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Questions and Answers
What is the main focus of the text above?
What is the main focus of the text above?
Which receptors are mentioned in the learning objectives for detecting pathogens?
Which receptors are mentioned in the learning objectives for detecting pathogens?
What is the role of inflammasome in cytokine responses?
What is the role of inflammasome in cytokine responses?
Which molecules are associated with the acute phase response?
Which molecules are associated with the acute phase response?
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What is the outcome associated with local release of TNF-α?
What is the outcome associated with local release of TNF-α?
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What are the effector functions of IL-1β?
What are the effector functions of IL-1β?
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Which receptors are involved in the detection of pathogens within cells?
Which receptors are involved in the detection of pathogens within cells?
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What is the next line of defense after the cellular and molecular defenses against pathogens?
What is the next line of defense after the cellular and molecular defenses against pathogens?
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Which cell type is responsible for releasing TNF-α?
Which cell type is responsible for releasing TNF-α?
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What is the primary effect of IL-1β on endothelium?
What is the primary effect of IL-1β on endothelium?
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Which cell type is targeted by Type I IFN (IFN-α and IFN-β)?
Which cell type is targeted by Type I IFN (IFN-α and IFN-β)?
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What effect does IL-6 have on hepatocytes?
What effect does IL-6 have on hepatocytes?
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Which cell type is responsible for increasing the bone marrow output of neutrophils?
Which cell type is responsible for increasing the bone marrow output of neutrophils?
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What is the primary effect of TNF-α on endothelium?
What is the primary effect of TNF-α on endothelium?
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Which cell type is responsible for releasing Type I IFN (IFN-α and IFN-β)?
Which cell type is responsible for releasing Type I IFN (IFN-α and IFN-β)?
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Which cell type is responsible for increasing glucose metabolism?
Which cell type is responsible for increasing glucose metabolism?
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Which type of receptors are expressed on cellular barriers and immune cells to detect 'conserved' structures of microbes?
Which type of receptors are expressed on cellular barriers and immune cells to detect 'conserved' structures of microbes?
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Which type of receptors can trigger phagocytosis without cell signaling?
Which type of receptors can trigger phagocytosis without cell signaling?
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Which protein plays a primary role in the acute phase response?
Which protein plays a primary role in the acute phase response?
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Which receptor type has an extracellular domain for pathogen engagement and a cytoplasmic signaling domain?
Which receptor type has an extracellular domain for pathogen engagement and a cytoplasmic signaling domain?
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What complex plays a key role in the production of IL-1β, a pro-inflammatory cytokine?
What complex plays a key role in the production of IL-1β, a pro-inflammatory cytokine?
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Which molecule is produced by macrophages and plays roles in fever, vasodilation, and increased vascular permeability?
Which molecule is produced by macrophages and plays roles in fever, vasodilation, and increased vascular permeability?
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Which protein deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
Which protein deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
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Which cytokine can trigger fever by binding to receptors on hypothalamic endothelium?
Which cytokine can trigger fever by binding to receptors on hypothalamic endothelium?
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What is responsible for the maturation and secretion of IL-1β?
What is responsible for the maturation and secretion of IL-1β?
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Which cells can be activated by IL-1β and IL-12, and have their cytotoxicity enhanced by IFNγ and cytotoxins?
Which cells can be activated by IL-1β and IL-12, and have their cytotoxicity enhanced by IFNγ and cytotoxins?
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Which protein interacts with the C1 component of the classical pathway of complement activation?
Which protein interacts with the C1 component of the classical pathway of complement activation?
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What can binding of LPS from Gram-negative bacteria to TLR4, CD14, and MD2 lead to?
What can binding of LPS from Gram-negative bacteria to TLR4, CD14, and MD2 lead to?
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What part of the immune system helps to destroy pathogens and induces inflammatory responses?
What part of the immune system helps to destroy pathogens and induces inflammatory responses?
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What is the role of TNF-α in preventing pathogen entry?
What is the role of TNF-α in preventing pathogen entry?
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What is activated by the binding of mannose-binding lectin (MBL) to mannose-containing structures on pathogens?
What is activated by the binding of mannose-binding lectin (MBL) to mannose-containing structures on pathogens?
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What plays a crucial role in the early stages of the immune response and helps to eliminate pathogens?
What plays a crucial role in the early stages of the immune response and helps to eliminate pathogens?
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Which type of receptors are NLRs?
Which type of receptors are NLRs?
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What is the role of NOD1 in pathogen recognition?
What is the role of NOD1 in pathogen recognition?
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What is the function of RIPK2 when NOD binds to its ligand?
What is the function of RIPK2 when NOD binds to its ligand?
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What is the outcome of IKK activation?
What is the outcome of IKK activation?
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What is the role of RIG-I-like receptors (RLR) in viral detection?
What is the role of RIG-I-like receptors (RLR) in viral detection?
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How do early responder cells like neutrophils infiltrate the site of inflammation?
How do early responder cells like neutrophils infiltrate the site of inflammation?
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What weakens tight junctions, allowing neutrophils to penetrate the extracellular matrix?
What weakens tight junctions, allowing neutrophils to penetrate the extracellular matrix?
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What induces chemokine production by macrophages?
What induces chemokine production by macrophages?
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Which type of receptors are expressed on cellular barriers and immune cells to detect 'conserved' structures of microbes?
Which type of receptors are expressed on cellular barriers and immune cells to detect 'conserved' structures of microbes?
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What is the primary effect of TNF-α on endothelium?
What is the primary effect of TNF-α on endothelium?
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Which type of receptors can trigger phagocytosis without cell signaling?
Which type of receptors can trigger phagocytosis without cell signaling?
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What is the role of RIG-I-like receptors (RLR) in viral detection?
What is the role of RIG-I-like receptors (RLR) in viral detection?
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What is the outcome associated with local release of TNF-α?
What is the outcome associated with local release of TNF-α?
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Which molecule is involved in the acute phase response and plays roles in fever, vasodilation, and increased vascular permeability?
Which molecule is involved in the acute phase response and plays roles in fever, vasodilation, and increased vascular permeability?
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Which receptor type has an extracellular domain for pathogen engagement and a cytoplasmic signaling domain?
Which receptor type has an extracellular domain for pathogen engagement and a cytoplasmic signaling domain?
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What is the primary function of RIG-I-like receptors (RLRs) in viral detection?
What is the primary function of RIG-I-like receptors (RLRs) in viral detection?
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Which protein deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
Which protein deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
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What is responsible for the maturation and secretion of IL-1β?
What is responsible for the maturation and secretion of IL-1β?
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Which protein plays a key role in the production of IL-1β, a pro-inflammatory cytokine?
Which protein plays a key role in the production of IL-1β, a pro-inflammatory cytokine?
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What is the outcome of IKK activation?
What is the outcome of IKK activation?
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Which molecule deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
Which molecule deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
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Which cytokine can trigger fever by binding to receptors on hypothalamic endothelium?
Which cytokine can trigger fever by binding to receptors on hypothalamic endothelium?
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What is the role of RIPK2 when NOD binds to its ligand?
What is the role of RIPK2 when NOD binds to its ligand?
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What is the primary role of NOD1 in the detection of pathogens?
What is the primary role of NOD1 in the detection of pathogens?
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What is the outcome associated with the local release of TNF-α?
What is the outcome associated with the local release of TNF-α?
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What is the primary function of RIG-I-like receptors (RLR) in viral detection?
What is the primary function of RIG-I-like receptors (RLR) in viral detection?
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Which molecule is responsible for inducing chemokine production by macrophages?
Which molecule is responsible for inducing chemokine production by macrophages?
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What is the main function of integrins on the surface of neutrophils during inflammation?
What is the main function of integrins on the surface of neutrophils during inflammation?
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Which type of cells release Type I IFN (IFN-α and IFN-β)?
Which type of cells release Type I IFN (IFN-α and IFN-β)?
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What is the primary role of IL-8?
What is the primary role of IL-8?
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Which protein deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
Which protein deficiency leads to susceptibility to meningitis caused by Neisseria meningitidis?
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What is the outcome associated with local release of TNF-α?
What is the outcome associated with local release of TNF-α?
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What is the function of RIPK2 when NOD binds to its ligand?
What is the function of RIPK2 when NOD binds to its ligand?
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Study Notes
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Inflammation is the body's response to harmful stimuli, such as pathogens or damaged cells (The pillars of inflammation).
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Two types of Pattern Recognition Receptors (PRR) are involved in the detection of harmful stimuli: Toll-like receptors (TLR) and NOD-like receptors (NLR).
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NLRs are intracellular receptors that detect degraded products from phagocytosed pathogens. They include NOD1 and NOD2.
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NOD1 recognizes the degraded peptidoglycan of Gram-negative bacteria, while NOD2 recognizes the degraded peptidoglycan of many bacteria.
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NOD receptors have a CARD (caspase-recruitment domain) at their terminal end, which allows binding to the CARD on the ends of RIPK2 (receptor interacting serine/threonine kinase 2).
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When NOD binds to its ligand, it dimerizes and RIPK2 binds, leading to the phosphorylation and activation of TAK1 (transforming growth factor beta-activated kinase 1).
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Activated TAK1 then phosphorylates and activates IKK (Iκβ kinase). IKK degrades Iκβ, which is bound to NF-κB (nuclear factor-kappa B).
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NF-κB translocates to the nucleus and induces cytokine production, phagocytosis and defensin synthesis.
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RIG-I-like receptors (RLR) are cytoplasmic detection proteins for viral RNA.
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RLRs consist of RIG-I and MDA-5, which bind to viral RNA and through CARDs interact with MAVS (mitochondrial antiviral signaling proteins).
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Resulting in the phosphorylation of IRF3 (interferon response factor 3), which dimerizes and becomes a transcription factor for type I interferons (IFNs).
-
Type I IFN signaling induces the interferon response, which prevents viral protein synthesis and production of new virions.
-
Early responder cells such as neutrophils infiltrate the site of inflammation through selectin and integrin interactions.
-
Selectins on the surface of vascular endothelial cells are induced by IL-1 and TNF-α, allowing immune cells to roll along the vascular surface.
-
Integrins on the surface of neutrophils interact with vascular endothelia to firmly adhere the neutrophils to the blood vessel surface.
-
Neutrophils produce CXCL8 (IL-8) in response to the presence of pathogens, which attracts more neutrophils to the site of inflammation.
-
Chemokines increase integrin binding and selectin interactions, allowing neutrophils to move through the endothelial cell layer and penetrate the extracellular matrix (diapedesis).
-
Macrophages also play a role in inflammation by producing chemokines that attract neutrophils to the site of infection.
-
TNF-α weakens tight junctions and neutrophil proteases loosen PECAM-1 interactions, allowing neutrophils to slide through the endothelial cell layer and penetrate the extracellular matrix.
-
Neutrophils use chemokine gradients to navigate towards the source of infection, and undergo cytoskeletal rearrangements to migrate through the tissue.
-
Inflammation is the body's response to harmful stimuli, such as pathogens or damaged cells (The pillars of inflammation).
-
Two types of Pattern Recognition Receptors (PRR) are involved in the detection of harmful stimuli: Toll-like receptors (TLR) and NOD-like receptors (NLR).
-
NLRs are intracellular receptors that detect degraded products from phagocytosed pathogens. They include NOD1 and NOD2.
-
NOD1 recognizes the degraded peptidoglycan of Gram-negative bacteria, while NOD2 recognizes the degraded peptidoglycan of many bacteria.
-
NOD receptors have a CARD (caspase-recruitment domain) at their terminal end, which allows binding to the CARD on the ends of RIPK2 (receptor interacting serine/threonine kinase 2).
-
When NOD binds to its ligand, it dimerizes and RIPK2 binds, leading to the phosphorylation and activation of TAK1 (transforming growth factor beta-activated kinase 1).
-
Activated TAK1 then phosphorylates and activates IKK (Iκβ kinase). IKK degrades Iκβ, which is bound to NF-κB (nuclear factor-kappa B).
-
NF-κB translocates to the nucleus and induces cytokine production, phagocytosis and defensin synthesis.
-
RIG-I-like receptors (RLR) are cytoplasmic detection proteins for viral RNA.
-
RLRs consist of RIG-I and MDA-5, which bind to viral RNA and through CARDs interact with MAVS (mitochondrial antiviral signaling proteins).
-
Resulting in the phosphorylation of IRF3 (interferon response factor 3), which dimerizes and becomes a transcription factor for type I interferons (IFNs).
-
Type I IFN signaling induces the interferon response, which prevents viral protein synthesis and production of new virions.
-
Early responder cells such as neutrophils infiltrate the site of inflammation through selectin and integrin interactions.
-
Selectins on the surface of vascular endothelial cells are induced by IL-1 and TNF-α, allowing immune cells to roll along the vascular surface.
-
Integrins on the surface of neutrophils interact with vascular endothelia to firmly adhere the neutrophils to the blood vessel surface.
-
Neutrophils produce CXCL8 (IL-8) in response to the presence of pathogens, which attracts more neutrophils to the site of inflammation.
-
Chemokines increase integrin binding and selectin interactions, allowing neutrophils to move through the endothelial cell layer and penetrate the extracellular matrix (diapedesis).
-
Macrophages also play a role in inflammation by producing chemokines that attract neutrophils to the site of infection.
-
TNF-α weakens tight junctions and neutrophil proteases loosen PECAM-1 interactions, allowing neutrophils to slide through the endothelial cell layer and penetrate the extracellular matrix.
-
Neutrophils use chemokine gradients to navigate towards the source of infection, and undergo cytoskeletal rearrangements to migrate through the tissue.
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Description
Test your knowledge of acute phase proteins, phagocytosis, complement activation, cytokines, and the inflammatory response with this quiz. Explore the key players and processes involved in the acute phase response and inflammation.
