Lecture 18: Innate Immunity III: Induced Cellular Response

Which of the following is the primary function of neutrophils upon infiltrating infected tissues?

Which of the following pathways do neutrophils and macrophages utilize to eliminate engulfed pathogens?

Which immune cell is responsible for secreting type I interferons upon detecting viral presence?

What is the outcome of NK cells being stimulated by IL-1, IL-2, IL-12, and type I IFNs?

Which process involves neutrophils releasing DNA fibers decorated with histones and granular proteins to trap microbes?

Which of the following is NOT a characteristic of neutrophils?

What is the effect of vasodilation and increased vascular permeability during inflammation?

Receptor ligation on phagocytes triggers which of the following?

What is the purpose of opsonization in the context of phagocytosis?

What is the role of NADPH oxidase (Phox) in the early reactions within the phagosome?

What is the function of inducible nitric oxide synthase (iNOS) within the phagosome?

What is the role of the vacuolar ATPase in the late reactions within the phagosome?

Which of the following is NOT a typical component of Neutrophil Extracellular Traps (NETs)?

What is the primary function of plasmacytoid dendritic cells (pDCs)?

What is the function of NK cells expressing CD56 and CD16?

What role does inflammation play in NK cell function?

Which of the following cytokines do NOT activate NK cells?

What is the role of MHC class I molecules in the regulation of NK cell cytotoxicity?

What is the effect of interferon-gamma (IFN-γ) released by activated NK cells on macrophages?

What generally induces M2 macrophage polarization?

What is the primary role of eosinophils in innate immunity?

Which of the following best describes the primary function of mast cells in innate immunity?

Which cell type secretes histamine, heparin, TNF-α, proteases, and degrading enzymes?

What is the initial response of a mast cell upon activation?

What is the role of Leukotrienes that are produced by mast cells?

What is the MOST important function of VEGF (vascular endothelial growth factor) that is produced by mast cells?

What is the significance of neutrophils undergoing NETosis?

How does the absence of MHC class I molecules on a target cell affect NK cell activity?

A researcher is investigating a new drug that aims to enhance the innate immune response against viral infections. Which cell type should the drug target to maximize type I interferon production?

A biopsy from a patient with a helminth infection shows a large number of immune cells surrounding the parasite. Which of the following cell types is MOST likely to be present in high numbers and directly involved in killing the worm?

A patient with a chronic inflammatory condition has elevated levels of both pro-inflammatory and anti-inflammatory cytokines. Which of the following macrophage phenotypes is MOST likely to be contributing to this mixed inflammatory profile?

A researcher discovers a novel protein that inhibits the fusion of lysosomes with phagosomes in macrophages. How would this protein MOST likely affect the macrophage's ability to clear intracellular bacteria?

A patient has a genetic defect that results in non-functional myeloperoxidase (MPO) in their neutrophils. Which of the following processes would be MOST directly impaired in these neutrophils?

A novel virus has evolved a mechanism to specifically inhibit the production of IL-12 by macrophages. Which of the following immune cell functions would be MOST directly compromised by this viral strategy?

Imagine a scenario where a new drug selectively blocks the S1PR receptor on mast cells. How would you anticipate this drug influencing the immediate and delayed phases of an allergic reaction, considering the role of mast cell activation?

Which of the following is the MOST accurate description of NETosis?

During an inflammatory response, a tissue is infiltrated with immune cells, including mast cells. What is a primary mechanism by which mast cells contribute to vasodilation?

A researcher is investigating the activation of NK cells in response to a viral infection. The researcher notices that the cells infected with the virus do not express Interferon Type 1. How will this affect the NK cell's response?

Which of the following represents the correct order of granule mobilization in neutrophils upon activation, from earliest to latest?

A patient presents with a genetic defect leading to the inability of neutrophils to produce Arginase 1 upon rolling contact with the endothelium. How will this affect the inflammatory response?

Given the sequential mobilization of neutrophil granules, which granule type's deficiency would MOST severely compromise the early stages of neutrophil transmigration across the endothelium during acute inflammation?

A researcher is investigating therapeutic strategies to modulate NETosis in severe sepsis. Targeting which of the following enzymatic activities would MOST effectively inhibit NET formation while preserving other neutrophil functions?

In the context of macrophage polarization, consider a scenario where a novel cytokine selectively inhibits the expression of transcription factor IRF5. How would this cytokine MOST likely influence macrophage phenotype and function in a tumor microenvironment?

Following a bee sting, an individual experiences a severe allergic reaction characterized by systemic vasodilation and bronchoconstriction. To counteract these effects rapidly, which of the following therapeutic interventions would be MOST physiologically effective, considering the immediate mediators released by activated mast cells?

A pharmaceutical company is developing a novel drug to enhance the cytotoxic activity of NK cells against tumor cells that have downregulated MHC class I expression. Which of the following approaches would be MOST effective in selectively amplifying NK cell responses in this context?

In a patient with chronic granulomatous disease (CGD) characterized by a defective NADPH oxidase enzyme, which of the following intracellular events would be MOST directly impaired in their neutrophils and macrophages, leading to increased susceptibility to catalase-positive organisms?

Consider a scenario where macrophages are exposed to immune complexes opsonized with IgG1. Which intracellular signaling pathway within the macrophage would be MOST directly activated, leading to enhanced phagocytosis and cytokine production?

A researcher is investigating the role of eosinophils in an experimental model of allergic asthma. If they selectively ablated eosinophils in this model, which of the following outcomes would be MOST likely?

A patient presents with a novel genetic mutation that results in a complete loss of Arginase-1 production specifically in neutrophils. During an acute inflammatory response, how would this deficiency MOST likely impact vasodilation and endothelial permeability at the affected site?

Considering the role of plasmacytoid dendritic cells (pDCs) in antiviral immunity, which of the following mechanisms would be MOST effective for a virus to evade detection and subsequent activation of innate immune responses mediated by pDCs?

Within the context of neutrophil-mediated NETosis, what consequence would arise MOST directly from inhibiting histone citrullination by peptidylarginine deiminase 4 (PAD4)?

A researcher is investigating the mechanisms by which mast cells contribute to the pathogenesis of rheumatoid arthritis. Which of the following mast cell-derived mediators would MOST directly promote joint inflammation and cartilage degradation?

A novel bacterial pathogen has evolved a mechanism to secrete a protease that specifically cleaves and inactivates C3a and C5a anaphylatoxins. How would this virulence strategy MOST effectively compromise the host's innate immune response?

A patient with a genetic defect exhibits impaired production of both IL-4 and IL-13. Considering the coordinated action of innate immune cells, which of the following processes would be MOST significantly affected in the context of helminth infection?

An experimental drug is designed to selectively inhibit the interaction between the leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1). During an inflammatory response, which of the following stages of neutrophil recruitment would be MOST directly affected by this drug?

Upon encountering a microbial pathogen, a tissue-resident macrophage initiates phagocytosis. Which signaling molecule predominantly governs non-inflammatory phagocytosis?

What is the MOST LIKELY reason that a neutrophil's secretion of resistin would be beneficial during an inflammatory immune response?

What is the MOST LIKELY outcome from a virally infected, stressed or tumor cell developing a complete loss of MHC-1 molecules?

You are investigating the MOA (mechanism of action) in a novel immune cell. You find it up-regulates stress-induced ligands to promote the killing of altered self-cells, What is the MOST LIKELY cell type?

How can the cytokine IFN-γ facilitate innate immune cellular responses?

If someone had a significant helminth infection, how would that MOST LIKELY affect the body overall?

During the innate immune response to a pathogenic threat, how do mast cells and other sentinel innate immune cells MAINTAIN the integrity of the tissue.

If a patient has the novel genetic defect of a non-functioning vacoular ATPase, what is the MOST likely direct outcome of this mutation?

Within the context of NETosis, how would a deficiency in histone citrullination by peptidylarginine deiminase 4 (PAD4) affect the biophysical properties of NETs and their subsequent interaction with circulating immune complexes?

Following exposure to a novel fungal pathogen, a subset of macrophages upregulates the expression of both iNOS and Arginase-1. How does this simultaneous expression influence the regulation of the inflammatory response and tissue homeostasis in the immediate microenvironment, taking into account the compartmentalization of enzymatic activity?

Upon activation by pathogen-associated molecular patterns (PAMPs), plasmacytoid dendritic cells (pDCs) initiate a signaling cascade culminating in the secretion of copious amounts of type I interferons (IFN-I). Which post-translational modification of interferon regulatory factor 7 (IRF7) is indispensable for its nuclear translocation and subsequent transcriptional activation of IFN-I genes, and how does this modification integrate with other signaling events?

In the context of helminth infections, how does the interplay between mast cell-derived TNF-α and eosinophil-derived major basic protein (MBP) contribute to the pathogenesis of tissue damage, considering the impact on both innate and adaptive immune responses?

Considering the sequential mobilization of neutrophil granules, what is the most plausible implication of a genetic polymorphism that selectively impairs the translocation of Arginase-1 into gelatinase granules, and how would this impact the regulatory balance of the inflammatory response?