Podcast
Questions and Answers
The immune system's goal for extracellular pathogens is to kill the pathogen.
The immune system's goal for extracellular pathogens is to kill the pathogen.
True (A)
Antibodies are primarily involved in the immune response against intracellular pathogens.
Antibodies are primarily involved in the immune response against intracellular pathogens.
False (B)
Neutrophils and macrophages are important for responding to extracellular bacteria.
Neutrophils and macrophages are important for responding to extracellular bacteria.
True (A)
Cytotoxic T cells are essential for eliminating infected cells due to intracellular pathogens.
Cytotoxic T cells are essential for eliminating infected cells due to intracellular pathogens.
Th2 cells and IgE antibodies are primarily involved in the immune response to helminths.
Th2 cells and IgE antibodies are primarily involved in the immune response to helminths.
Viruses can evade the immune response by down-regulating MHC class I.
Viruses can evade the immune response by down-regulating MHC class I.
Antigenic drift involves major changes in viral antigens.
Antigenic drift involves major changes in viral antigens.
The Epstein Barr Virus has a protein that inhibits antigen processing.
The Epstein Barr Virus has a protein that inhibits antigen processing.
Influenza virus evasion is primarily due to antigenic drift and antigenic shift.
Influenza virus evasion is primarily due to antigenic drift and antigenic shift.
Down-regulated MHC class I makes cells immune to NK cells.
Down-regulated MHC class I makes cells immune to NK cells.
Point mutations lead to antigenic drift in viruses.
Point mutations lead to antigenic drift in viruses.
Antigenic shift does not occur in influenza viruses.
Antigenic shift does not occur in influenza viruses.
Viral genetic variation can prevent recognition by the immune system.
Viral genetic variation can prevent recognition by the immune system.
HSV aids in peptide generation for immune response.
HSV aids in peptide generation for immune response.
Cells can become targets for NK cells after down-regulating MHC class I.
Cells can become targets for NK cells after down-regulating MHC class I.
Innate immune cells have specific antigen receptors.
Innate immune cells have specific antigen receptors.
NK cells can detect 'altered self' cells.
NK cells can detect 'altered self' cells.
The primary function of NK cells is to directly kill pathogens.
The primary function of NK cells is to directly kill pathogens.
NK cells possess both inhibitory and activatory receptors.
NK cells possess both inhibitory and activatory receptors.
Normal, uninfected cells trigger NK cell activation.
Normal, uninfected cells trigger NK cell activation.
Infected cells down-regulate MHC class I to escape NK cell detection.
Infected cells down-regulate MHC class I to escape NK cell detection.
NK cells kill infected cells in a similar manner to cytotoxic T cells.
NK cells kill infected cells in a similar manner to cytotoxic T cells.
NK cells require a positive signal from either inhibitory or activatory receptors to function.
NK cells require a positive signal from either inhibitory or activatory receptors to function.
Perforin forms pores in the membrane of infected cells.
Perforin forms pores in the membrane of infected cells.
Cytotoxic T lymphocytes (CTL) kill pathogens directly.
Cytotoxic T lymphocytes (CTL) kill pathogens directly.
Granzyme is involved in activating apoptosis in infected cells.
Granzyme is involved in activating apoptosis in infected cells.
Cytotoxic T cells recognize viral antigens presented on MHC class II molecules.
Cytotoxic T cells recognize viral antigens presented on MHC class II molecules.
The cytokine IFN-γ drives Th1 responses.
The cytokine IFN-γ drives Th1 responses.
Antibody effector mechanisms are significant for anti-viral immunity.
Antibody effector mechanisms are significant for anti-viral immunity.
A virally-infected cell displays viral antigens on MHC class II molecules.
A virally-infected cell displays viral antigens on MHC class II molecules.
Activated cytotoxic T cells release vesicles containing toxic enzymes.
Activated cytotoxic T cells release vesicles containing toxic enzymes.
Genetic recombination between different viruses can create a completely new virus with no historical immunity.
Genetic recombination between different viruses can create a completely new virus with no historical immunity.
Th1 cells are primarily important for fighting viral infections.
Th1 cells are primarily important for fighting viral infections.
IFN-γ enhances the activation of macrophages by upregulating costimulatory molecules.
IFN-γ enhances the activation of macrophages by upregulating costimulatory molecules.
Granulomas can form as a result of Th1 induced macrophage activation.
Granulomas can form as a result of Th1 induced macrophage activation.
The center of a granuloma may become hyperoxic and undergo necrosis.
The center of a granuloma may become hyperoxic and undergo necrosis.
The MTb bacteria can persist within granulomas for years while the host maintains good health.
The MTb bacteria can persist within granulomas for years while the host maintains good health.
Steroid treatment can reactivate dormant MTb infections.
Steroid treatment can reactivate dormant MTb infections.
Ongoing Th1 response is not necessary for lifelong control of infections.
Ongoing Th1 response is not necessary for lifelong control of infections.
Macrophages are activated by Th1 cells to kill Mycobacterium tuberculosis (MTb).
Macrophages are activated by Th1 cells to kill Mycobacterium tuberculosis (MTb).
IL-12 is a factor that promotes the activation of Th2 cells.
IL-12 is a factor that promotes the activation of Th2 cells.
Interferons play a significant role in the anti-viral response.
Interferons play a significant role in the anti-viral response.
Natural Killer cells are exclusively responsible for the adaptive immune response.
Natural Killer cells are exclusively responsible for the adaptive immune response.
Granulomas are involved in the response to intracellular bacteria.
Granulomas are involved in the response to intracellular bacteria.
The immune system recognizes both viruses and extracellular bacteria with the same response.
The immune system recognizes both viruses and extracellular bacteria with the same response.
Cytotoxic T cells are important for dealing with intracellular infections.
Cytotoxic T cells are important for dealing with intracellular infections.
The innate immune response comes days to weeks after infection.
The innate immune response comes days to weeks after infection.
Pathogenic fungi are only recognized by the adaptive immune system.
Pathogenic fungi are only recognized by the adaptive immune system.
The use of influenza helps describe a typical immune response to viral infection.
The use of influenza helps describe a typical immune response to viral infection.
Adaptive immunity is not involved in the response to extracellular fungi.
Adaptive immunity is not involved in the response to extracellular fungi.
Viruses can escape immune detection and may contribute to disease pathology.
Viruses can escape immune detection and may contribute to disease pathology.
Type I interferons (IFNs) induce an anti-viral immune state that potentially shuts down nearby infected cells.
Type I interferons (IFNs) induce an anti-viral immune state that potentially shuts down nearby infected cells.
Natural Killer (NK) cells solely rely on MHC class I molecules for activation.
Natural Killer (NK) cells solely rely on MHC class I molecules for activation.
Viral RNA is recognized by TLR2 and TLR6 receptors.
Viral RNA is recognized by TLR2 and TLR6 receptors.
The innate immune response to viruses is characterized by the activation of NK cells and macrophages.
The innate immune response to viruses is characterized by the activation of NK cells and macrophages.
Cytotoxic T cells directly kill infected cells by releasing antibodies.
Cytotoxic T cells directly kill infected cells by releasing antibodies.
Activation of dendritic cells and macrophages is a significant effect of Type I IFNs on the immune response.
Activation of dendritic cells and macrophages is a significant effect of Type I IFNs on the immune response.
Cells that down-regulate MHC class I become targets for NK cells.
Cells that down-regulate MHC class I become targets for NK cells.
Granzyme is involved in the metabolic activation of macrophages by T cells.
Granzyme is involved in the metabolic activation of macrophages by T cells.
Inhibitory receptors on NK cells bind to MHC class II molecules.
Inhibitory receptors on NK cells bind to MHC class II molecules.
NK cells can be activated when there is no positive signal from the inhibitory receptor.
NK cells can be activated when there is no positive signal from the inhibitory receptor.
Viruses have developed strategies solely to enhance their reproduction, disregarding immune evasion.
Viruses have developed strategies solely to enhance their reproduction, disregarding immune evasion.
Uninfected cells do not provide any inhibitory signaling to NK cells.
Uninfected cells do not provide any inhibitory signaling to NK cells.
Type I interferons play a critical role in the innate immune response to viruses.
Type I interferons play a critical role in the innate immune response to viruses.
Virally-infected cells down-regulate MHC class I to avoid detection by cytotoxic T cells (CTLs).
Virally-infected cells down-regulate MHC class I to avoid detection by cytotoxic T cells (CTLs).
The goal of viruses is to thrive in a hostile environment rather than to survive.
The goal of viruses is to thrive in a hostile environment rather than to survive.
NK cells have antigen-specific receptors similar to those of cytotoxic T cells.
NK cells have antigen-specific receptors similar to those of cytotoxic T cells.
Cytokines, including pro-inflammatory cytokines, are not involved in the innate immune response to viruses.
Cytokines, including pro-inflammatory cytokines, are not involved in the innate immune response to viruses.
Activation of NK cells involves recognizing the presence of tumor cells.
Activation of NK cells involves recognizing the presence of tumor cells.
The immune system is a versatile opponent against viruses aimed at survival.
The immune system is a versatile opponent against viruses aimed at survival.
The presence of activatory receptors on NK cells prevents them from killing infected cells.
The presence of activatory receptors on NK cells prevents them from killing infected cells.
NK cells kill infected cells using a mechanism similar to cytotoxic T lymphocytes (CTLs).
NK cells kill infected cells using a mechanism similar to cytotoxic T lymphocytes (CTLs).
Cytotoxic T Lymphocytes (CTL) are programmed to kill cells that display viral antigens on MHC class I molecules.
Cytotoxic T Lymphocytes (CTL) are programmed to kill cells that display viral antigens on MHC class I molecules.
Perforin and granzymes are involved in the killing of extracellular pathogens.
Perforin and granzymes are involved in the killing of extracellular pathogens.
The cytokine IFN-γ plays a significant role in driving Th2 responses.
The cytokine IFN-γ plays a significant role in driving Th2 responses.
Activated cytotoxic T cells release perforin to promote apoptosis in infected cells.
Activated cytotoxic T cells release perforin to promote apoptosis in infected cells.
Virally-infected cells do not express any antigens.
Virally-infected cells do not express any antigens.
Cytotoxic T cells primarily attack pathogens directly rather than the cells infected by them.
Cytotoxic T cells primarily attack pathogens directly rather than the cells infected by them.
Granzymes activate apoptosis regardless of the presence of perforin.
Granzymes activate apoptosis regardless of the presence of perforin.
Cytotoxic T cells play an insignificant role in anti-viral immunity.
Cytotoxic T cells play an insignificant role in anti-viral immunity.
Eosinophils and mast cells are important for the immune response to helminths.
Eosinophils and mast cells are important for the immune response to helminths.
The primary goal of the immune system when dealing with intracellular pathogens is to kill the pathogens directly.
The primary goal of the immune system when dealing with intracellular pathogens is to kill the pathogens directly.
Th17 cells are primarily involved in the immune response against extracellular bacteria.
Th17 cells are primarily involved in the immune response against extracellular bacteria.
Interferon response is crucial for managing infections caused by viruses.
Interferon response is crucial for managing infections caused by viruses.
Intracellular bacteria activate Th2 cells to promote the immune response.
Intracellular bacteria activate Th2 cells to promote the immune response.
Antigenic drift refers to subtle changes in surface antigens of viruses due to major mutations.
Antigenic drift refers to subtle changes in surface antigens of viruses due to major mutations.
Influenza viruses evade the immune response through antigenic shift and antigenic drift.
Influenza viruses evade the immune response through antigenic shift and antigenic drift.
Down-regulating MHC class I protects cells from being targeted by NK cells.
Down-regulating MHC class I protects cells from being targeted by NK cells.
Major changes in viral antigens caused by genetic recombination are a characteristic of antigenic drift.
Major changes in viral antigens caused by genetic recombination are a characteristic of antigenic drift.
Viral genetic variation can lead to mutations that prevent recognition by immune cells.
Viral genetic variation can lead to mutations that prevent recognition by immune cells.
Interfering with antigen processing does not impact the detection of viruses by the immune system.
Interfering with antigen processing does not impact the detection of viruses by the immune system.
Cells that successfully down-regulate MHC class I are likely to experience increased immune recognition.
Cells that successfully down-regulate MHC class I are likely to experience increased immune recognition.
Antigenic shift occurs rarely compared to antigenic drift in influenza viruses.
Antigenic shift occurs rarely compared to antigenic drift in influenza viruses.
HSV aids in efficient peptide generation for the immune response.
HSV aids in efficient peptide generation for the immune response.
Type I interferons (IFNs) are produced by uninfected cells.
Type I interferons (IFNs) are produced by uninfected cells.
The activation of cytotoxic T cells is solely dependent on the presence of TLR receptors.
The activation of cytotoxic T cells is solely dependent on the presence of TLR receptors.
Natural Killer (NK) cells have no role in recognizing 'altered self' cells.
Natural Killer (NK) cells have no role in recognizing 'altered self' cells.
MHC class I upregulation is a direct effect of type I interferons on immune cells.
MHC class I upregulation is a direct effect of type I interferons on immune cells.
Intracellular infections primarily trigger an adaptive immune response without the involvement of innate immunity.
Intracellular infections primarily trigger an adaptive immune response without the involvement of innate immunity.
RIG-I receptors are involved in recognizing viral capsid proteins.
RIG-I receptors are involved in recognizing viral capsid proteins.
Cytotoxic T lymphocytes (CTL) are primarily activated by type I interferons.
Cytotoxic T lymphocytes (CTL) are primarily activated by type I interferons.
Type I IFNs can directly shut down infected cells to limit the spread of viruses.
Type I IFNs can directly shut down infected cells to limit the spread of viruses.
Virally-infected cells primarily produce IL-10 as their main cytokine.
Virally-infected cells primarily produce IL-10 as their main cytokine.
CTLs and NK cells are responsible for killing virally-infected cells.
CTLs and NK cells are responsible for killing virally-infected cells.
Antibodies have only one role, which is to neutralize viruses.
Antibodies have only one role, which is to neutralize viruses.
Viruses can evade the host immune response by mutating their surface proteins.
Viruses can evade the host immune response by mutating their surface proteins.
Th17 and Th1 cells are equally effective in eliminating virally-infected cells.
Th17 and Th1 cells are equally effective in eliminating virally-infected cells.
Complement activation is not a function of antibodies against viruses.
Complement activation is not a function of antibodies against viruses.
Down-regulation of MHC class I enhances the recognition of infected cells by NK cells.
Down-regulation of MHC class I enhances the recognition of infected cells by NK cells.
The innate immune response in humans occurs within hours of infection.
The innate immune response in humans occurs within hours of infection.
Granzyme is responsible for forming pores in the membrane of infected cells.
Granzyme is responsible for forming pores in the membrane of infected cells.
Cytotoxic T lymphocytes primarily kill pathogens directly rather than infected cells.
Cytotoxic T lymphocytes primarily kill pathogens directly rather than infected cells.
IFN-γ is a cytokine that enhances Th2 responses.
IFN-γ is a cytokine that enhances Th2 responses.
Virally-infected cells display viral antigens on MHC class I molecules to be recognized by cytotoxic T cells.
Virally-infected cells display viral antigens on MHC class I molecules to be recognized by cytotoxic T cells.
Granulomas are primarily formed in response to viral infections.
Granulomas are primarily formed in response to viral infections.
Activated cytotoxic T cells release perforin and granzymes to eliminate infected cells.
Activated cytotoxic T cells release perforin and granzymes to eliminate infected cells.
The expression of MHC class I on a cell is irrelevant for the activation of cytotoxic T cells.
The expression of MHC class I on a cell is irrelevant for the activation of cytotoxic T cells.
Natural Killer cells are unable to recognize cells that down-regulate MHC class I molecules.
Natural Killer cells are unable to recognize cells that down-regulate MHC class I molecules.
The primary mechanisms of the innate immune response occur instantaneously, within minutes to hours.
The primary mechanisms of the innate immune response occur instantaneously, within minutes to hours.
Adaptive immunity primarily targets extracellular pathogens without any involvement of innate immunity.
Adaptive immunity primarily targets extracellular pathogens without any involvement of innate immunity.
Natural Killer cells are mainly responsible for targeting only extracellular bacteria during the immune response.
Natural Killer cells are mainly responsible for targeting only extracellular bacteria during the immune response.
Granulomas are formed as an adaptive immune response to control intracellular bacteria like Mycobacterium tuberculosis.
Granulomas are formed as an adaptive immune response to control intracellular bacteria like Mycobacterium tuberculosis.
Interferons are crucial mediators that enhance the body's antiviral response.
Interferons are crucial mediators that enhance the body's antiviral response.
Th1 cells are essential for the effective immune response against helminths.
Th1 cells are essential for the effective immune response against helminths.
The process of antigenic drift in viruses results from gradual mutations that escape immune detection.
The process of antigenic drift in viruses results from gradual mutations that escape immune detection.
NK cells kill uninfected cells by utilizing their activatory receptors.
NK cells kill uninfected cells by utilizing their activatory receptors.
Cytokines play an essential role in the inflammatory response but are not involved in adaptive immunity.
Cytokines play an essential role in the inflammatory response but are not involved in adaptive immunity.
The immune system's recognition of both viruses and extracellular bacteria utilizes identical mechanisms.
The immune system's recognition of both viruses and extracellular bacteria utilizes identical mechanisms.
Virally-infected cells down-regulate MHC class I to avoid detection by cytotoxic T cells.
Virally-infected cells down-regulate MHC class I to avoid detection by cytotoxic T cells.
NK cells can directly kill pathogens by themselves.
NK cells can directly kill pathogens by themselves.
Inhibitory receptors on NK cells increase their activation when they bind to MHC class I.
Inhibitory receptors on NK cells increase their activation when they bind to MHC class I.
Normal cells trigger a positive signal for NK cell activation.
Normal cells trigger a positive signal for NK cell activation.
The mechanism of NK cell killing is fundamentally the same as that of cytotoxic T cells.
The mechanism of NK cell killing is fundamentally the same as that of cytotoxic T cells.
NK cells have only inhibitory receptors and cannot activate without a positive signal.
NK cells have only inhibitory receptors and cannot activate without a positive signal.
MHC class I down-regulation on infected cells leads to NK cell inactivation.
MHC class I down-regulation on infected cells leads to NK cell inactivation.
Antigenic drift results in major alterations on the surface of the influenza virus due to events such as point mutations.
Antigenic drift results in major alterations on the surface of the influenza virus due to events such as point mutations.
Viruses can evade immune detection by up-regulating MHC class I expression.
Viruses can evade immune detection by up-regulating MHC class I expression.
Antigenic shift occurs less frequently than antigenic drift and involves significant changes in the viral antigens.
Antigenic shift occurs less frequently than antigenic drift and involves significant changes in the viral antigens.
Epstein Barr Virus enhances antigen processing to help with immune evasion.
Epstein Barr Virus enhances antigen processing to help with immune evasion.
The down-regulation of MHC class I makes cells more susceptible to attacks from NK cells.
The down-regulation of MHC class I makes cells more susceptible to attacks from NK cells.
Cellular mechanisms that interfere with peptide generation can enhance a virus's ability to evade immune response.
Cellular mechanisms that interfere with peptide generation can enhance a virus's ability to evade immune response.
Small mutations in viral genes can result in loss of recognition by the immune system and contribute to ongoing infections.
Small mutations in viral genes can result in loss of recognition by the immune system and contribute to ongoing infections.
Major changes to viral antigens can occur due to genetic recombination of influenza viruses.
Major changes to viral antigens can occur due to genetic recombination of influenza viruses.
The protein produced by Epstein Barr Virus enhances MHC class I expression on the cell surface.
The protein produced by Epstein Barr Virus enhances MHC class I expression on the cell surface.
Cells that up-regulate MHC class I are less likely to be targeted by NK cells.
Cells that up-regulate MHC class I are less likely to be targeted by NK cells.
Flashcards
Intracellular Infection
Intracellular Infection
An infection where the pathogen resides inside host cells.
Immune Response to Viral Infection
Immune Response to Viral Infection
The body's reaction to a viral invader, including both innate and adaptive responses.
Interferons
Interferons
Anti-viral proteins produced by infected cells to prevent viral spread.
Natural Killer (NK) Cells
Natural Killer (NK) Cells
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Cytotoxic T Cells
Cytotoxic T Cells
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Adaptive Immune Response
Adaptive Immune Response
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Granulomas
Granulomas
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Innate Immune Response
Innate Immune Response
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Extracellular vs Intracellular Infections
Extracellular vs Intracellular Infections
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Immune Recognition of Viruses
Immune Recognition of Viruses
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Innate immune cells
Innate immune cells
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NK cells
NK cells
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MHC Class I
MHC Class I
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Infected cells
Infected cells
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Mechanism of NK cell killing
Mechanism of NK cell killing
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Viral infection's effect on MHC class I
Viral infection's effect on MHC class I
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Inhibitory receptor and NK cell activation
Inhibitory receptor and NK cell activation
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Perforin
Perforin
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Granzyme
Granzyme
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CTL Killing Mechanism
CTL Killing Mechanism
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CTL Target
CTL Target
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IFN-γ
IFN-γ
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Antibody Effector Mechanisms against Viruses
Antibody Effector Mechanisms against Viruses
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CTL's Role
CTL's Role
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CTL vs. Pathogen
CTL vs. Pathogen
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Extracellular Pathogens
Extracellular Pathogens
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Intracellular Pathogens
Intracellular Pathogens
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Immune Response to Extracellular Pathogens
Immune Response to Extracellular Pathogens
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Immune Response to Intracellular Pathogens
Immune Response to Intracellular Pathogens
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How does the immune system distinguish infected cells?
How does the immune system distinguish infected cells?
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Genetic recombination between viruses
Genetic recombination between viruses
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What does IFN-γ do?
What does IFN-γ do?
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What is the role of CD40?
What is the role of CD40?
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Why is nitric oxide synthase important?
Why is nitric oxide synthase important?
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What are granulomas?
What are granulomas?
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How do granulomas affect Mycobacterium tuberculosis?
How do granulomas affect Mycobacterium tuberculosis?
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Hypoxia in granulomas
Hypoxia in granulomas
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Reactivation of Mycobacterium tuberculosis
Reactivation of Mycobacterium tuberculosis
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Why is ongoing Th1 response crucial?
Why is ongoing Th1 response crucial?
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How viruses evade immune response
How viruses evade immune response
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Viral genetic variation
Viral genetic variation
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Down-regulating MHC class I
Down-regulating MHC class I
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Interfering with antigen processing
Interfering with antigen processing
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Antigenic drift
Antigenic drift
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Impact of antigenic drift
Impact of antigenic drift
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Antigenic shift
Antigenic shift
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NK cells and MHC downregulation
NK cells and MHC downregulation
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Why influenza can evade the immune response
Why influenza can evade the immune response
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How antigenic shift differs from drift
How antigenic shift differs from drift
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Viral RNA Receptors
Viral RNA Receptors
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TLR2/6 & TLR4
TLR2/6 & TLR4
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Type I Interferons
Type I Interferons
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Effects of Type I IFNs
Effects of Type I IFNs
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NK Cell Function
NK Cell Function
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MHC Class I & NK Cells
MHC Class I & NK Cells
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Perforin and Granzyme
Perforin and Granzyme
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Adaptive Immunity & Viruses
Adaptive Immunity & Viruses
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Viral Survival Goal
Viral Survival Goal
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Viral Immune Evasion Strategies
Viral Immune Evasion Strategies
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Immune System vs. Virus
Immune System vs. Virus
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Viral Strategies for Evasion
Viral Strategies for Evasion
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Host Cell vs. Virus
Host Cell vs. Virus
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How CTLs kill infected cells
How CTLs kill infected cells
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Antibody's role in viral infections
Antibody's role in viral infections
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CTL's importance
CTL's importance
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Altered Self Cells
Altered Self Cells
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How do NK cells kill infected cells?
How do NK cells kill infected cells?
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Viral downregulation of MHC Class I
Viral downregulation of MHC Class I
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NK cells vs. CTLs
NK cells vs. CTLs
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Extracellular Pathogen Defense
Extracellular Pathogen Defense
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Intracellular Pathogen Defense
Intracellular Pathogen Defense
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NK Cell Activation
NK Cell Activation
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IFN-γ's Role
IFN-γ's Role
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Granulomas: Immune Wall
Granulomas: Immune Wall
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Viral Evasion Mechanisms
Viral Evasion Mechanisms
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Influenza Evasion
Influenza Evasion
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TLR3 and RIG-I
TLR3 and RIG-I
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Viral Evasion Strategies
Viral Evasion Strategies
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Viral Pattern Recognition Receptors (PRRs)
Viral Pattern Recognition Receptors (PRRs)
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TLR3
TLR3
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RIG-I
RIG-I
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Type I Interferons (IFNs)
Type I Interferons (IFNs)
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MHC Class I Down-regulation
MHC Class I Down-regulation
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IFN-α/β
IFN-α/β
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CTLs and NK cells
CTLs and NK cells
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Neutralization
Neutralization
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Type I Interferons (IFN-α/β)
Type I Interferons (IFN-α/β)
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Viral Immune Evasion
Viral Immune Evasion
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Study Notes
Responses to Intracellular Infections
- Presentation given by Dr. Patrick Walsh
- Class Year 1
- Module BMF
- Date: November 2024
Immunology Lectures Outline
- Barrier Immunity: Physical, mechanical, and chemical barriers
- Innate Immunity: Cytokines, inflammation, complement, antigen presentation
- Adaptive Immunity: Response to extracellular and intracellular infections, including cytotoxic and helper T cells, and antibodies
Lecture Learning Outcomes
- Describe a typical immune response to viral infection (using influenza as an example) and the role of interferons, Natural Killer cells, and cytotoxic T cells in the anti-viral response
- Define the adaptive immune response to viral infection and how viruses escape immune detection, leading to disease pathology
- Using mycobacterium as an example, describe the innate and adaptive immune response to intracellular bacteria and granuloma development/maintenance
Extracellular vs. Intracellular
- Extracellular: Bacteria, fungi, protozoa, helminths, interstitial spaces, blood, lymph, epithelial surfaces
- Intracellular: Viruses, bacteria, fungi, protozoa, cytoplasmic, vesicular
How Does the Immune System Recognize Viruses?
- Viral pattern recognition receptors, including:
- Viral capsid proteins: TLR2/6 & TLR4
- Viral RNA (RNA virus): TLR3
- Cytoplasmic RNA receptors: RIG-I
Overview of Immune Response to Intracellular Infections
- Innate immunity: NK cells, Type I IFNs
- Adaptive immunity: Virus-specific CTLs, antibodies
- Timeline (graph shown) indicates the relative timing of responses
Innate Immune Response to Viruses
- Recognition by infected cells
- Production of type I interferons (IFNs)
- Induction of an anti-viral state in infected and nearby cells
- Increase of antigen presentation in all cells
- Activation of innate immune cells (NK cells, macrophages, dendritic cells)
- Induction of adaptive immunity
Effects of Type I IFNs on Immune Cells
- Up-regulation of MHC class I
- Activation of dendritic cells and macrophages
- Activation of cytotoxic T cells (directly kill infected cells)
- Activation of NK cells (directly kill infected cells)
NK Cells in Anti-viral Innate Immune Response
- Innate immune cells
- No specific antigen receptor
- Detect "altered self" cells
- Kill virally-infected and tumor cells
- Do not kill pathogens, though they kill infected cells Mechanism: -Inhibitory receptor bound to MHC class I
- Activatory receptor bound to virally-infected cells
- Cytotoxic action (pore formation, enzyme release)
NK Cells Mechanism of Action
- Kill virally infected cells by the same way as CTLs
- Perforin
- Granzyme
- Cell death (apoptosis)
- Release of cytokine IFN-y (drives Th1 responses and CTL activity)
Antibody effector mechanisms against viruses
- Neutralization (prevents adherence)
- Opsonization ( antibody blocks microbe binding)
- Complement activation (insignificant for anti-viral immunity)
Cytotoxic T Lymphocytes (CTL) Activation
- Virally infected cells display viral antigens on MHC class I molecules
- CTLs recognize the displayed antigens and bind
- CTLs release cytotoxic granules to execute infected cells via apoptosis
Cytotoxic T Lymphocyte (CTL) Killing
- Recognition of virally infected cells via MHC Class I molecules displayed on their surfaces
- Activation of the CTLs
- Vesicle release containing perforin and granzymes to kill the infected cells
- Killing of infected cells due to the activation of apoptosis
Follow the Influenza Virus
- Main cytokine produced by virally-infected cells: IFN-a/b
- Immune cells responsible for killing virally-infected cells: CTLs and NK cells
- Role of antibodies against viruses: Insignificant for killing viruses (neutralization/opsonization, etc.)
How can Viruses Learn to Evade the Host Immune Response?
- Viruses evolve evasion techniques
Mechanisms of How Viruses Evade the Immune Response
- Viral genetic variation: mutations prevent recognition by MHC class 1
- Downregulation of MHC class I
- Interference with antigen processing (Epstein Barr Virus and HSV)
Other Immune Evasion by Influenza
- Antigenic shift: major changes in viral antigens caused by genetic recombination between different viruses
- Completely new virus created. Nobody has previous or historical immunity
- Doesn't happen frequently
Th1 Cells and Mycobacterial Infections
- Th1 cells are important in fighting mycobacterial infections
- Key functions:
- Potent macrophage activation
- Increased MHC class I and II expression for antigen presentation
- Induction of nitric oxide synthase and ROS production
Th1 Cells and the Killing of MTB
- IFN-γ activates the macrophages to kill mycobacteria (MTB) by upregulating various molecules (e.g., CD80/86, CD40), increasing MHC expression, and activating nitric oxide synthase
- Enhanced microbial activity and activation of Th1 and cytotoxic T cells
Granuloma Formation
- Th1 induced macrophage maturation and granuloma formation
- Infection sealed off by immune cells
- Hypoxic center and necrosis
- MTB persistence for prolonged periods
- Reactivation by treatment (e.g., steroids, or malnutrition)
Immune Responses - Summary of Today's Lectures
- Extracellular pathogens: Neutrophils, macrophages, Th17, antibodies, eosinophils, and mast cells (for helminths)
- Intracellular pathogens: IFN response, NK cells, CTLs, antibody neutralization (viruses), and Th1 and IFN-γ for intracellular bacteria
SGT - A Healthy Immune Response
- XX November Immunology tutorial, divided into small groups
- Students must pre-read the reference
- Feedback on the lecture content or delivery can be given via www.menti.com
Studying That Suits You
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Description
This quiz focuses on the immune responses to intracellular infections as outlined in Dr. Patrick Walsh's lecture. It covers key concepts like barrier immunity, innate and adaptive immunity, and the role of various immune cells in response to viral infections. Prepare to test your knowledge on critical concepts that underlie the immune system's function against pathogens.
