About this Research Topic
When cells are infected by microorganisms, the body's inflammatory response is activated. This initial detection is mediated by pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), NOD-like receptors (NLRs), C-type lectin receptors (CLRs), absent in melanoma-2 (AIM2)-like receptors (ALRs), and scavenger receptor cysteine-rich (SRCR) receptors. These receptors recognize pathogen-associated molecular patterns (PAMPs) and initiate immune responses.
PRRs activate intracellular signaling pathways that lead to the expression of inflammatory molecules like cytokines, chemokines, and interferons. These molecules coordinate efforts to eliminate pathogens and infected cells. Key inflammatory mechanisms include:
• Cytokine Production: Activation of PRRs induces the production of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β, which enhance the immune response.
• Chemokine Release: PRRs stimulate the release of chemokines like CXCL8 (IL-8) that attract immune cells to the site of infection.
• Interferon Response: PRRs, especially RLRs, trigger the production of type I interferons (IFN-α and IFN-β), which have antiviral effects and modulate the activity of immune cells.
• Activation of NF-κB and MAPK Pathways: These pathways are crucial for the transcription of inflammatory genes following PRR activation.
Crucially, PRRs also perform anti-inflammatory functions to maintain immune balance and prevent excessive inflammation. Key mechanisms include:
• Inhibition of PRR Signaling: Proteins like A20, CYLD, and SOCS inhibit PRR signaling, reducing the production of inflammatory molecules.
• Production of Anti-Inflammatory Cytokines: PRRs stimulate the production of anti-inflammatory cytokines such as IL-10 and TGF-β, helping to resolve inflammation.
• Cross-Talk with Other Pathways: PRR pathways interact with other pathways that promote tissue repair and regeneration, aiding in the resolution of inflammation.
• Phagocytosis of Apoptotic Cells: Certain PRRs, especially CLRs and SRCRs, help clear apoptotic cells and dead cell debris, preventing the release of pro-inflammatory substances.
Dysregulation of PRR signaling can lead to immunodeficiency or autoimmune diseases. Chronic activation can result in prolonged inflammation and tissue damage.
This research topic explores the roles of PRRs in both pro-inflammatory and anti-inflammatory responses, detailing their signaling pathways, regulatory mechanisms, and the implications of their dysregulation. Understanding these roles is crucial for developing therapies to modulate immune responses in various diseases.
We will compile observations, commentaries, and perspectives from researchers working on different PRRs. These researchers will have developed and utilized a wide range of molecular and cellular experimental systems and disease models, including those related to infection and inflammation. Collectively, these studies, in the form of research articles, opinion articles, mini-reviews, and full reviews, will inform on current and future efforts to develop therapeutic strategies targeting mediators of inflammation arising from PRR recognition of microorganisms.
PRRs activate intracellular signaling pathways that lead to the expression of inflammatory molecules like cytokines, chemokines, and interferons. These molecules coordinate efforts to eliminate pathogens and infected cells. Key inflammatory mechanisms include:
• Cytokine Production: Activation of PRRs induces the production of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β, which enhance the immune response.
• Chemokine Release: PRRs stimulate the release of chemokines like CXCL8 (IL-8) that attract immune cells to the site of infection.
• Interferon Response: PRRs, especially RLRs, trigger the production of type I interferons (IFN-α and IFN-β), which have antiviral effects and modulate the activity of immune cells.
• Activation of NF-κB and MAPK Pathways: These pathways are crucial for the transcription of inflammatory genes following PRR activation.
Crucially, PRRs also perform anti-inflammatory functions to maintain immune balance and prevent excessive inflammation. Key mechanisms include:
• Inhibition of PRR Signaling: Proteins like A20, CYLD, and SOCS inhibit PRR signaling, reducing the production of inflammatory molecules.
• Production of Anti-Inflammatory Cytokines: PRRs stimulate the production of anti-inflammatory cytokines such as IL-10 and TGF-β, helping to resolve inflammation.
• Cross-Talk with Other Pathways: PRR pathways interact with other pathways that promote tissue repair and regeneration, aiding in the resolution of inflammation.
• Phagocytosis of Apoptotic Cells: Certain PRRs, especially CLRs and SRCRs, help clear apoptotic cells and dead cell debris, preventing the release of pro-inflammatory substances.
Dysregulation of PRR signaling can lead to immunodeficiency or autoimmune diseases. Chronic activation can result in prolonged inflammation and tissue damage.
This research topic explores the roles of PRRs in both pro-inflammatory and anti-inflammatory responses, detailing their signaling pathways, regulatory mechanisms, and the implications of their dysregulation. Understanding these roles is crucial for developing therapies to modulate immune responses in various diseases.
We will compile observations, commentaries, and perspectives from researchers working on different PRRs. These researchers will have developed and utilized a wide range of molecular and cellular experimental systems and disease models, including those related to infection and inflammation. Collectively, these studies, in the form of research articles, opinion articles, mini-reviews, and full reviews, will inform on current and future efforts to develop therapeutic strategies targeting mediators of inflammation arising from PRR recognition of microorganisms.
Keywords: Immune Homeostasis, Inflammation, Pattern Recognition Receptors
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
