Unlike traditional cancer therapies, such as surgery, radiation and chemotherapy that are typically non-specific, cancer immunotherapy harnesses the high specificity of a patient's own immune system to selectively kill cancer cells. The immune system is the body's main cancer surveillance system, but cancers may evade destruction thanks to various immune-suppressing mechanisms. We therefore need to deploy various immunotherapy-based strategies to help bolster the anti-tumour immune responses. These include engineering T cells to express chimeric antigen receptors (CARs) to specifically recognise tumour neoantigens, inactivating immune checkpoints, oncolytic viruses and dendritic cell (DC) vaccines, which have all shown clinical benefit in certain cancers. However, treatment efficacy remains poor due to drug-induced adverse events and immunosuppressive tendencies of the tumour microenvironment. Recent preclinical studies have unveiled novel therapies such as anti-cathepsin antibodies, galectin-1 blockade and anti-OX40 agonistic antibodies, which may be utilised as adjuvant therapies to modulate the tumour microenvironment and permit more ferocious anti-tumour immune response.
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http://dx.doi.org/10.3390/cancers12071826 | DOI Listing |
Sci Immunol
January 2025
Koch Institute at MIT, Cambridge, MA 02139, USA.
Immune responses against cancer are dominated by T cell exhaustion and dysfunction. Recent advances have underscored the critical role of early priming interactions in establishing T cell fates. In this review, we explore the importance of dendritic cell (DC) signals in specifying CD8 T cell fates in cancer, drawing on insights from acute and chronic viral infection models.
View Article and Find Full Text PDFJ Cell Mol Med
January 2025
Institute of Molecular Medicine, Huaqiao University, Quanzhou, China.
Recombinant adeno-associated virus (rAAV) has emerged as one of the best gene delivery vectors for human gene therapy in vivo. However, the clinical efficacy of rAAV gene therapy is often hindered by the host immune response against its transgene products. Endoplasmic reticulum aminopeptidase 1 (ERAP1) is specialised to process peptides presented by class I molecules of major histocompatibility complex.
View Article and Find Full Text PDFParasitol Res
January 2025
Department of Medical Biology, Faculty of Science, University of South Bohemia, Branišovská 1760, CZ-37005, České Budějovice, Czech Republic.
Tick-borne encephalitis virus (TBEV) is flavivirus transmitted to the host via tick saliva which contains various molecules with biological impacts. One of such molecules is Iristatin, a cysteine protease inhibitor from Ixodes ricinus that has been shown to have immunomodulatory properties. To characterize Iristatin in the relation to TBEV, we investigate whether this tick inhibitor has any capacity to influence TBEV infection.
View Article and Find Full Text PDFSemin Immunopathol
January 2025
Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
The management of autoimmune diseases is currently limited by therapies that largely suppress the immune system, often resulting in partial and temporary remissions. Cellular immunotherapies offer a targeted approach by redirecting immune cells to correct the underlying autoimmunity. This review explores the latest advances in cellular immunotherapies for autoimmune diseases, focusing on various strategies, such as the use of chimeric antigen receptor (CAR) T cells, chimeric auto-antibody receptor (CAAR) T cells, regulatory T cells (Tregs), and tolerogenic dendritic cells (TolDCs).
View Article and Find Full Text PDFJ Appl Toxicol
January 2025
Department of Pharmacotherapeutics and Toxicology, Faculty of Pharmacy, Osaka Medical and Pharmaceutical University, Osaka, Japan.
Although the pathophysiology of idiosyncratic drug-induced liver injury (IDILI) is unclear, it is presumed to be immune-mediated, involving complex interactions between drug metabolism and activation of the immune system. The following four reactive metabolite production patterns are considered: (1) parent compounds into reactive metabolites within neutrophils or antigen-presenting cells (APCs), (2) reactive metabolites produced by cytochrome P450 (CYP), (3) nonreactive metabolites produced by CYP into reactive metabolites within APCs, and (4) reactive metabolites produced by non-CYPs. Reactive metabolites indirectly activate inflammasomes in APCs, leading to IDILIs.
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