Q5. The primary immune function of mucus is to:
A. Directly kill microbes by phagocytosis

B. Serve as a physical and chemical barrier that traps microbes and limits contact with epithelium

C. Allow microbes to colonize epithelium safely

D. Replace epithelial cells during damage

B. Serve as a physical and chemical barrier that traps microbes and limits contact with epithelium

Q6. Glycan decoys on mucins:
A. Enhance pathogen invasion

B. Act as binding sites that prevent microbial adhesion to host cells

C. Induce apoptosis in epithelial cells

D. Inhibit mucus secretion

B. Act as binding sites that prevent microbial adhesion to host cells

Q7. Commensal microorganisms:
A. Always cause disease
B. Live on mucosal surfaces without causing harm and often benefit the host
C. Are sterile environments in the body
D. Only exist in germ-free animals

B. Live on mucosal surfaces without causing harm and often benefit the host

Q8. Gnotobiotic mice differ from conventional mice because they:
A. Have no immune system
B. Are exposed to all environmental microbes
C. Lack microbiota-driven immune stimulation
D. Contain more Peyer’s patches

C. Lack microbiota-driven immune stimulation

Q9. Which of the following is an anatomical change in germ-free mice?
A. Thickened mucosal epithelium
B. Larger Peyer’s patches
C. Reduced goblet cells and thinner mucus
D. Increased villus length

C. Reduced goblet cells and thinner mucus

Q10. The microbiome contributes to host health by:
A. Reducing vitamin synthesis
B. Suppressing mucus production
C. Competing with pathogens and supporting epithelial integrity
D. Destroying regulatory T cells

C. Competing with pathogens and supporting epithelial integrity

Q11. Which of the following is not a symbiotic function of the microbiome?
A. Detoxifying xenobiotics
B. Inducing immune tolerance
C. Inhibiting epithelial repair
D. Producing short-chain fatty acids

C. Inhibiting epithelial repair

Q12. Which of the following is an example of GALT?
A. Peyer’s patches
B. Spleen
C. Thymus
D. Bone marrow

A. Peyer’s patches

Q13. The effector compartment of the mucosa primarily contains:
A. Sites for antigen sampling
B. Activated lymphocytes and IgA-producing plasma cells
C. Naïve lymphocytes
D. Bone marrow stem cells

B. Activated lymphocytes and IgA-producing plasma cells

Q14. Which of the following is true of mucosal immunity compared to systemic immunity?
A. Relies primarily on IgG antibodies
B. Promotes tolerance and is dominated by secretory IgA
C. Allows strong inflammatory responses
D. Has unrestricted complement activation

B. Promotes tolerance and is dominated by secretory IgA

Q15. Mucosal immune responses are typically:
A. Highly inflammatory
B. Complement-dependent
C. Anti-inflammatory and tolerance-oriented
D. Systemic in distribution

C. Anti-inflammatory and tolerance-oriented

Q16. Crohn’s disease involves:
A. Autoantibody destruction of red blood cells
B. Dysregulated immune response to gut microbiota
C. Viral infection of Peyer’s patches
D. Deficiency in mucus production only

B. Dysregulated immune response to gut microbiota

Q17. Intestinal epithelial cells (IECs) contribute to immunity by:
A. Blocking cytokine production
B. Serving as a barrier, producing antimicrobial peptides, and communicating with immune cells
C. Producing IgA directly
D. Lacking pattern recognition receptors

B. Serving as a barrier, producing antimicrobial peptides, and communicating with immune cells

Q18. Which of the following is not a PRR found in intestinal epithelial cells?
A. TLR4
B. NOD2
C. RIG-I
D. IgA receptor

D. IgA receptor

Q19. Activation of PRRs on IECs results in:
A. Reduced antimicrobial activity
B. Induction of cytokines, chemokines, and antimicrobial peptides
C. Suppression of epithelial repair
D. Inhibition of tight junction formation

B. Induction of cytokines, chemokines, and antimicrobial peptides

Q20. Overactivation of NFκB in the gut can lead to:
A. Enhanced tolerance
B. Chronic inflammation (as in IBD)
C. Increased IgA secretion
D. Immunodeficiency

B. Chronic inflammation (as in IBD)

Q21. Which epithelial cell type produces mucins?
A. Paneth cells
B. Goblet cells
C. Enterocytes
D. Tuft cells

B. Goblet cells

Q22. Follicle-associated epithelium (FAE) differs from normal epithelium because it:
A. Contains more goblet cells
B. Has a thicker mucus layer
C. Contains M cells that facilitate antigen uptake
D. Lacks immune cells

C. Contains M cells that facilitate antigen uptake

Q23. M cells function by:
A. Producing defensins
B. Transcytosing antigens from the lumen to immune cells
C. Secreting IgA
D. Strengthening tight junctions

B. Transcytosing antigens from the lumen to immune cells

Q24. Oral tolerance prevents:
A. Tolerance to commensals
B. Immune responses to dietary antigens
C. Antibody production
D. Mucus secretion

B. Immune responses to dietary antigens

Q25. CD103⁺ DCs promote gut homeostasis by:
A. Inducing Th1 cells
B. Producing retinoic acid and TGFβ to generate Tregs and IgA
C. Activating NK cells
D. Enhancing inflammation

B. Producing retinoic acid and TGFβ to generate Tregs and IgA

Q26. During infection, CD103⁺ DCs primarily:
A. Induce Tregs
B. Promote effector T cell differentiation and IgG responses
C. Reduce co-stimulation
D. Decrease cytokine production

B. Promote effector T cell differentiation and IgG responses

Q27. Which molecule pair directs lymphocytes back to mucosal tissues?
A. CD28 – CD80
B. α4β7 – MAdCAM-1
C. CD40 – CD40L
D. CCR5 – CCL5

B. α4β7 – MAdCAM-1

Q28. Intraepithelial lymphocytes (IELs) are mainly:
A. Naïve CD4⁺ T cells
B. CD8⁺ or γδ T cells between epithelial cells that provide rapid cytotoxic defense
C. Circulating B cells
D. NK cells only

B. CD8⁺ or γδ T cells between epithelial cells that provide rapid cytotoxic defense

Q29. The first wave of mucosal IgA response is:
A. T-dependent, high-affinity
B. T-independent, lower-affinity and rapid
C. IgG-mediated
D. Complement-dependent

B. T-independent, lower-affinity and rapid

Q30. The poly-Ig receptor (pIgR):
A. Degrades IgA before secretion
B. Transports dimeric IgA across epithelial cells
C. Replaces the Fc receptor
D. Produces cytokines

B. Transports dimeric IgA across epithelial cells

Q31. The secretory component of IgA:
A. Is a microbial enzyme
B. Protects IgA from degradation and anchors it to mucus
C. Signals epithelial apoptosis
D. Recruits macrophages

B. Protects IgA from degradation and anchors it to mucus

Q32. Secretory IgA maintains mucosal tolerance primarily by:
A. Activating complement
B. Inducing inflammation
C. Neutralizing antigens non-inflammatorily and preventing epithelial penetration
D. Enhancing neutrophil recruitment

C. Neutralizing antigens non-inflammatorily and preventing epithelial penetration

Q33. Which statement about IgA1 and IgA2 is correct?
A. IgA1 is resistant to bacterial proteases
B. IgA2 predominates in serum
C. IgA2 is more abundant in the colon and resistant to proteases
D. IgA1 is shorter and found mainly in the colon

C. IgA2 is more abundant in the colon and resistant to proteases

Q34. A major consequence of selective IgA deficiency is:
A. Reduced systemic inflammation
B. Increased risk of mucosal infections
C. Decreased allergy risk
D. Increased complement activation

B. Increased risk of mucosal infections

Q35. Some IgA-deficient patients experience transfusion reactions due to:
A. Formation of anti-IgA antibodies
B. Lack of complement proteins
C. Low IgG
D. Excessive mucus production

A. Formation of anti-IgA antibodies

Q36. A hallmark antibody of mucosal immunity is:
A. IgG
B. IgA
C. IgE
D. IgM

B. IgA

Q37. The mucosal immune system is distinct because it:
A. Encourages strong complement activation
B. Prioritizes tolerance over inflammation
C. Has minimal epithelial participation
D. Lacks antigen sampling

B. Prioritizes tolerance over inflammation

Q38. Which statement best summarizes the mucosal immune strategy?
A. Destroy microbes with inflammation
B. Maintain barrier function while promoting immune tolerance
C. Use complement and neutrophil activation
D. Avoid microbial recognition

B. Maintain barrier function while promoting immune tolerance

39. Why must mucosal tissues balance immune defense and tolerance?

A. They are rarely exposed to antigens
B. They cannot tolerate any activation
C. They constantly encounter harmless antigens like food and commensals
D. They lack immune cells

C. They constantly encounter harmless antigens like food and commensals

40. How does mucosal tissue structure support immune function?

A. Narrow surface area reduces antigen exposure
B. Mucus and epithelial barriers block pathogens
C. Loose junctions increase permeability
D. Lack of mucus improves surveillance

B. Mucus and epithelial barriers block pathogens

41. A defect in mucin glycosylation leads to infections because:

A. Mucins become toxic
B. Mucus becomes too thick
C. Mucins cannot form a proper gel layer to trap microbes
D. IgG production decreases

C. Mucins cannot form a proper gel layer to trap microbes

42. Why is mucus both a physical and biochemical barrier?

A. Only physical
B. Only biochemical
C. It traps microbes and contains defensins, IgA, and lysozyme
D. It replaces epithelial cells

C. It traps microbes and contains defensins, IgA, and lysozyme

43. Germ-free mice have fewer Peyer’s patches, showing that:

A. Diet controls immunity
B. The microbiome directs immune development
C. Genetics fully determines IgA levels
D. Infections are necessary for immunity

B. The microbiome directs immune development

44. What results from drastically reducing gut microbiota?

A. Stronger IgA responses
B. More Peyer’s patches
C. Weaker mucosal immunity and higher infection risk
D. Reduced nutrient absorption stress-free

C. Weaker mucosal immunity and higher infection risk

45. Which best compares IgA and IgG at mucosal surfaces?

A. IgG is less inflammatory
B. IgA is non-inflammatory and protects tissues
C. IgA activates complement strongly
D. IgG promotes tolerance

B. IgA is non-inflammatory and protects tissues

46. Why are strong inflammatory responses harmful in mucosal tissues?

A. Mucosa lacks immune cells
B. Inflammation disrupts absorption and damages epithelium
C. Inflammation improves tolerance
D. Mucosa cannot regenerate

B. Inflammation disrupts absorption and damages epithelium

47. In Crohn’s disease, inappropriate activation occurs because:

A. Commensals never stimulate PRRs
B. Defective PRRs or mucus allow commensals to trigger chronic inflammation
C. IgA is overproduced
D. Cytokines are absent

B. Defective PRRs or mucus allow commensals to trigger chronic inflammation

48. How do intestinal epithelial cells act as dual barriers?

A. They only produce mucus
B. They have no immune functions
C. Tight junctions block microbes; PRRs trigger cytokines/defensins
D. They rely completely on IgG

C. Tight junctions block microbes; PRRs trigger cytokines/defensins

49. PRR activation in epithelial cells leads to:

A. Complement activation only
B. NFκB signaling → defensins and cytokines
C. IgE production
D. No significant response

B. NFκB signaling → defensins and cytokines

50. Chronic NFκB activation in gut epithelium causes:

A. Tolerance
B. Reduced cytokines
C. Persistent inflammation and tissue damage
D. Increased mucus only

C. Persistent inflammation and tissue damage

51. Which correctly matches cell type with function?

A. Paneth cells → mucus secretion
B. Goblet cells → antigen transcytosis
C. M cells → defensin release
D. Paneth = antimicrobials; Goblet = mucus; M cells = antigen delivery

• D. Paneth = antimicrobials; Goblet = mucus; M cells = antigen delivery

52. Why does the FAE have fewer goblet cells?

A. To increase digestion
B. To reduce mucus and allow antigen sampling
C. To increase mucus thickness
D. To promote IgG secretion

B. To reduce mucus and allow antigen sampling

53. How do M cells and DCs coordinate in Peyer’s patches?

A. DCs bring antigens to M cells
B. M cells digest microbes
C. M cells deliver antigens to DCs, which present them to T/B cells
D. Both destroy pathogens directly

C. M cells deliver antigens to DCs, which present them to T/B cells

54. Feeding antigen before injection causes:

A. Allergy
B. Oral tolerance and weaker systemic responses
C. Stronger antibody responses
D. Autoimmunity

B. Oral tolerance and weaker systemic responses

55. CD103⁺ DCs maintain tolerance by:

A. Producing IL-6 and IL-12
B. Activating NK cells
C. Producing IL-10 and TGF-β to induce Tregs and IgA switching
D. Triggering inflammation

C. Producing IL-10 and TGF-β to induce Tregs and IgA switching

56. During infection, CD103⁺ DCs shift to:

A. Producing IL-10 only
B. Promoting Th1/Th17 via IL-6 and IL-12
C. Shutting down all cytokines
D. Enhancing tolerance

B. Promoting Th1/Th17 via IL-6 and IL-12

57. α4β7 integrin and MAdCAM-1 enable:

A. Neutrophil activation
B. Lymphocyte homing back to mucosal tissues
C. Complement activation
D. NK cell killing

B. Lymphocyte homing back to mucosal tissues

58. Which describes first vs. second wave IgA responses?

A. Both T-dependent
B. First = IgA2 only
C. First: T-independent, IgA1; Second: T-dependent, IgA2
D. Second is T-independent

• C. First: T-independent, IgA1; Second: T-dependent, IgA2

59. Role of the poly-Ig receptor (pIgR) in IgA transport:

A. Degrades IgA
B. Transports dimeric IgA across epithelium and adds secretory component
C. Blocks antibody release
D. Activates complement

B. Transports dimeric IgA across epithelium and adds secretory component

60. Secretory IgA promotes tolerance because it:

A. Strongly activates inflammation
B. Neutralizes microbes without triggering complement
C. Acts like IgE
D. Destroys epithelial cells

B. Neutralizes microbes without triggering complement

61. Selective IgA deficiency leads to:

A. Stronger mucosal immunity
B. Recurrent infections and allergies; IgM compensates only partially
C. High IgA in semen
D. Only systemic infections

B. Recurrent infections and allergies; IgM compensates only partially

62. An effective probiotic should:

A. Reduce IgA
B. Increase harmful commensals
C. Strengthen epithelial barriers and promote IgA/defensins
D. Block TGF-β

C. Strengthen epithelial barriers and promote IgA/defensins

63. Chronic stress increases disease risk because:

A. It strengthens tight junctions
B. It makes the gut sterile
C. Barrier weakening allows microbes to cross, causing inflammation
D. It increases IgA production

C. Barrier weakening allows microbes to cross, causing inflammation