Cancer Immunotherapy: Reprogramming the Tumor Microenvironment through Second‐Near‐Infrared‐Window Photothermal Genome Editing of PD‐L1 Mediated by Supramolecular Gold Nanorods for Enhanced Cancer Immunotherapy (Adv. Mater. 12/2021)

Abstract

In article number 2006003, Yuan Ping and co‐workers, by means of photothermal transcription of CRISPR/Cas9 in the second near‐infrared window, demonstrate genome editing of PD‐L1 to be effective to reprogram the tumor microenvironment. The photothermal genome editing for the disruption of PD‐L1 mediated by supramolecular gold nanorods also simultaneously activates T cells to infiltrate and attack tumor cells in the deep tissues, which can substantially improve cancer immunotherapy.

Advanced Nanotheranostics of CRISPR/Cas for Viral Hepatitis and Hepatocellular Carcinoma

“…Lately, they changed the target into PD‐L1 gene for cancer immunotherapy, and the results demonstrated significant gene disruption and heat‐induced activation of immunogenic cell death (ICD). [ 108 ]…”

Reshaping the Tumor Immune Microenvironment Based on a Light‐Activated Nanoplatform for Efficient Cancer Therapy

“…[ 1 ] The immunosuppressive tumor microenvironment (TME), which is called the “cold” tumor immune microenvironment (TIME), which is featured by low presentation efficiency of antigen‐presenting cells (APC), insufficient infiltration of cytotoxic T lymphocytes (CTLs) in tumor tissues, high expression of tumor‐promoting phenotype tumor‐associated macrophages (TAMs), and large amounts of lactic acid, glutathione (GSH), regulatory T cells (Tregs), etc., leads to an inefficient antitumor immunity effect. [ 2,3 ] Notably, reshaping the TIME is emerging as a promising strategy to boost anticancer immune responses as well as prevent cancer metastasis and recurrence, for example, intra/extracellular lactic acid exhaustion synergistic anti‐PDL1 immunotherapy, [ 4 ] GSH depletion to upregulate the reactive oxygen species (ROS) level to promote an immunity effect, [ 5 ] and inhibition of myeloid‐derived suppressive cells (MDSCs) to decrease Tregs and increase the infiltration of CD8 + T cells, [ 6 ] etc. It is well known that the inadequate infiltration of CTLs and anti‐inflammatory M2 phenotype of TAMs are the main culprits leading to the low antitumor immune response, as well as cancer metastasis and recurrence.…”

“…It is well known that the inadequate infiltration of CTLs and anti‐inflammatory M2 phenotype of TAMs are the main culprits leading to the low antitumor immune response, as well as cancer metastasis and recurrence. [ 3 ] Oxygen (O 2 ) plays an essential role in the life activity and energy metabolism, simultaneously in the application of anticancer. [ 7,8 ] Alleviating hypoxia in solid tumors can reprogram the immunosuppressive TME, leading to the recruitment of large numbers of macrophages, as well as their subsequent polarization from M2 to M1 phenotype, which also inhibits the growth of tumor cells and promotes the infiltration of T‐cells, and even reduces the immune escape of cancer cells.…”

Biomimetic Active Materials Guided Immunogenic Cell Death for Enhanced Cancer Immunotherapy

“…[ 3 ] One of the promising approaches for achieving high immunogenicity is to induce the immunogenic cell death (ICD) to reshape TME. [ 4 ] ICD is a major cell death subroutines, which is sufficient to activate an adaptive immune response specific for endogenous (cellular) or exogenous antigens expressed by dying cells. [ 5 ] During the progress of ICD, cell death undergoes damage‐associated molecular patterns (DAMPs), endogenous immunogenic tumor‐associated antigens (TAAs), and proinflammatory cytokines released from tumor cells to break the immunologic tolerance and initiate antitumor immune responses.…”