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The role of innate immune signals in antitumor immunity.

Jinushi M - Oncoimmunology (2012)

Bottom Line: Recent evidence demonstrates that these pattern-sensing systems are also applicable to the recognition of tumor-derived stress-related factors.In particular, toll-like receptors and cytosolic sensors for DNA and RNA recognition utilize endogenous host elements containing microbial components, danger-associated molecules, and/or nucleic acids to stimulate innate signaling pathways and generate protective immune responses against nascent tumors in animal models and humans.In this review, we describe recent advances and perspectives about antitumor mechanisms and clinical application of innate immune signals and pathways.

View Article: PubMed Central - PubMed

Affiliation: Research Center for Infection-Associated Cancer; Institute for Genetic Medicine; Hokkaido University; Sapporo, Hokkaido, Japan.

ABSTRACT
Innate immunity serves as a first line of defense against infectious agents, and germ-line-encoded pattern recognition receptors detect stressed and infected cells and elicit potent effector activities that accomplish efficient microbe containment. Recent evidence demonstrates that these pattern-sensing systems are also applicable to the recognition of tumor-derived stress-related factors. In particular, toll-like receptors and cytosolic sensors for DNA and RNA recognition utilize endogenous host elements containing microbial components, danger-associated molecules, and/or nucleic acids to stimulate innate signaling pathways and generate protective immune responses against nascent tumors in animal models and humans. In this review, we describe recent advances and perspectives about antitumor mechanisms and clinical application of innate immune signals and pathways.

No MeSH data available.


Related in: MedlinePlus

Figure 1. TLR and DC cross-presentation of tumor antigens. Upon pahgocytosis of dying tumor cells, the cargo is internalized into phagosomes. If microbial or endogenous danger signals serving as TLR agonists are contained in tumor cells, the engagements of TLR along with phagosomal membranes facilitates the assembly of phagosomal-lysosomal fusion machinery and the processing of tumor-associated antigens, and makes MHC class II amenable to binding of antigenic peptides. The resultant peptide-MHC comlex enables tumor-specific CD4+T cells to recognize and kill tumors.
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Figure 1: Figure 1. TLR and DC cross-presentation of tumor antigens. Upon pahgocytosis of dying tumor cells, the cargo is internalized into phagosomes. If microbial or endogenous danger signals serving as TLR agonists are contained in tumor cells, the engagements of TLR along with phagosomal membranes facilitates the assembly of phagosomal-lysosomal fusion machinery and the processing of tumor-associated antigens, and makes MHC class II amenable to binding of antigenic peptides. The resultant peptide-MHC comlex enables tumor-specific CD4+T cells to recognize and kill tumors.

Mentions: Furthermore, recent studies have explored that TLR ligands in antigen-presenting cells preferentially target ingested apoptotic cells to endosomal pathways in dendritic cells, and support forming peptide-MHC class II complex and enhance the recognition of immunogenic targets by antigen-specific T lymphocytes.9,10 In this regard, the administration of TLR agonists may sense APCs to facilitate cross-presentation of immunogenic tumor antigens and trigger specific T cell responses (Fig. 1).


The role of innate immune signals in antitumor immunity.

Jinushi M - Oncoimmunology (2012)

Figure 1. TLR and DC cross-presentation of tumor antigens. Upon pahgocytosis of dying tumor cells, the cargo is internalized into phagosomes. If microbial or endogenous danger signals serving as TLR agonists are contained in tumor cells, the engagements of TLR along with phagosomal membranes facilitates the assembly of phagosomal-lysosomal fusion machinery and the processing of tumor-associated antigens, and makes MHC class II amenable to binding of antigenic peptides. The resultant peptide-MHC comlex enables tumor-specific CD4+T cells to recognize and kill tumors.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3376990&req=5

Figure 1: Figure 1. TLR and DC cross-presentation of tumor antigens. Upon pahgocytosis of dying tumor cells, the cargo is internalized into phagosomes. If microbial or endogenous danger signals serving as TLR agonists are contained in tumor cells, the engagements of TLR along with phagosomal membranes facilitates the assembly of phagosomal-lysosomal fusion machinery and the processing of tumor-associated antigens, and makes MHC class II amenable to binding of antigenic peptides. The resultant peptide-MHC comlex enables tumor-specific CD4+T cells to recognize and kill tumors.
Mentions: Furthermore, recent studies have explored that TLR ligands in antigen-presenting cells preferentially target ingested apoptotic cells to endosomal pathways in dendritic cells, and support forming peptide-MHC class II complex and enhance the recognition of immunogenic targets by antigen-specific T lymphocytes.9,10 In this regard, the administration of TLR agonists may sense APCs to facilitate cross-presentation of immunogenic tumor antigens and trigger specific T cell responses (Fig. 1).

Bottom Line: Recent evidence demonstrates that these pattern-sensing systems are also applicable to the recognition of tumor-derived stress-related factors.In particular, toll-like receptors and cytosolic sensors for DNA and RNA recognition utilize endogenous host elements containing microbial components, danger-associated molecules, and/or nucleic acids to stimulate innate signaling pathways and generate protective immune responses against nascent tumors in animal models and humans.In this review, we describe recent advances and perspectives about antitumor mechanisms and clinical application of innate immune signals and pathways.

View Article: PubMed Central - PubMed

Affiliation: Research Center for Infection-Associated Cancer; Institute for Genetic Medicine; Hokkaido University; Sapporo, Hokkaido, Japan.

ABSTRACT
Innate immunity serves as a first line of defense against infectious agents, and germ-line-encoded pattern recognition receptors detect stressed and infected cells and elicit potent effector activities that accomplish efficient microbe containment. Recent evidence demonstrates that these pattern-sensing systems are also applicable to the recognition of tumor-derived stress-related factors. In particular, toll-like receptors and cytosolic sensors for DNA and RNA recognition utilize endogenous host elements containing microbial components, danger-associated molecules, and/or nucleic acids to stimulate innate signaling pathways and generate protective immune responses against nascent tumors in animal models and humans. In this review, we describe recent advances and perspectives about antitumor mechanisms and clinical application of innate immune signals and pathways.

No MeSH data available.


Related in: MedlinePlus