Abstract
The pathogen recognition receptors (PRRs) initiate immediate responses against infection and tissue damage to protect the host from microbial invasion. In response to mucosal damage, intestinal PRR signaling initiates damage repair processes. Recent advances appear to link PRR abnormalities and inflammatory as well as neoplastic intestinal disorders. Emerging evidence suggests a dual role of PRRs, in which they may simultaneously induce tumorigenesis and antitumor immunity. PRR may induce tumor cell proliferation by activating cell survival signaling mainly via NF-kappaB, but this signal can activate dendritic cells to promote antitumor immunity. TLR signaling within the tumor cells may result in evasion of immune surveillance, propagation of metastatic growth, or rather, induction of tumor cell apoptosis depending on ligands. Epithelial cells induce endogenous PRR ligands when damaged or during neoplastic transformation. Targeted manipulation of PRR signaling may provide emerging opportunities for the development of new therapeutic strategies for many gastrointestinal diseases.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anti-Inflammatory Agents / pharmacology
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Anti-Inflammatory Agents / therapeutic use
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Drug Delivery Systems / methods
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Enterocolitis
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Gastrointestinal Neoplasms / drug therapy
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Gastrointestinal Neoplasms / etiology
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Gastrointestinal Neoplasms / immunology
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Gastrointestinal Neoplasms / metabolism*
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Gastrointestinal Tract / drug effects
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Gastrointestinal Tract / immunology
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Gastrointestinal Tract / metabolism*
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Humans
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Immunity, Innate / drug effects
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Immunity, Innate / physiology
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Nod Signaling Adaptor Proteins / drug effects
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Nod Signaling Adaptor Proteins / metabolism
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RNA Helicases / drug effects
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RNA Helicases / metabolism
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Receptors, Pattern Recognition / immunology
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Receptors, Pattern Recognition / physiology*
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Toll-Like Receptors / drug effects
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Toll-Like Receptors / metabolism
Substances
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Anti-Inflammatory Agents
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Antineoplastic Agents
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Nod Signaling Adaptor Proteins
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Receptors, Pattern Recognition
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Toll-Like Receptors
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RNA Helicases