Lecture 17: Innate Immunity II: receptors & Cytokines

Which outcome is associated with the activation of innate immune receptors upon antigen exposure?

Which of the following cytokines are classified as inflammatory cytokines?

What is the primary function of Type I interferons?

Which acute phase protein activates the lectin pathway of complement?

What is the role of selectins during inflammation?

What is the function of integrins during the process of inflammation?

Which of the following outcomes is associated with local TNF-α release?

What cellular process do most innate receptors trigger without initiating cell signaling?

Which domain of Toll-like receptors (TLRs) is responsible for PAMP engagement?

What is the immediate consequence of MD2 binding to the LPS-CD14 complex associated with TLR4?

Which transcription factor is activated by TLR signaling and leads to the production of inflammatory cytokines?

A deficiency in the γ subunit of IKK leads to which condition?

After TLR signaling, what is the direct effect of IL-1β and TNF-α on capillary endothelial cells?

What is the role of prostaglandin E2 (PGE2) in the development of fever?

What condition results from the systemic presence of TNF-α leading to blood clotting in small vessels and organ failure?

What is the role of the NLRP3 protein in the inflammasome complex?

Which of the following best describes the role of C-reactive protein (CRP) in the complement pathway?

How does mannose-binding lectin (MBL) contribute to the innate immune response?

What process does CXCL8 (IL-8) facilitate in the inflammatory response?

Which of the following occurs during the 'rolling' phase of leukocyte extravasation?

What is the role of RIPK2 in NOD-like receptor signaling?

Which event directly follows the binding of viral RNA to RIG-I and MDA-5 in RLR signaling?

What direct effect do type I interferons have on viral protein synthesis?

What is the significance of a nonfunctional MBL allele in approximately 10% of the population?

In a patient with Cryopyrin-Associated Periodic Syndrome (CAPS), what is the primary mechanism driving the inflammatory symptoms?

Which of the following is the MOST accurate description of how deficiency of C5-C9 affect complement function?

A researcher is studying the effects of a novel drug on the innate immune system. They discover that the drug significantly enhances the production of type I interferons in response to viral infection in vitro. Which of the following receptors is the MOST likely target of this drug?

What is the MOST critical mechanistic difference between the action of C-reactive protein (CRP) and antibodies on pathogen surfaces with respect to complement activation?

Which intracellular sensor is responsible for detecting the presence of cytoplasmic dsDNA, typically associated with bacterial or viral infection, and subsequently activating the production of type I interferons?

Based on the provided information, what is NOT a primary mechanism by which Type 1 Interferons (IFNs) establish an antiviral state?

Which statement accurately differentiates the local versus systemic effects of TNF-α release?

In the context of extravasation, which event typically occurs IMMEDIATELY after a leukocyte establishes tight binding to the endothelium via chemokine-mediated integrin activation?

A researcher discovers a novel pathogen-associated molecular pattern (PAMP) that triggers a strong innate immune response. Initial experiments indicate that this PAMP primarily activates intracellular receptors. Which of the following receptor types would BEST fit this characteristic?

In a patient undergoing treatment for a severe bacterial infection, a physician observes a significant increase in the level of serum amyloid A (SAA). What is the MOST likely role of SAA in modulating the immune response in this scenario?

A pharmaceutical company is developing a therapeutic agent targeting the inflammasome to treat chronic inflammatory diseases. Which of the following mechanisms of action would be MOST effective in reducing IL-1β production?

Select the TLR homodimer-ligand pair with incorrect pairing.

Match the acute phase protein with its correct function.

Assuming an individual has a mutation that disrupts the function of MyD88, which function is most likely to be impaired?

Which cellular component is responsible for initiating intracellular signaling following PAMP recognition by Toll-like receptors (TLRs)?

What is the MOST immediate consequence of type I interferon (IFN) secretion from a virus-infected cell?

What direct effect does the binding of lipopolysaccharide (LPS) and LBP to CD14 have on TLR4?

Which acute phase protein directly enhances the phagocytosis of pathogens?

In the context of leukocyte extravasation, what event is mediated by the interaction between integrins and their respective ligands?

Which of the following best describes the function of NOD-like receptors (NLRs) in innate immunity?

What is the MOST direct mechanism by which TNF-α contributes to increased vascular permeability during the inflammatory response?

A patient presents with a genetic defect resulting in non-functional IKKγ. Which of the following would MOST accurately describe the immunological consequence?

In the absence of inflammation, what is the MOST likely state of neutrophils?

A novel therapeutic agent is designed to specifically inhibit the interaction between C4b and C2b. Which complement pathway would be MOST directly affected by this agent?

If an individual exhibits a complete absence of functional TLR signaling, which subsequent immunological process would be MOST severely compromised?

Considering the intricacies of TLR4 signaling, what outcome would be expected in a patient with a homozygous loss-of-function mutation in the MD2 gene?

Given the complex interplay of intracellular signaling cascades downstream of PRRs, what cellular event would be MOST directly affected by a mutation that prevents the phosphorylation of IκB?

In the context of systemic inflammation, which of the following best illustrates the mechanistic link between TNF-α and the development of disseminated intravascular coagulation (DIC)?

Assuming a genetically engineered mouse lacks the capacity to produce prostaglandin E2 (PGE2), what specific physiological response would be MOST directly affected following peripheral IL-1β release?

Considering the pathogenesis of Cryopyrin-Associated Periodic Syndromes (CAPS), which therapeutic intervention would MOST directly target the underlying mechanism of disease?

What is the MOST consequential difference between the activation of the lectin pathway by mannose-binding lectin (MBL) versus C-reactive protein (CRP) with respect to initiating complement activation?

In the cellular context of a virally infected cell undergoing apoptosis, what would be the MOST direct effect of type I interferon (IFN) secretion on neighboring, uninfected cells?

Given the redundancy and specificity of NOD-like receptors (NLRs), how would a targeted mutation eliminating the CARD domain of NOD2 MOST directly impact downstream signaling?

What would be the MOST critical mechanistic consequence of a genetic defect leading to the production of a non-functional form of the Mx GTPase proteins?

A researcher is investigating the effects of a novel compound that selectively enhances the generation of 'Oligo A'. Which cellular process would be MOST directly affected by this compound?

Given the complexity of leukocyte extravasation, what would be the immediate consequence of blocking the function of CXCL8 (IL-8) at a site of infection?

If a patient's neutrophils expressed a constitutively active form of LFA-1, independent of chemokine signaling, what would be the MOST likely immunological outcome?

Considering the multistep nature of leukocyte trafficking, which event is MOST immediately dependent on TNF-α-mediated changes to endothelial cell-cell junctions?

In a scenario where a novel immunosuppressive drug selectively inhibits the function of selectins in vivo, what would be the MOST immediate effect on leukocyte migration during an inflammatory response?

A newly discovered viral pathogen expresses a protein that directly inhibits IRF3 dimerization. What would be the MOST immediate effect of this viral protein on the host's innate immune response?

How would a mutation that disrupts the ability of macrophages to synthesize and secrete IL-6 impact the acute phase response in the liver?

If an individual possesses a mutation causing constitutive activation of the inflammasome, resulting in chronic IL-1β production, what compensatory mechanism, if any, would MOST likely mitigate the resulting inflammation?

What would be the PRIMARY consequence of a mutation leading to complete deficiency of MyD88 in an individual exposed to a bacterial infection?

Considering the role of acute phase proteins (APPs) in the inflammatory response, what would be the MOST direct consequence of significantly reduced serum levels of C4?

A patient with a genetic mutation exhibits impaired function of plasmacytoid dendritic cells (pDCs). How would this MOST directly impact the initial immune response to a systemic viral infection?

If a novel pathogen evolved a mechanism to specifically inhibit the function of RNase L, what stage of the antiviral response initiated by type I interferons would be MOST directly compromised?

In a scenario where an individual has a genetic mutation that leads to a complete loss of function of the protein kinase R (PKR), how would this MOST directly impact the cellular response to viral infection?

Considering the critical role of selectins in leukocyte trafficking, what would be the MOST likely consequence of a genetic defect that results in a complete deficiency of E-selectin expression on endothelial cells?

Given the physiological mechanisms underlying fever, which therapeutic intervention would MOST directly counteract the effects of prostaglandin E2 (PGE2) in the hypothalamus to reduce fever during an infection?

In the context of leukocyte adhesion deficiency (LAD), a genetic defect that prevents the expression of functional β2 integrins, what specific step in leukocyte extravasation would be MOST directly impaired?

What would be the MOST direct consequence of a mutation leading to non-functional MASP-2 in the lectin pathway of complement activation?

Assuming a researcher discovers a novel cytokine that selectively targets and activates tissue fibroblasts, leading to increased production of extracellular matrix (ECM) components, what downstream immunological event would be MOST directly influenced?

In a patient with a functional defect in the C-type lectin receptor Dectin-1, what would be the most direct impact on the immune response to fungal infections?

A researcher is investigating the role of cellular location of various TLRs. What is the MOST accurate rationale for TLR3 being located in endosomes rather than the plasma membrane?

For a patient with a deficiency in nucleotide-binding oligomerization domain-containing protein 2 (NOD2), what innate immune event would be MOST directly compromised during a bacterial infection

How would a loss-of-function mutation in the gene encoding serum amyloid A (SAA) PRIMARILY affect the host's response to bacterial infection?

Where are PAMP generally found?

In the context of viral infections, what critical event is MOST directly dependent on the synthesis and activation of 2',5'-oligoadenylate synthetase (OAS) by interferon-stimulated genes (ISGs)?

Considering the intricate crosstalk between innate immune cells and tissue cells, what is the MOST immediate consequence of IL-1β and TNF-α on tissue fibroblasts during the inflammatory response?

What is the MOST accurate description of how a deficiency in the γ subunit of IKK (IKKγ) would impact NF-κB activation in macrophages stimulated with LPS?

Given the complexity of leukocyte trafficking, what cellular event is MOST critically reliant upon the local effects of TNF-α on post-capillary venule endothelial cells during inflammation?

In the context of pathogen recognition, what feature is DISTINCTIVE about NOD-like receptors (NLRs) compared to Toll-like receptors (TLRs)?

If an individual expresses a constitutively active form of protein kinase R (PKR), independent of dsRNA binding, what signaling outcome is MOST likely?

Considering the roles of acute phase proteins (APPs), what outcome would be expected from significantly reduced serum levels of C-reactive protein (CRP)?

Based on current understanding, what would be the MOST consequential difference between complement activation initiated by C-reactive protein (CRP) versus mannose-binding lectin (MBL)?

In the context of viral infections, how does released type I interferon (IFN) MOST directly mediate resistance to viral replication in neighboring, uninfected cells?

A researcher discovers a novel pathogen-associated molecular pattern (PAMP) that strongly activates NF-κB in macrophages. Further investigation reveals that this PAMP's activity is ENTIRELY dependent on MyD88. Which Toll-like receptor (TLR) is MOST likely involved in the recognition of this PAMP?