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TH2 cells coordinate type 2 responses to expel intestinal helminths and repair tissue injury. The immune response to helminthic worm infections in the gastrointestinal tract requires specialized mechanisms due to the fact that helminths are too large to be ingested and destroyed by phagocytes. For example, cytokines made by TH2 cells elicit responses from multiple non-hematopoietic cell types that aid in
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- Mycobacteria are intracellular pathogens that have adapted to life inside phagocytic cells, such as macrophages. These intracellular bacteria are taken up by phagocytosis, similar to other pathogens, but the bacteria are not killed. One possible mechanism that could account for this immune evasion by mycobacteria is their ability to: Prevent induction of nitric oxide production in the phagosome Prevent the acidification of phagosomes Prevent the expression of antimicrobial peptides in the phagosome Prevent fusion of phagosomes with lysosomes Kill the macrophage before it kills themIn addition to phagocytosis, neutrophils use a process called NETs. Which one of the following describes this process? Group of answer choices A. NETs is a neutrophil process that activates the complement system of proteins, which destroys pathogens. B. A net-like structure of DNA, histones, lactoferrins, gelatinase, cathepsin G, and myeloperoxidase is secreted at pathogens. Together these chemicals destroy pathogens. C. NETs works when neutrophils secrete major basic proteins onto pathogens, destroying the pathogens' cell membranes. D. NETs are chemicals secreted by neutrophils that trigger the rapid maturation of lymphoid stem cells into lymphocytes.In addition to phagocytosis, neutrophils use a process called NETs. Which one of the following describes this process? A. NETs is a neutrophil process that activates the complement system of proteins, which destroys pathogens. B. NETs are chemicals secreted by neutrophils that trigger the rapid maturation of lymphoid stem cells into lymphocytes. C. A net-like structure of DNA, histones, lactoferrins, gelatinase, cathepsin G, and myeloperoxidase is secreted at pathogens. Together these chemicals destroy pathogens. D. NETs works when neutrophils secrete major basic proteins onto pathogens, destroying the pathogens' cell membranes.
- Opsonization of pathogens by both antibodies and complement proteins (C3b) leads to uptake and destruction of the pathogen by phagocytic cells that express both Fc receptors and complement receptors. Which of the following in the figure below is the most efficient form of dual opsonization of the pathogen by antibody and C3b to maximize phagocytosis?The entry of naive T cells from the blood into lymph nodes and mucosal lymphoid tissues occurs by a process that involves similar steps and similar adhesion molecules to the process by which leukocytes are recruited into sites of inflammation. Yet naive T cells do not enter tissues at sites of inflammation, but rather, home to lymphoid tissues. Which class of adhesion molecules direct the specific homing of naive T cells to lymphoid tissues?The Gram-negative bacterium Yersinia pestis, thecausative agent of the plague, is extremely virulent. Uponinfection, Y. pestis injects a set of effector proteins intomacrophages that suppresses their phagocytic behaviorand also interferes with their innate immune responses.One of the effector proteins, YopJ, acetylates serines andthreonines on various MAP kinases, including the MAPkinase kinase kinase TAK1, which controls a key signalingstep in the innate immune response pathway. To deter-mine how YopJ interferes with TAK1, you transfect humancells with active YopJ (YopJWT) or inactive YopJ (YopJCA)and with FLAG-tagged active TAK1 (TAK1WT) or inactiveTAK1 (TAK1K63W), and assay for total TAK1 and for phos-phorylated TAK1, using antibodies against the FLAG tag oragainst phosphorylated TAK1 (Figure Q23–1). How doesYopJ block the TAK1 signaling pathway? How do you sup-pose the serine/threonine acetylase activity of YopJ mightinterfere with TAK1 activation?
- The small fragments of some complement proteins initiate a local inflammatory response. Recent studies using mouse models of pulmonary inflammation (a model for human asthma) have found that mice deficient in the C3a receptor have greatly reduced disease symptoms when challenged with inhaled preparations containing extracts of the fungal pathogen Aspergillus fumigatus. Specifically, the C3a receptor-deficient mice showed reduced influx of granulocytes and lymphocytes into the lung and reduced fluid in the lung after challenge. What is the explanation for these findings?Some viruses have mechanisms to down-regulate MHC class I protein expression on the surface of cells in which the virus is replicating. This immune evasion strategy might prevent effector CD8 cytotoxic T cells from recognizing and killing the virus-infected cells. Would this immune evasion strategy also prevent the initial activation of virus-specific CD8 T cells? Yes, because no viral peptide:MHC class I complexes would form to activate CD8 T cells. No, because dendritic cells would take up infected cells and cross-present viral peptides to activate CD8 T cells. No, because some presentation of MHC class I complexes with viral peptides would occur before the virus could down-regulate all the surface MHC class I protein. Yes, because this immune evasion strategy would also function in dendritic cells, even if the virus doesn’t replicate in dendritic cells. No, because the type I interferon response induced by the virus infection will up-regulate MHC class I expression and override the…Human immune system During the inflammatory response, histamine plays a key role in causing capillaries to become more permeable to phagocytic cells such as neutrophils. Antibodies directly kill bacterial cells by activating cell death programs that lead to apoptosis. Interferons are signaling molecules produced by bacteria that block (or interfere) with the ability of plasma cells to release antibodies.
- B cells express a complement receptor that binds to C3b cleavage products, such as iC3b and C3dg. When a B cell with an antigen receptor that specifically recognizes that pathogen also has its complement receptor stimulated because the pathogen is opsonized with these C3 fragments, B cell activation is greatly enhanced. Due to this mechanism, B cells can be activated by much lower concentrations of antigen (in this case, the pathogen) than if the antigen is devoid of complement components. This mechanism functions to: Ensure that pathogens are readily detected by the adaptive immune system before they replicate to high levels in the host Prevent B cells from being activated in response to antigens that are not pathogens Allow B cells to phagocytose the pathogen and help destroy it Induce increased rounds of B cell replication to make more pathogen-specific B cells Allow the B cell to block pathogen replication by interfering with multiple pathogen surface functionsAn adaptive immune response underlying coeliac disease pathogenesis involves: a) Production of Th1 (T helper cell 1 type) cytokines that act to promote the production of antibodies to gluten peptides b) Production of anti-gliadin and anti-tissue transglutaminase antibodies via TH2 cytokines c) Conversion of glutamate to glutamine by deamination d) The early recognition of gluten peptides via pattern recognition receptors on epithelial cells and the subsequent release of Interleukin 15During the chemotaxis phase of the inflammatory response,a. C-reactive protein is secreted by damaged parenchymal cells in the tissue, which attracts neutrophils, which secrete leukotrienes and prostaglandins to attract macrophages; a purulent exudate is formed.b. Band cells respond to hyperthermia by producing TNF-α and interleukins, which then cause a left shift that results in the accumulation of neutrophils within the tissue.c. Damaged parenchymal cells release prostaglandins and leukotrienes to attract macrophages, causing a left shift and the formation of a purulent exudate.d. Cytokines, such as TNF-α, are released by damaged parenchymal cells, while leukotrienes and prostaglandins produced by neutrophils cause smooth muscle constriction and the further accumulation of leukocytes.
