeremy Beach, Ambikaipakan Senthilselvan
TLR2-16934 (rs4696480) is a promoter variant of TLR2 gene. An experimental study of cord blood mononuclear cells showed the carriers of AA genotype of this SNP exhibited significantly increased gene expression of several Treg (regulatory T cells) marker genes including FOXP3 (forkhead box protein p3), GITR (glucocorticoid-induced tumor necrosis factor receptor) and LAG3 (lymphocyte activation gene 3) as well as Th2 (T helper cell type 2) cytokines and TNF-α (tumor necrosis factor alpha) secretion in the presence of maternal atopy and postulated modification effects of maternal atopy status on this association may be partially explained by epigenetic regulation (Liu et al. 2011). Eder et al. (2004) reported that farm children from rural areas in Austria and Germany with a T allele of TLR2-16934 (rs4696480) were less susceptible to the diagnosis of asthma and atop, but not among children who did not reside on a farm. Kerkhof et al (2010) noted that this SNP significantly modified the influence of PM2.5 exposure on doctor-diagnosed asthma in children in the Netherlands.