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Intratumoural immunotherapy: activation of nucleic acid sensing pattern recognition receptors.

ABSTRACT: Recently, it has become clear that the tumour microenvironment (TME) is important in cancer immunotherapy. While immune checkpoint inhibitors are effective for some patients, the heterogeneous nature and status of the TME ('cold' tumours) play a critical role in suppressing antitumour immunity in non-responding patients. Converting 'cold' to 'hot' tumours through modulation of the TME may enable expansion of the therapeutic efficacy of immunotherapy to a broader patient population. This paper describes advances in intratumoural immunotherapy, specifically activation of nucleic acid sensing pattern recognition receptors to modulate the TME.

SUBMITTER: Agrawal S

PROVIDER: S-EPMC9216656 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Intratumoural immunotherapy: activation of nucleic acid sensing pattern recognition receptors.

Agrawal Sudhir S Kandimalla Ekambar R ER

Immuno-oncology technology 20191016

Recently, it has become clear that the tumour microenvironment (TME) is important in cancer immunotherapy. While immune checkpoint inhibitors are effective for some patients, the heterogeneous nature and status of the TME ('cold' tumours) play a critical role in suppressing antitumour immunity in non-responding patients. Converting 'cold' to 'hot' tumours through modulation of the TME may enable expansion of the therapeutic efficacy of immunotherapy to a broader patient population. This paper de ...[more]

PMID: 35757301

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Project description:Chronic inflammation has been associated with an increased risk of several human malignancies, a classic example being gastric adenocarcinoma (GC). Development of GC is known to result from infection of the gastric mucosa by Helicobacter pylori, which initially induces acute inflammation and, in a subset of patients, progresses over time to chronic inflammation, gastric atrophy, intestinal metaplasia, dysplasia, and finally intestinal-type GC. Germ-line encoded receptors known as pattern-recognition receptors (PRRs) are critical for generating mature pro-inflammatory cytokines that are crucial for both Th1 and Th2 responses. Given that H. pylori is initially targeted by PRRs, it is conceivable that dysfunction within genes of this arm of the immune system could modulate the host response against H. pylori infection, and subsequently influence the emergence of GC. Current evidence suggests that Toll-like receptors (TLRs) (TLR2, TLR3, TLR4, TLR5, and TLR9), nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) (NOD1, NOD2, and NLRP3), a C-type lectin receptor (DC-SIGN), and retinoic acid-inducible gene (RIG)-I-like receptors (RIG-I and MDA-5), are involved in both the recognition of H. pylori and gastric carcinogenesis. In addition, polymorphisms in genes involved in the TLR (TLR1, TLR2, TLR4, TLR5, TLR9, and CD14) and NLR (NOD1, NOD2, NLRP3, NLRP12, NLRX1, CASP1, ASC, and CARD8) signaling pathways have been shown to modulate the risk of H. pylori infection, gastric precancerous lesions, and/or GC. Further, the modulation of PRRs has been suggested to suppress H. pylori-induced inflammation and enhance GC cell apoptosis, highlighting their potential relevance in GC therapeutics. In this review, we present current advances in our understanding of the role of the TLR and NLR signaling pathways in the pathogenesis of GC, address the involvement of other recently identified PRRs in GC, and discuss the potential implications of PRRs in GC immunotherapy.

Dataset Information

Intratumoural immunotherapy: activation of nucleic acid sensing pattern recognition receptors.

Publications

Intratumoural immunotherapy: activation of nucleic acid sensing pattern recognition receptors.

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