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pubmed, article, google, scholar, cas, cells, cancer, tumor, tlr, immune, central, proteins, protein, hmgb, damp, tolllike, cell, receptor, signaling, immunol, tlrs, inflammation, expression, receptors, tumors, activation, released, human, damps, metastasis, cytokines, patients, pauf, res, inflammatory, apoptosis, molecular, pancreatic, response, immunity, reported, kim, chemotherapy, nature, microenvironment, induce, rps, role, activate, factor,

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nature portfolio national research foundation privacy policy nature advertising tumour-derived microparticles obtained social media multi-institutional case–control study nab-pxl-treated tlr4−/− tumors anti-tumor double-edged sword reprints eosinophil-derived neurotoxin acts author information authors clearing t-cell trafficking damp-tlr-cytokine axis dictates promotes tumor development b-cell development rage/nf-κb signaling pathway generating kaplan–meier plots noise-induced hearing loss acquire pro-tumorigenic properties chemo-/radiotherapy-induced inflammation results dendritic cell-based vaccine produce pro-inflammatory cytokines individual patient data helicobacter pylori-induced invasion multiple leucine-rich repeats original author uv-induced dna damage63 yeong-min park tae heung kang secreting pro-inflammatory cytokines tumor-derived secretory proteins cancer-testis antigen spag9 tlr4-mediated signaling pathway anti-tlr2 antibody resulted asbestos-exposed individuals compared s100a4-mediated metastatic progression secrete pro-inflammatory cytokines myeloid-derived suppressor cells receptors gun-young jang tumor-derived damp proteins enhances anti-tumor immunity sh-sy5y neuroblastoma cells pro-inflammatory cytokines secreted cell-dependent antitumor immunity tumor-derived damps interact dc-based vaccines require rage-transfected ht1080 cells activates tlr2-myd88 signaling

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• Adjuvant role for cell death during chemo- and radiotherapy of cancer?
• Danger signals in tumor cells: a risk factor for autoimmune disease?
• Differential Expression of Neurodegeneration-Related Genes in SH-SY5Y Neuroblastoma Cells Under the Influence of Cyclophilin A: Could the Enzyme be a Likely Trigger and Therapeutic Target for Alzheimer’s Disease?
• Endogenous ligands of TLR2 and TLR4: agonists or assistants?
• Toll-like receptor 3 expressed by melanoma cells as a target for therapy?
• Toll-like receptor signalling on Tregs: to suppress or not tosuppress?

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         headline:Interactions between tumor-derived proteins and Toll-like receptors
         description:Damage-associated molecular patterns (DAMPs) are danger signals (or alarmins) alerting immune cells through pattern recognition receptors (PRRs) to begin defense activity. Moreover, DAMPs are host biomolecules that can initiate a noninflammatory response to infection, and pathogen-associated molecular pattern (PAMPs) perpetuate the inflammatory response to infection. Many DAMPs are proteins that have defined intracellular functions and are released from dying cells after tissue injury or chemo-/radiotherapy. In the tumor microenvironment, DAMPs can be ligands for Toll-like receptors (TLRs) expressed on immune cells and induce cytokine production and T-cell activation. Moreover, DAMPs released from tumor cells can directly activate tumor-expressed TLRs that induce chemoresistance, migration, invasion, and metastasis. Furthermore, DAMP-induced chronic inflammation in the tumor microenvironment causes an increase in immunosuppressive populations, such as M2 macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). Therefore, regulation of DAMP proteins can reduce excessive inflammation to create an immunogenic tumor microenvironment. Here, we review tumor-derived DAMP proteins as ligands of TLRs and discuss their association with immune cells, tumors, and the composition of the tumor microenvironment. Tumor cells killed by radiotherapy or chemotherapy release signaling molecules that stimulate both immune response and tumor aggressiveness; regulating these molecules could improve treatment efficacy. Tae Heung Kang, Yeong-Min Park, and co-workers at Konkuk University, Seoul, South Korea, have reviewed the role of damage-associated molecular patterns (DAMPs) in immunity and cancer. These signaling molecules act as danger signals, activating immune cells by binding to specific receptors. However, tumor cells have the same receptors, and DAMPs binding triggers chemoresistance and increases invasiveness. The researchers report that although DAMPs can trigger a helpful immune response, they can also cause chronic inflammation, which in turn promotes an immune suppression response, allowing tumors to escape immune detection. Improving our understanding of the functions of different DAMPs could improve our ability to boost the immune response and decrease tumor aggressiveness.
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      headline:Interactions between tumor-derived proteins and Toll-like receptors
      description:Damage-associated molecular patterns (DAMPs) are danger signals (or alarmins) alerting immune cells through pattern recognition receptors (PRRs) to begin defense activity. Moreover, DAMPs are host biomolecules that can initiate a noninflammatory response to infection, and pathogen-associated molecular pattern (PAMPs) perpetuate the inflammatory response to infection. Many DAMPs are proteins that have defined intracellular functions and are released from dying cells after tissue injury or chemo-/radiotherapy. In the tumor microenvironment, DAMPs can be ligands for Toll-like receptors (TLRs) expressed on immune cells and induce cytokine production and T-cell activation. Moreover, DAMPs released from tumor cells can directly activate tumor-expressed TLRs that induce chemoresistance, migration, invasion, and metastasis. Furthermore, DAMP-induced chronic inflammation in the tumor microenvironment causes an increase in immunosuppressive populations, such as M2 macrophages, myeloid-derived suppressor cells (MDSCs), and regulatory T cells (Tregs). Therefore, regulation of DAMP proteins can reduce excessive inflammation to create an immunogenic tumor microenvironment. Here, we review tumor-derived DAMP proteins as ligands of TLRs and discuss their association with immune cells, tumors, and the composition of the tumor microenvironment. Tumor cells killed by radiotherapy or chemotherapy release signaling molecules that stimulate both immune response and tumor aggressiveness; regulating these molecules could improve treatment efficacy. Tae Heung Kang, Yeong-Min Park, and co-workers at Konkuk University, Seoul, South Korea, have reviewed the role of damage-associated molecular patterns (DAMPs) in immunity and cancer. These signaling molecules act as danger signals, activating immune cells by binding to specific receptors. However, tumor cells have the same receptors, and DAMPs binding triggers chemoresistance and increases invasiveness. The researchers report that although DAMPs can trigger a helpful immune response, they can also cause chronic inflammation, which in turn promotes an immune suppression response, allowing tumors to escape immune detection. Improving our understanding of the functions of different DAMPs could improve our ability to boost the immune response and decrease tumor aggressiveness.
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