Lecture 4 Microbial Immunity Flashcards
Q1: Define microbial pathogenicity and explain how it can be influenced by host immune responses.
A: Microbial pathogenicity refers to the ability of a microbe to cause disease, which is often defined by its capacity to evade or resist the host immune response or by inducing a pathological immune reaction. For example, Hepatitis B virus causes liver injury not through cytopathic effects, but via immune-mediated damage due to cytotoxic T cell responses against infected hepatocytes.
Q2: Describe how the complement system aids in defending against extracellular bacteria.
A: The complement system contributes via:
Opsonization: C3b coats microbes to enhance phagocytosis.
Membrane Attack Complex (MAC): Forms pores causing lysis.
Leukocyte Recruitment: C3a and C5a act as chemoattractants and inflammatory mediators.
Q3: What roles do innate lymphoid cells (ILCs) play in microbial immunity?
A: ILCs, particularly group 3 ILCs, lack antigen-specific receptors but secrete cytokines like IL-17 and IL-22, enhancing neutrophil recruitment and mucosal defense. They act rapidly and reside at barrier surfaces.
Q4: How does E. coli use antigenic variation to evade the immune system?
A: E. coli varies its pili (pilin proteins), of which over 100 antigenic variants exist. This antigenic variation prevents antibody recognition, allowing the bacteria to persist.
Q5: Describe two other immune evasion strategies used by extracellular bacteria.
A:
Membrane blebbing: Releases vesicles that decoy antibodies.
LPS sialylation: Masks PAMPs, mimicking host cells and reducing immune recognition.
Q6: Compare the roles of CD4+ Th1 and CD8+ cytotoxic T cells in controlling intracellular bacteria.
A:
Th1 cells secrete IFN-γ to activate macrophages, enhancing phagolysosome fusion and RONS production.
CD8+ T cells kill infected cells directly if bacteria escape into the cytosol and present antigens on MHC class I.
Q7: How do intracellular bacteria evade the host immune response? Give examples.
A:
Preventing phagolysosome fusion (e.g., Mycobacterium tuberculosis).
Escaping into the cytosol, avoiding lysosomal enzymes (e.g., Listeria monocytogenes).
Producing catalase, detoxifying hydrogen peroxide and reducing ROS effectiveness.
Q8: What is the role of type I interferons in antiviral immunity?
A: Produced by infected cells, type I IFNs (e.g., IFN-α/β) induce antiviral states in neighboring cells by activating the STING pathway, increasing expression of RNA-degrading enzymes and inhibiting viral protein synthesis.
Q9: Explain how NK cells distinguish between healthy and virally infected cells.
A: NK cells recognize cells lacking MHC class I (which viruses may downregulate). The absence of MHC I removes inhibitory signals, prompting NK-mediated cytotoxicity.
Q10: Differentiate between antigenic drift and antigenic shift. Provide viral examples.
A:
Antigenic drift: Gradual mutations in viral genes (e.g., influenza spike proteins), evading existing antibodies.
Antigenic shift: Sudden genetic reassortment forming new viral strains (e.g., H1N1 from human, avian, and swine influenza).
Q11: How does Epstein-Barr virus evade immune detection?
A: EBV secretes an IL-10 homolog that suppresses macrophage and dendritic cell function, dampening the immune response.
