Toll-like receptors (TLRs) are a class of pattern recognition receptors that play a bridging role in innate immunity and adaptive immunity. The activated TLRs not only induce inflammatory responses, but also elicit the development of antigen specific immunity. TLR7, a member of TLR family, is an intracellular receptor expressed on the membrane of endosomes. TLR7 can be triggered not only by ssRNA during viral infections, but also by immune modifiers that share a similar structure to nucleosides. Its powerful immune stimulatory action can be potentially used in the anti-tumor therapy. This article reviewed the anti-tumor activity and mechanism of TLR7 agonists that are frequently applied in preclinical and clinical investigations, and mainly focused on small synthetic molecules, including imiquimod, resiquimod, gardiquimod, and 852A, etc.

/pdf/anti-tumor-activity-of-toll-like-receptor-7-agonists-4nccx6c9c7.pdf

Anti-tumor Activity of Toll-Like Receptor 7 Agonists

Pattern recognition receptors: immune targets to enhance cancer immunotherapy.

The occurrence of the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), responsible for coronavirus disease 2019 (COVD-19), represents a catastrophic threat to global health. Protruding from the viral surface is a densely glycosylated spike (S) protein, which engages angiotensin-converting enzyme 2 (ACE2) to mediate host cell entry. However, studies have reported viral susceptibility in intra- and extrapulmonary immune and non-immune cells lacking ACE2, suggesting that the S protein may exploit additional receptors for infection. Studies have demonstrated interactions between S protein and innate immune system, including C-lectin type receptors (CLR), toll-like receptors (TLR) and neuropilin-1 (NRP1), and the non-immune receptor glucose regulated protein 78 (GRP78). Recognition of carbohydrate moieties clustered on the surface of the S protein may drive receptor-dependent internalization, accentuate severe immunopathological inflammation, and allow for systemic spread of infection, independent of ACE2. Furthermore, targeting TLRs, CLRs, and other receptors (Ezrin and dipeptidyl peptidase-4) that do not directly engage SARS-CoV-2 S protein, but may contribute to augmented anti-viral immunity and viral clearance, may represent therapeutic targets against COVID-19.

Can SARS-CoV-2 Virus Use Multiple Receptors to Enter Host Cells?

Acute myeloid leukemia (AML) is a common and lethal hematopoietic malignancy that is highly dependent on the bone marrow (BM) microenvironment. Infiltrating immune and stromal cells are important components of the BM microenvironment and significantly influence the progression of AML. This study aimed to elucidate the value of immune/stromal cell-associated genes for AML prognosis by integrated bioinformatics analysis. We obtained expression profiles from The Cancer Genome Atlas (TCGA) database and used the ESTIMATE algorithm to calculate immune scores and stromal scores; we then identified differentially expressed genes (DEGs) based on these scores. Overall survival analysis was applied to reveal common DEGs of prognostic value. Subsequently, we conducted a functional enrichment analysis, generated a protein-protein interaction (PPI) network and performed an interrelation analysis of immune system processes, showing that these genes are mainly associated with the immune/inflammatory response. Finally, eight genes (CD163, CYP27A1, KCNA5, PPM1J, FOLR1, IL1R2, MYOF, VSIG2) were verified to be significantly associated with AML prognosis in the Gene Expression Omnibus (GEO) database. In summary, we identified key microenvironment-related genes that affect the outcomes of AML patients and might serve as therapeutic targets.

Identification of prognostic genes in the acute myeloid leukemia immune microenvironment based on TCGA data analysis

S100A9 induces differentiation of acute myeloid leukemia cells through TLR4

Acute myeloid leukemia (AML) is an aggressive disease with a poor 5-year survival of 21% that is characterized by the differentiation arrest of immature myeloid cells. For a rare subtype of AML (acute promyeloctyic leukemia, 5-10% of cases), all-trans retinoic acid therapy removes the differentiation block, yielding over a 90% cure rate. However, this treatment is not effective for the other 90-95% of AML patients, suggesting that new differentiation strategies are needed. Interestingly, differentiation is induced in normal hematopoietic cells through Toll-like receptor (TLR) stimulation and TLRs are expressed on AML cells. We present evidence that the TLR8 activation promotes AML differentiation and growth inhibition in a TLR8/MyD88/p38-dependent manner. We also show that that TLR7/TLR8 agonist, R848, considerably impairs the growth of human AML cells in immunodeficient mice. Our data suggests TLR8 activation has direct anti-leukemic effects independent of its immunomodulating properties that are currently under investigation for cancer therapy. Taken together, our results suggest that treatment with TLR8 agonists may be a promising new therapeutic strategy for AML.

/pdf/the-role-of-tlr8-signaling-in-acute-myeloid-leukemia-4ydow39p7x.pdf

The role of TLR8 signaling in acute myeloid leukemia differentiation.

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The role of TLR8 signaling in acute myeloid leukemia differentiation.