Block C - Mucosal Immunity Flashcards
(170 cards)
1
Q
What is the approximate surface area of the gastrointestinal (GI) tract?
A) 1m²
B) 10m²
C) 400m²
D) 1000m²
A
C) 400m² ✅
2
Q
Which of the following is NOT a challenge faced by the gut mucosal immune system?
A) Distinguishing between harmful and harmless antigens
B) Absorbing food while preventing pathogen entry
C) Producing red blood cells
D) Preventing infections from microbes
A
C) Producing red blood cells ✅
3
Q
Which of the following statements about the gut microbiota is true?
A) The small intestine has a more diverse microbiota than the large intestine
B) The large intestine contains a higher density of bacteria than the small intestine
C) The gut microbiota consists of only 10 species
D) The gut microbiota is not involved in immune regulation
A
B) The large intestine contains a higher density of bacteria than the small intestine ✅
4
Q
Which of the following is NOT a non-specific defense mechanism of the gut?
A) Peristalsis
B) Lysozyme secretion
C) IgA production
D) Defensin production
A
C) IgA production ✅ (IgA is part of the adaptive immune response)
5
Q
What is the primary role of Paneth cells in the gut mucosa?
A) Absorbing nutrients
B) Producing mucus
C) Secreting antimicrobial peptides
D) Transporting antigens
A
C) Secreting antimicrobial peptides ✅
6
Q
What percentage of the body’s lymphocytes are found in the gut?
A) 10%
B) 25%
C) 50%
D) 70%
A
D) 70%
7
Q
Which of the following is NOT part of the Gut-Associated Lymphoid Tissue (GALT)?
A) Peyer’s patches
B) Mesenteric lymph nodes
C) Bone marrow
D) Cryptopatches
A
C) Bone marrow ✅
8
Q
Which immunoglobulin is the most abundantly secreted antibody in the gut?
A) IgM
B) IgG
C) IgA
D) IgE
A
C) IgA ✅
9
Q
What is the primary function of IgA in the gut?
A) Activating complement
B) Promoting phagocytosis
C) Preventing attachment of bacteria and toxins
D) Inducing inflammation
A
C) Preventing attachment of bacteria and toxins ✅
10
Q
Which type of T cell is found in high numbers in the gut and plays a role in early immune responses?
A) CD4+ T cells
B) CD8+ T cells
C) γδ T cells
D) Regulatory T cells
A
C) γδ T cells ✅
11
Q
How do γδ T cells differ from αβ T cells?
A) They require antigen processing via MHC
B) They are primarily found in the thymus
C) They can develop outside the thymus
D) They do not participate in mucosal immunity
A
C) They can develop outside the thymus ✅
12
Q
What is the main function of M (microfold) cells in Peyer’s patches?
A) Secreting IgA
B) Presenting antigens to T cells
C) Absorbing nutrients
D) Transporting antigens from the gut lumen to immune cells
A
D) Transporting antigens from the gut lumen to immune cells ✅
13
Q
Which molecule plays a key role in lymphocyte homing to the gut?
A) MAdCAM-1
B) CD4
C) IL-10
D) TLR4
A
A) MAdCAM-1 ✅
14
Q
Why is the interaction between MAdCAM-1 and α4β7 integrin important?
A) It allows neutrophils to enter the gut lumen
B) It regulates antigen presentation in Peyer’s patches
C) It directs lymphocytes primed in the gut back to the mucosal tissues
D) It enhances systemic immune responses
A
C) It directs lymphocytes primed in the gut back to the mucosal tissues ✅
15
Q
Which of the following best explains why the gut immune system must tolerate commensal bacteria while still being able to respond to pathogens?
A) The gut lacks antigen-presenting cells, preventing immune activation against commensals.
B) The gut microbiota actively suppresses immune responses through secretion of antimicrobial peptides.
C) The gut immune system uses regulatory T cells (Tregs) and secretory IgA to limit inflammation while maintaining surveillance against pathogens.
D) Commensal bacteria do not express antigens that can be recognized by pattern recognition receptors (PRRs).
A
C) The gut immune system uses regulatory T cells (Tregs) and secretory IgA to limit inflammation while maintaining surveillance against pathogens. ✅
16
Q
Which factor is most critical in maintaining intestinal homeostasis and preventing excessive immune activation in response to gut microbiota?
A) High expression of MHC class II by epithelial cells
B) Constant activation of γδ T cells in the lamina propria
C) Secretion of immunosuppressive cytokines such as IL-10 and TGF-β by regulatory T cells
D) Increased antigen uptake by microfold (M) cells to stimulate immune responses
A
C) Secretion of immunosuppressive cytokines such as IL-10 and TGF-β by regulatory T cells ✅
17
Q
Which of the following describes a mechanism by which antimicrobial peptides (AMPs) function in the gut?
A) They neutralize bacterial toxins by directly binding to lipopolysaccharides (LPS).
B) They disrupt microbial membranes by forming pores or altering membrane charge.
C) They promote bacterial aggregation, preventing colonization.
D) They stimulate epithelial cells to produce pro-inflammatory cytokines.
A
B) They disrupt microbial membranes by forming pores or altering membrane charge. ✅
18
Q
Which of the following statements about Paneth cells is false?
A) They produce α-defensins, which have broad antimicrobial activity.
B) They are found at the base of the crypts of Lieberkühn.
C) Their dysfunction has been linked to inflammatory bowel diseases (IBD).
D) They directly present antigens to naïve T cells in Peyer’s patches.
A
D) They directly present antigens to naïve T cells in Peyer’s patches. ✅ (Paneth cells do not function as antigen-presenting cells.)
19
Q
Which feature makes IgA uniquely suited for mucosal immunity?
A) IgA forms immune complexes that activate the complement system.
B) Secretory IgA is resistant to proteolytic cleavage by microbial enzymes.
C) IgA can cross-link pathogens and promote phagocytosis by macrophages.
D) IgA directly induces inflammatory responses to clear infections.
A
B) Secretory IgA is resistant to proteolytic cleavage by microbial enzymes. ✅
20
Q
Why do certain pathogens like Neisseria gonorrhoeae and Streptococcus pneumoniae produce IgA proteases?
A) To degrade IgA and facilitate colonization of mucosal surfaces
B) To promote the formation of immune complexes
C) To enhance phagocytosis by host immune cells
D) To convert IgA into a more inflammatory antibody class
A
A) To degrade IgA and facilitate colonization of mucosal surfaces ✅
21
Q
What is the consequence of IgA deficiency in the gut?
A) Increased susceptibility to bacterial infections and overgrowth of commensal bacteria
B) Hyperactivation of macrophages and T cells in Peyer’s patches
C) Increased production of IgG to compensate
D) Reduced antigen sampling by dendritic cells
A
A) Increased susceptibility to bacterial infections and overgrowth of commensal bacteria ✅
22
Q
What makes γδ T cells functionally distinct in the gut immune system?
A) They require antigen processing and MHC presentation before activation.
B) They act as a bridge between innate and adaptive immunity by recognizing lipid antigens and responding rapidly to stress signals.
C) They primarily function by promoting inflammation through IL-6 secretion.
D) They are exclusively found in Peyer’s patches.
A
B) They act as a bridge between innate and adaptive immunity by recognizing lipid antigens and responding rapidly to stress signals. ✅
23
Q
Which type of T cell is most critical in maintaining oral tolerance to food antigens?
A) CD8+ cytotoxic T cells
B) γδ T cells
C) Regulatory T cells (Tregs)
D) Follicular helper T cells
A
C) Regulatory T cells (Tregs) ✅
24
Q
Which of the following best describes how M (microfold) cells contribute to antigen sampling in the gut?
A) They process and present antigen directly to naïve T cells.
B) They transport antigens from the gut lumen to antigen-presenting cells in Peyer’s patches.
C) They secrete antimicrobial peptides to prevent bacterial colonization.
D) They stimulate goblet cells to produce mucus.
A
B) They transport antigens from the gut lumen to antigen-presenting cells in Peyer’s patches. ✅
25
What is the key role of MAdCAM-1 in gut immune responses?
A) It regulates antigen presentation in Peyer’s patches.
B) It serves as a homing signal for lymphocytes to return to the intestinal mucosa.
C) It enhances epithelial barrier integrity by interacting with tight junction proteins.
D) It promotes neutrophil infiltration into the gut during infection.
B) It serves as a homing signal for lymphocytes to return to the intestinal mucosa. ✅
26
Which statement best explains how dendritic cells contribute to gut-specific immune responses?
A) They remain in Peyer’s patches and only process antigens presented by M cells.
B) They extend dendrites across the epithelial barrier to capture antigens directly from the gut lumen.
C) They function primarily as phagocytic cells, without a role in T cell activation.
D) They inhibit antigen presentation to prevent inflammation.
B) They extend dendrites across the epithelial barrier to capture antigens directly from the gut lumen. ✅
27
Which of the following conditions is most likely to result from a breakdown in oral tolerance mechanisms?
A) Celiac disease
B) Tuberculosis
C) Influenza
D) Malaria
A) Celiac disease ✅
28
A mutation affecting α4β7 integrin would most likely impair which immune function?
A) Trafficking of immune cells to the gut mucosa
B) IgA secretion
C) Macrophage activation in the lamina propria
D) Antigen uptake by M cells
A) Trafficking of immune cells to the gut mucosa ✅
29
Which of the following is an experimental strategy for treating inflammatory bowel disease (IBD) based on mucosal immunity?
A) Blocking MAdCAM-1 to reduce gut-specific lymphocyte recruitment
B) Enhancing γδ T cell activation to increase inflammation
C) Inhibiting IgA production to prevent immune suppression
D) Increasing gut permeability to promote antigen exposure
A) Blocking MAdCAM-1 to reduce gut-specific lymphocyte recruitment ✅
30
How does the gut immune system distinguish between commensal bacteria and pathogenic microbes while preventing unnecessary inflammation? (4 marks)
-gut immune system differentiates between commensals and pathogens through pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs), which recognize microbial-associated molecular patterns (MAMPs).
-Commensal microorganisms promote regulatory responses, inducing Tregs and IL-10/TGF-β secretion, which suppress excessive inflammation.
-Bacteroides produce SCFAs and faecalibacterium produces butyrate, which fuels colonocytes and has anti-inflammatory properties
-Pathogens trigger strong immune activation via virulence factors, leading to NF-κB activation and inflammatory cytokine release.
31
Describe the role of regulatory T cells (Tregs) in maintaining oral tolerance and preventing food allergies (3 marks)
-Tregs suppress immune responses to dietary antigens and commensals by secreting IL-10 and TGF-β, which reduce inflammatory cytokine production such as activation of effector T cells (Th1, Th2, Th17) that might otherwise attack harmless food antigens.
-Foxp3+ Tregs are critical for suppressing dendritic cell activation and maintaining gut homeostasis.
-A failure in Treg function leads to increased IgE responses, contributing to allergic disorders, inflammatory bowel diseases (IBD), or celiac disease due to loss of immune regulation.
32
Why is the composition of the gut microbiota different between the small intestine and the large intestine? How does this affect immune responses? (3 marks)
-The small intestine has a lower microbial density (~10⁶ bacteria/mL) due to rapid flow, bile acids, and antimicrobial peptides. The large intestine harbors 10⁹-10¹² bacteria/mL, supporting anaerobic fermentation.
-Small Intestine: Favors antigen sampling by M cells and GALT activation.
-Large Intestine: More Tregs and IgA to maintain tolerance and prevent overgrowth of microbes.
33
What are the potential consequences of dysbiosis (imbalanced gut microbiota) on mucosal immunity and systemic health? (4 marks)
-Dysbiosis disrupts the balance of commensal and pathogenic microbes, leading to immune dysregulation.
-its effect on the gut include, Loss of barrier integrity → Leaky gut syndrome, allowing bacterial translocation.
-Overgrowth of pro-inflammatory bacteria (e.g., Proteobacteria) → Triggers IBD, Crohn’s disease, ulcerative colitis.
-the systemic results is that dysbiosis is linked to autoimmune diseases (e.g., rheumatoid arthritis, multiple sclerosis) and neurological disorders via the gut-brain axis.
34
Where are Paneth cells located?
Small intestine crypts (Lieberkühn crypts)
35
Where are Goblet cells located?
Throughout the intestinal epithelium
36
What is the function of paneth cells?
Secrete antimicrobial peptides (AMPs) (e.g., defensins, lysozyme)
37
What is the function of goblet cells?
Secrete mucins to form a protective mucus layer
38
what is the immune role of paneth cells?
directly kill bacteria
39
what is the immune role of goblet cells?
produces mucus which traps pathogens, allergens, and toxins and prevents direct contact between microbes and the epithelial surface
40
Explain how defensins function as antimicrobial peptides and describe the key differences between α-defensins and β-defensins. ( 3 marks)
-Defensins are cationic peptides that disrupt bacterial membranes by inserting into lipid bilayers, forming pores.
-α-Defensins: Produced by Paneth cells and neutrophils, most effective against gram-negative bacteria.
-β-Defensins: Produced by epithelial cells in response to inflammation, active against fungi and viruses.
41
How does peristalsis contribute to gut immunity, and why might disruption of gut motility lead to increased susceptibility to infection? (4 marks)
-peristaltic waves help flush out pathogens before they can colonize or damage the epithelium, minimizing the time microbes have to adhere to the mucosa, penetrate the barrier, or trigger inflammation.
-continuous movement prevents stagnation, particularly in the small intestine, reducing the risk of small intestinal bacterial overgrowth (SIBO).
-Disruption (e.g., in IBS, opioid use) allows pathogens to colonize, leading to SIBO (small intestinal bacterial overgrowth) and infections.
-Abnormal peristalsis or stasis (e.g., in IBS, opioid use) can lead to accumulation of microbial products like LPS, stimulating pattern recognition receptors (PRRs) and potentially triggering inflammation and immune activation.
42
Why is IgA the dominant immunoglobulin in the gut, and how does its structure contribute to its function in mucosal immunity? (4 marks)
-IgA is the primary antibody in mucosal secretions due to high production rate: ~3g/day, 70% of total body Ig production.
-Structure: Exists as dimeric linked by a J-chain, has a attached secretory component that protects it from enzymatic digestive in the gut lumen.
-while IgG and IgM, can be degraded by proteases, sIgA remains stable in the harsh proteolytic environment of the intestine
-Function is that it prevents bacterial adhesion and acts through neutralization, blocking toxins and viruses.
43
Some pathogenic bacteria (e.g., Neisseria gonorrhoeae) produce IgA proteases. What is the significance of this adaptation, and how does it aid bacterial survival in mucosal tissues? (2 marks)
-IgA proteases cleave the hinge region of IgA, preventing immune exclusion and allowing bacteria to adhere to mucosal surfaces.
-some examples include: Neisseria, Haemophilus, and Streptococcus species use this to evade immune defenses and establish infections.
44
How do gut-associated lymphoid tissues (GALT) support the generation of adaptive immune responses while maintaining immune tolerance? (3 marks)
-M cells in Peyer’s patches transport antigens to dendritic cells (DCs).
-DCs induce Tregs for tolerance or activate Th17 cells for infection defense.
-IgA secretion prevents bacterial colonization without causing inflammation
45
Explain the unique role of γδ T cells in mucosal immunity and describe how they differ from conventional αβ T cells. (5 marks)
-γδ T Cells do not require MHC antigen presentation
-since they typically respond to self and microbial stress-induced molecules like heat shock proteins released by stressed of infected cells, phosphoantigens produced by bacteria, and MHC related proteins like MIC-A which is found in tumor cells
-Bridge innate and adaptive immunity.
-αβ T Cells Require MHC-restricted antigen presentation.
-Have a more diverse receptor repertoire.
46
Who first described the concept of oral tolerance in 1911?
A) Louis Pasteur
B) H.G. Wells
C) Edward Jenner
D) Robert Koch
B) H.G. Wells ✅
47
What is oral tolerance (OT)?
A) The gut’s ability to absorb nutrients efficiently
B) A state of immune unresponsiveness to non-pathogenic antigens
C) The suppression of IgA production in the gut
D) The immune system’s overreaction to food proteins
B) A state of immune unresponsiveness to non-pathogenic antigens ✅
48
Which of the following statements about oral tolerance is TRUE?
A) It is a passive, non-specific immune suppression
B) It prevents immune responses to food antigens and commensal bacteria
C) It only affects B cell responses, not T cell responses
D) It requires the complete absence of immune system activation
B) It prevents immune responses to food antigens and commensal bacteria ✅
49
Which of the following is NOT a major mechanism of oral tolerance?
A) Clonal deletion
B) Clonal expansion
C) Clonal anergy
D) Regulatory T cell induction
B) Clonal expansion ✅
50
Which immune cell type is most responsible for maintaining oral tolerance?
A) Cytotoxic T cells
B) Regulatory T cells (Tregs)
C) Natural killer (NK) cells
D) Dendritic cells
B) Regulatory T cells (Tregs) ✅
51
Which of the following factors can influence the induction of oral tolerance?
A) Nature of the antigen
B) Dose and frequency of antigen exposure
C) Age and genetic background
D) All of the above
D) All of the above ✅
52
Which characteristic of an antigen is most likely to induce oral tolerance rather than active immunity?
A) Particulate and invasive
B) Soluble and non-living
C) Locally invasive and rapidly absorbed
D) Present in large numbers in Peyer’s patches
B) Soluble and non-living ✅
53
What is the primary difference between clonal deletion and clonal anergy in oral tolerance?
A) Clonal deletion removes B cells, while clonal anergy removes T cells
B) Clonal deletion occurs in response to high doses of antigen, while clonal anergy occurs with repeated low doses
C) Clonal deletion is reversible, while clonal anergy is not
D) Clonal anergy leads to cell death, while clonal deletion only suppresses cell function
B) Clonal deletion occurs in response to high doses of antigen, while clonal anergy occurs with repeated low doses ✅
54
Which of the following best describes clonal deletion in oral tolerance?
A) It is induced by exposure to low doses of antigen
B) It occurs through the apoptosis of self-reactive T cells
C) It enhances immune responses against food proteins
D) It can be reversed by IL-2 administration
B) It occurs through the apoptosis of self-reactive T cells ✅
55
Which factor is critical in preventing clonal anergy from occurring?
A) The presence of co-stimulatory signals
B) The absence of antigen exposure
C) The presence of memory B cells
D) High levels of IgE in circulation
A) The presence of co-stimulatory signals ✅
56
Which cytokine is MOST important for the function of regulatory T cells (Tregs) in oral tolerance?
A) IL-4
B) IFN-γ
C) IL-10
D) TNF-α
C) IL-10 ✅
57
Which of the following explains how Tregs contribute to oral tolerance?
A) They secrete IL-10 and TGF-β to suppress immune activation
B) They activate cytotoxic T cells to destroy food antigens
C) They increase IgE production to enhance tolerance
D) They prevent antigen uptake by M cells
A) They secrete IL-10 and TGF-β to suppress immune activation ✅
58
Which of the following cytokines is known to BREAK oral tolerance?
A) IL-10
B) TGF-β
C) IL-12
D) IL-35
C) IL-12 ✅
59
Which of the following is an example of a disease linked to a FAILURE of oral tolerance?
A) Celiac disease
B) Tuberculosis
C) Influenza
D) Multiple sclerosis
A) Celiac disease ✅
60
How does oral tolerance contribute to preventing allergic reactions?
A) It inhibits IgE production and mast cell activation
B) It enhances IgG production against allergens
C) It stimulates Th1 immune responses
D) It blocks histamine release from B cells
A) It inhibits IgE production and mast cell activation ✅
61
Which of the following statements about oral tolerance and vaccine development is TRUE?
A) Oral vaccines can be less effective due to the risk of inducing tolerance
B) Oral vaccines are the only effective way to generate mucosal immunity
C) The immune system cannot develop memory from oral vaccines
D) Oral vaccines are ineffective in stimulating T cell responses
A) Oral vaccines can be less effective due to the risk of inducing tolerance ✅
62
What is the main challenge of using oral tolerance as a therapy for autoimmune diseases?
A) It only works for bacterial infections
B) It may suppress beneficial immune responses
C) It enhances inflammatory reactions
D) It leads to increased antibody production
B) It may suppress beneficial immune responses ✅
63
Why are oral vaccines potentially useful for treating autoimmune diseases such as multiple sclerosis?
A) They induce Tregs that suppress autoimmune responses
B) They activate Th1 responses to attack self-antigens
C) They increase IgE production to desensitize the immune system
D) They block antigen uptake by dendritic cells
A) They induce Tregs that suppress autoimmune responses ✅
64
What is bystander suppression in the context of oral tolerance?
A) The ability of Tregs to suppress immune responses to unrelated antigens
B) The suppression of antigen uptake by epithelial cells
C) The inhibition of cytokine secretion by dendritic cells
D) The process by which IgG neutralizes food allergens
A) The ability of Tregs to suppress immune responses to unrelated antigens ✅
65
How do γδ T cells contribute to oral tolerance?
A) They suppress IgE-mediated allergic responses
B) They enhance Th1 responses in Peyer’s patches
C) They increase antigen uptake by M cells
D) They promote clonal expansion of B cells
A) They suppress IgE-mediated allergic responses ✅
66
How does clonal deletion contribute to immune suppression in oral tolerance? (2 marks)
High doses of antigen cause apoptosis of antigen-specific T cells, similar to negative selection in the thymus. This prevents activation of self-reactive T cells.
67
How does clonal anergy contribute to immune suppression in oral tolerance? (2 marks)
Repeated low doses of antigen lead to T cell inactivation due to the absence of co-stimulatory molecules (CD80/CD86). These T cells remain alive but are functionally unresponsive.
68
How does regulatory T cells (Tregs) contribute to immune suppression in oral tolerance? (2 marks)
Regulatory T cells (FoxP3⁺ Tregs) are induced in response to TGF-β and IL-10 in the gut. They actively suppress immune responses through cytokine secretion and direct inhibition of effector T cells.
69
What are the key differences in antigen uptake and presentation that lead to oral tolerance instead of an immune response? (5 marks)
-oral tolerance is ensured through tolerogenic presentation where antigens are taken up by epithelial cells, M cells, and dendritic cells (DCs) in the gut
-Gut DCs lack co-stimulatory molecules (CD80/CD86), preventing full T cell activation.
-DCs promote Treg induction via TGF-β and IL-10 secretion.
-while with immunogenic presentation, the antigens taken up during inflammation activate DCs, which express CD80/CD86 and MHC-II, leading to T cell activation.
-This results in Th1 or Th17 differentiation and an active immune response.
70
Why does a high dose of antigen tend to induce clonal deletion, whereas a low dose induces clonal anergy? (2 marks)
-with a high dose antigen, overwhelming antigen exposure triggers activation-induced cell death (AICD) in T cells
-with a low dose antigen, insufficient TCR stimulation and lack of co-stimulatory molecules lead to T cell anergy rather than deletion
71
Explain the roles of TGF-β and IL-10 in oral tolerance. (3 marks)
-TGF-β induces Treg differentiation and promotes IgA class switching in B cells.
-Suppresses Th1 and Th17 responses.
-IL-10 inhibits pro-inflammatory cytokines like IL-12 and IFN-γ, preventing effector T cell activation.
72
What factors can break oral tolerance and lead to food allergies or autoimmune diseases? (3 marks)
-Inflammation through infection-driven cytokines (e.g., IL-12) override Treg suppression.
-Gut Barrier Dysfunction which Increases antigen exposure due to leaky gut.
-Genetics for example HLA mutations linked to diseases like celiac disease.
73
What is the oral administration of autoantigens as a treatment method?
its a experimental treatment used to reduce the severity of autoimmune diseases by feeding autoantigens to induce immune suppression rather than an inflammatory response. the goal being to induce the immune system to tolerate self-antigens instead of attacking them.
74
Why would we induce Tregs into a immune system in the oral administration of autoantigens as a treatment method? (4 marks)
-When autoantigens are ingested, gut dendritic cells (DCs) process them in a non-inflammatory environment.
-the absence of PAMPs and DAMPs, prevents them from upregulating co-stimulatory molecules (CD80/CD86). Instead, they express indoleamine 2,3-dioxygenase (IDO), a key enzyme that promotes immune suppression.
-the gut environment is rich in anti-inflammatory cytokines, DCs start producing TGF-β and IL-10, and in the presence of these cytokines, naïve CD4+ T cells differentiate into FoxP3+ Tregs.
-Tregs suppress effector T cells (Th1, Th17) and prevent autoimmunity.
75
How do γδ T cells suppress IgE responses and contribute to immune regulation in the gut? (5 marks)
-γδ T cells suppress IgE responses by secreting IL-10 and TGF-β
-this directly inhibits B cells from class-switching to IgE by downregulating necessary transcription factors.
-Suppress excess Th2 cells, reducing IL-4 and IL-13 production needed for IgE synthesis.
-Promote regulatory T cells (Tregs), enhancing immune tolerance and reducing allergic responses.
-Modulate dendritic cells and macrophages, lowering allergen presentation and Th2 activation.
76
What diseases are associated with FoxP3+ Treg dysfunction?
-Loss of Treg Function leads to excessive immune activation.
-Diseases include IPEX syndrome (FoxP3 mutation)
-Inflammatory bowel disease (IBD)
-Celiac disease
77
What does IBD stand for?
A) Irritable Bowel Disorder
B) Inflammatory Bowel Disease
C) Intestinal Bacterial Dysbiosis
D) Immune Barrier Dysfunction
B) Inflammatory Bowel Disease
78
Which of the following is a type of IBD?
A) Celiac Disease
B) Crohn's Disease
C) Graft versus Host Disease
D) GI Helminth Infection
B) Crohn's Disease
79
Which immune cells are involved in Ulcerative Colitis?
A) Th1 and Th17
B) Th2 and Mast Cells
C) Macrophages and Neutrophils
D) Tregs and CD8+ T cells
B) Th2 and Mast Cells
80
Which cytokine drives fibrosis in Colitis?
A) IL-10
B) IL-13
C) IL-18
D) TNF-α
B) IL-13
81
What is the auto-antigen associated with Crohn’s Disease?
A) Microbiome
B) GP2 in M-cells
C) Gluten
D) Milk Proteins
B) GP2 in M-cells
82
What is a common factor inducing IBD?
A) Excess Vitamin K
B) Genetic Susceptibility (e.g., MHC, TNF)
C) High levels of Tregs
D) Lack of dietary fiber
B) Genetic Susceptibility (e.g., MHC, TNF)
83
Which immune pathway is primarily associated with Crohn's Disease?
A) Th1/Th17
B) Th2
C) Treg-mediated tolerance
D) CD8+ T cell cytotoxicity
A) Th1/Th17
84
Which of the following is NOT a potential immunological intervention for IBD?
A) Anti-IL-12 antibodies
B) Anti-TNF-α antibodies
C) Haptenised colonic proteins
D) CD8+ T cell enhancers
D) CD8+ T cell enhancers
85
How do probiotics help in IBD?
A) By increasing Th1/Th17 responses
B) By inducing Tregs and increasing IgA secretion
C) By enhancing Th2 cytokine production
D) By blocking IL-4Rα signaling
B) By inducing Tregs and increasing IgA secretion
86
Which model is used to study epithelial perturbation in IBD?
A) IL-10 KO
B) TCR-α KO
C) Gai2 KO
D) CD4 CD45RB hi into SCID
C) Gai2 KO
87
Which mechanism underlies the autoimmune response in Crohn's Disease?
A) Loss of Treg-mediated tolerance to dietary antigens
B) Cross-reactivity to GP2 auto-antigen located in M-cells
C) IL-13 driven Th2-mediated mast cell activation
D) Overexpression of IL-4Rα leading to excessive Th2 response
B) Cross-reactivity to GP2 auto-antigen located in M-cells
88
Which genetic model demonstrates the role of T cell/MHC perturbations in IBD pathogenesis?
A) IL-10 KO mice
B) TCR-α KO mice
C) N-cadherin transgenic mice
D) CD4 CD45RB hi into SCID mice
B) TCR-α KO mice
89
What is the primary role of IL-18 in Crohn's Disease?
A) Inducing Treg differentiation to resolve inflammation
B) Driving Th1/Th17 responses and recruitment of macrophages and neutrophils
C) Promoting fibrosis through mast cell hyperplasia
D) Enhancing IgA secretion for barrier protection
B) Driving Th1/Th17 responses and recruitment of macrophages and neutrophils
90
Which of the following best describes the role of IL-13 in Ulcerative Colitis?
A) Promotes Th1-mediated granuloma formation
B) Drives Th2 response, leading to mast cell hyperplasia and fibrosis
C) Induces Treg cells to downregulate chronic inflammation
D) Stimulates macrophages to produce TNF-α and IL-6
B) Drives Th2 response, leading to mast cell hyperplasia and fibrosis
91
Which environmental factor is most closely linked to the 'hygiene hypothesis' in IBD pathogenesis?
A) High dietary fiber intake
B) Reduced exposure to intestinal flora
C) Excessive intake of fermented foods
D) Chronic parasitic infections
B) Reduced exposure to intestinal flora
92
Which model demonstrates the impact of microbial products on IBD development?
A) N-cadherin transgenic mice
B) Dextran sulfate sodium (DSS) induced colitis
C) IL-2 knockout in germ-free mice
D) Haptenised colonic protein model
B) Dextran sulfate sodium (DSS) induced colitis
93
Which mechanism explains how anti-IL-4Rα therapy provides protection in Ulcerative Colitis?
A) Inhibition of Th2-mediated activation of mast cells and goblet cells
B) Enhancement of Th1/Th17 inflammatory responses
C) Direct suppression of Tregs leading to immune tolerance
D) Increased antigen presentation by dendritic cells
A) Inhibition of Th2-mediated activation of mast cells and goblet cells
94
In Crohn's Disease, which immune defect is most commonly observed?
A) TGF-β overexpression leading to excessive Treg activity
B) Epithelial cell permeability defects allowing microbial translocation
C) Overproduction of IL-4 driving Th2 responses
D) High IgA secretion preventing pathogen colonization
B) Epithelial cell permeability defects allowing microbial translocation (leaky gut syndrome)
95
Why does IL-10 knockout lead to spontaneous IBD development?
A) Loss of Treg induction and enhanced Th1/Th17 inflammation
B) Overactivation of Th2 cells and mast cell degranulation
C) Uncontrolled IgA production against dietary antigens
D) Reduced epithelial barrier function and increased antigen uptake
A) Loss of Treg induction and enhanced Th1/Th17 inflammation
96
Which therapeutic approach targets adhesion molecules to treat IBD?
A) Anti-IL-13 antibodies
B) Anti-sense oligonucleotide against ICAM-1
C) Small kinase inhibitors for NF-κB
D) Probiotic reconstitution with Bacteroides species
B) Anti-sense oligonucleotide against ICAM-1
97
Which transcription factor is crucial for driving Th1 responses in Crohn's Disease and is linked to IL-18 signaling?
A) GATA3
B) STAT4
C) T-bet
D) Foxp3
C) T-bet
98
In the context of IBD, how does a deficiency in NOD2 affect intestinal immunity?
A) Enhances Treg function leading to immune suppression
B) Reduces Paneth cell defensin production, compromising antimicrobial defense
C) Increases Th2 polarization, exacerbating allergic inflammation
D) Enhances epithelial barrier integrity, preventing antigen penetration
B) Reduces Paneth cell defensin production, compromising antimicrobial defense
99
Which of the following best explains the mechanism of fibrosis in Crohn’s Disease?
A) IL-13 induced activation of fibroblasts through STAT6 signaling
B) TGF-β activation by integrins, leading to myofibroblast differentiation and collagen deposition
C) IFN-γ mediated apoptosis of epithelial cells, allowing fibroblast infiltration
D) IL-10 suppression of matrix metalloproteinases (MMPs), reducing extracellular matrix degradation
B) TGF-β activation by integrins, leading to myofibroblast differentiation and collagen deposition
100
Which signaling pathway is critical for the maintenance of Tregs but paradoxically contributes to Th17 differentiation in IBD?
A) NF-κB
B) JAK-STAT3
C) mTORC1
D) TGF-β/SMAD3
D) TGF-β/SMAD3
101
Which microbiome-derived metabolite has been shown to induce Tregs and maintain intestinal homeostasis but is often reduced in IBD patients?
A) Butyrate
B) Lactate
C) Succinate
D) Acetate
A) Butyrate
102
What is the role of GP2 auto-antigen in Crohn's Disease pathology?
A) It enhances IgA transport across epithelial cells, maintaining mucosal barrier integrity.
B) It is recognized by auto-reactive antibodies leading to chronic inflammation in M-cells.
C) It acts as a TLR ligand promoting anti-inflammatory cytokine production.
D) It inhibits Th17 differentiation, reducing inflammatory responses.
B) It is recognized by auto-reactive antibodies leading to chronic inflammation in M-cells.
103
Which chemokine receptor is pivotal for Th17 cell recruitment to the inflamed gut mucosa in IBD?
A) CCR4
B) CCR6
C) CXCR3
D) CXCR5
B) CCR6
104
Which immune evasion strategy utilized by gut microbiota can exacerbate IBD by impairing host immune responses?
A) Secretion of SCFAs to enhance Treg differentiation
B) Expression of polysaccharide A (PSA) to inhibit Th17 polarization
C) Production of proteases that degrade mucins and disrupt epithelial barriers
D) Stimulation of IL-10 production by dendritic cells to induce tolerance
C) Production of proteases that degrade mucins and disrupt epithelial barriers
105
In the context of IBD, which role does the integrin αvβ6 play in Ulcerative Colitis?
A) Promotes TGF-β activation leading to fibrosis and tissue remodeling
B) Inhibits Th1/Th17 responses, reducing chronic inflammation
C) Enhances IL-10 signaling in epithelial cells, promoting barrier repair
D) Suppresses mast cell degranulation, preventing mucosal damage
A) Promotes TGF-β activation leading to fibrosis and tissue remodeling
106
Which experimental IBD model demonstrates the role of innate lymphoid cells (ILCs) in initiating chronic inflammation?
A) CD4 CD45RB hi into SCID mice
B) IL-10 KO in germ-free mice
C) RAG KO mice reconstituted with ILC3s
D) Dextran sulfate sodium (DSS) induced colitis
C) RAG KO mice reconstituted with ILC3s
107
Which test is most commonly used to diagnose Coeliac Disease?
A) Skin prick test
B) tTG-IgA antibody test
C) Fecal calprotectin test
D) MRI enterography
B) tTG-IgA antibody test
108
Which condition is ruled out by a negative HLA-DQ2 and HLA-DQ8 genetic test?
A) Crohn's Disease
B) Coeliac Disease
C) Ulcerative Colitis
D) Oat Allergy
B) Coeliac Disease
109
Which of the following is a key diagnostic marker for intestinal inflammation in IBD?
A) IgE antibodies
B) Fecal calprotectin
C) Total IgA levels
D) Vitamin K levels
B) Fecal calprotectin
110
Which test is used to differentiate Non-Coeliac Gluten Sensitivity (NCGS) from Coeliac Disease?
A) Genetic testing for HLA-DQ2/DQ8
B) tTG-IgA antibody test
C) Oral gluten challenge test
D) Skin prick test
C) Oral gluten challenge test
111
Which diagnostic procedure is considered the gold standard for confirming Coeliac Disease?
A) Specific IgE blood test
B) Endoscopy with small intestine biopsy
C) Stool culture for pathogens
D) MRI enterography
B) Endoscopy with small intestine biopsy
112
In which condition would you expect to see "skip lesions" and transmural inflammation on endoscopy?
A) Coeliac Disease
B) Crohn's Disease
C) Ulcerative Colitis
D) Oat Allergy
B) Crohn's Disease
113
Which biomarker is specifically used to distinguish IBD from Irritable Bowel Syndrome (IBS)?
A) tTG-IgA
B) Fecal calprotectin
C) IL-13 levels
D) Specific IgE for food antigens
B) Fecal calprotectin
114
Which of the following findings is most indicative of Ulcerative Colitis on colonoscopy?
A) Cobblestone appearance with skip lesions
B) Continuous inflammation starting from the rectum
C) Villous atrophy and crypt hyperplasia
D) Transmural inflammation with fistulas
B) Continuous inflammation starting from the rectum
115
Which diagnostic test is most appropriate for confirming an oat allergy?
A) tTG-IgA antibody test
B) Skin prick test and specific IgE blood test
C) Fecal calprotectin test
D) Genetic testing for HLA-DQ2/DQ8
B) Skin prick test and specific IgE blood test
116
Why is a total IgA test recommended when diagnosing Coeliac Disease?
A) To confirm IgE-mediated allergy
B) To rule out IgA deficiency which may cause false negatives in tTG-IgA testing
C) To assess inflammation in Ulcerative Colitis
D) To diagnose Crohn's Disease-related immune dysregulation
B) To rule out IgA deficiency which may cause false negatives in tTG-IgA testing
117
Which histological feature is most specific for diagnosing Coeliac Disease in a small intestine biopsy?
A) Transmural inflammation with granulomas
B) Villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (IELs)
C) Cobblestone appearance with skip lesions
D) Continuous inflammation limited to the mucosal layer
B) Villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes (IELs)
118
Which cytokine profile would you expect to find in the intestinal mucosa of a patient with Crohn’s Disease?
A) Elevated IL-13 and IL-5
B) High IL-18, IFN-γ, and IL-17
C) Increased TGF-β and IL-10
D) Elevated IL-4 and IL-10
B) High IL-18, IFN-γ, and IL-17
119
Which advanced imaging technique is preferred for assessing transmural complications (e.g., fistulas) in Crohn's Disease?
A) Colonoscopy
B) Capsule endoscopy
C) MRI enterography
D) Abdominal ultrasound
C) MRI enterography
120
In diagnosing NCGS, which finding would strongly suggest an alternative diagnosis of wheat allergy instead?
A) Positive tTG-IgA antibodies
B) Elevated serum specific IgE to wheat proteins
C) Villous atrophy on small intestine biopsy
D) High fecal calprotectin
B) Elevated serum specific IgE to wheat proteins
121
Which of the following endoscopic findings is most characteristic of Crohn’s Disease rather than Ulcerative Colitis?
A) Continuous inflammation starting at the rectum
B) Pseudopolyps with superficial ulceration
C) Aphthous ulcers, cobblestoning, and skip lesions
D) Diffuse erythema with loss of vascular pattern
C) Aphthous ulcers, cobblestoning, and skip lesions
122
Which serological marker is highly specific for Ulcerative Colitis?
A) Anti-Saccharomyces cerevisiae antibodies (ASCA)
B) Perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA)
C) tTG-IgA antibodies
D) Anti-gliadin antibodies
B) Perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA)
123
Which cytokine imbalance is most closely linked to the pathogenesis of Ulcerative Colitis?
A) IL-12 and IFN-γ overexpression
B) IL-13 driven Th2 response leading to epithelial damage
C) IL-17 and IL-22 mediated epithelial hyperplasia
D) IL-10 and TGF-β suppression leading to loss of Treg function
B) IL-13 driven Th2 response leading to epithelial damage
124
Which immunological defect is most commonly associated with early-onset IBD?
A) IL-10 receptor mutation leading to impaired anti-inflammatory signaling
B) STAT4 overactivation causing excessive Th1 responses
C) Reduced IL-4Rα expression leading to weak Th2 differentiation
D) Increased IL-22 production leading to epithelial hyperproliferation
A) IL-10 receptor mutation leading to impaired anti-inflammatory signaling
125
Why is fecal calprotectin a preferred biomarker for assessing IBD activity?
A) It differentiates between Crohn's Disease and Ulcerative Colitis.
B) It specifically indicates neutrophil migration to the gut mucosa, reflecting intestinal inflammation.
C) It is a marker of epithelial cell apoptosis in Coeliac Disease.
D) It indicates IgE-mediated allergic inflammation in food intolerances.
B) It specifically indicates neutrophil migration to the gut mucosa, reflecting intestinal inflammation.
126
Which genetic mutation is most commonly associated with Crohn's Disease and affects innate immune responses to gut microbiota?
A) HLA-DQ2/DQ8
B) NOD2/CARD15 mutation
C) IL-10 receptor mutation
D) FOXP3 mutation
B) NOD2/CARD15 mutation
127
Which of the following best describes the primary role of the mucosal immune system?
To maintain homeostasis by balancing immune responses and tolerance
## Footnote
The mucosal immune system aims to balance immunity and tolerance to prevent excessive inflammation while maintaining defense against pathogens.
128
What is a key component of the Gut-Associated Lymphoid Tissue (GALT)?
Peyer’s patches
## Footnote
Peyer’s patches are specialized lymphoid follicles found in the intestine that play a crucial role in the immune response.
129
What is the primary function of M cells in the gut?
To transport antigens from the gut lumen to underlying immune cells
## Footnote
M cells facilitate the uptake and presentation of antigens to the immune system.
130
Oral tolerance (OT) is best defined as:
The suppression of immune responses to harmless orally administered antigens
## Footnote
Oral tolerance is a mechanism that prevents the immune system from reacting to non-harmful substances, such as food proteins.
131
Which factors influence the induction of oral tolerance?
All of the above
* Antigen dose and frequency
* Age and genetic background
* Microbiome composition and nutrition
## Footnote
Multiple factors contribute to the establishment of oral tolerance, highlighting its complexity.
132
Which dose of orally administered antigen is most likely to induce clonal deletion?
Very high doses
## Footnote
High doses of antigen can lead to the deletion of specific T cells that react against that antigen.
133
Which of the following is NOT one of the three main mechanisms of oral tolerance?
Activation of cytotoxic T cells
## Footnote
The three main mechanisms of oral tolerance include clonal deletion, clonal anergy, and induction of regulatory T cells (Tregs).
134
Clonal deletion in oral tolerance occurs due to:
Apoptosis of antigen-reactive T cells
## Footnote
Clonal deletion is a process by which T cells that recognize specific antigens are eliminated to prevent inappropriate immune responses.
135
Clonal anergy is best described as:
The functional inactivation of T cells due to lack of co-stimulation
## Footnote
Anergic T cells are unable to respond to their specific antigens, contributing to immune tolerance.
136
Which subset of Tregs plays a critical role in oral tolerance?
FoxP3+ Tregs
## Footnote
FoxP3+ Tregs are essential for maintaining tolerance to food antigens and preventing allergic responses.
137
Bystander suppression in oral tolerance refers to:
The ability of Tregs to suppress immune responses to other antigens nearby
## Footnote
This mechanism allows Tregs to maintain tolerance not only to specific antigens but also to those present in the vicinity.
138
Which antigen-presenting cells (APCs) are primarily involved in the induction of oral tolerance?
Gut dendritic cells
## Footnote
Gut dendritic cells play a crucial role in capturing antigens and promoting tolerance in the mucosal immune system.
139
What is a defining feature of tolerogenic dendritic cells (DCs) in the gut?
They lack co-stimulatory molecules and promote Treg differentiation
## Footnote
Tolerogenic DCs are specialized in inducing tolerance rather than activating inflammatory responses.
140
Which cytokines are crucial for promoting regulatory T cell (Treg) differentiation in the gut?
IL-10 and TGF-β
## Footnote
These cytokines play a significant role in the differentiation and function of Tregs.
141
Which of the following diseases is associated with a failure of oral tolerance?
Crohn’s disease
## Footnote
Crohn's disease is an inflammatory bowel disease linked to the immune system's failure to tolerate gut antigens.
142
Food allergies can arise due to:
All of the above
* A lack of exposure to gut microbiota early in life
* Failure to induce regulatory T cells in response to dietary antigens
* Genetic predisposition
## Footnote
These factors can contribute to the development of food allergies by disrupting normal tolerance mechanisms.
143
Which cytokine is most commonly involved in breaking oral tolerance and promoting allergy?
IL-4
## Footnote
IL-4 is known to drive allergic responses and is often elevated in allergic conditions.
144
Which of the following antigen characteristics is most likely to induce oral tolerance?
Soluble, rapidly absorbed
## Footnote
Soluble antigens that are quickly absorbed are more likely to promote tolerance rather than an immune response.
145
What is the role of intraepithelial lymphocytes (IELs) in oral tolerance?
They promote regulatory mechanisms and immune homeostasis
## Footnote
IELs contribute to maintaining balance in the gut immune environment.
146
Why is the induction of Tregs considered the most important mechanism of oral tolerance?
Because Tregs suppress unwanted immune responses to gut antigens
## Footnote
The induction of Tregs is key to maintaining tolerance and preventing overreaction to non-harmful antigens.
147
Briefly describe inflammatory bowel disease (IBD)?
A chronic inflammatory condition of the gastrointestinal tract
## Footnote
IBD includes conditions like Crohn's disease and ulcerative colitis.
148
Which are the two main types of IBD?
Ulcerative colitis and Crohn’s disease
## Footnote
These are the primary classifications of inflammatory bowel disease.
149
Which part of the gastrointestinal tract is primarily affected in ulcerative colitis?
Colon and rectum
## Footnote
Ulcerative colitis specifically affects the colon and rectum.
150
Which feature is characteristic of Crohn’s disease but NOT ulcerative colitis?
Granuloma formation
## Footnote
Granulomas are a hallmark of Crohn's disease.
151
What is a primary defect in the gut epithelium that contributes to IBD?
Breach of the epithelial barrier
## Footnote
This defect allows for increased permeability and inflammation.
152
What is the role of tight junction proteins in gut barrier integrity?
They create a barrier that prevents microbial invasion
## Footnote
Tight junctions are crucial for maintaining the gut's protective barrier.
153
Which cytokine is involved in maintaining epithelial barrier integrity but is reduced in IBD?
IL-10
## Footnote
IL-10 plays a significant role in modulating the immune response.
154
IBD is considered a T-cell mediated disease due to:
A failure of Tregs to regulate inflammation
## Footnote
Regulatory T cells are crucial for maintaining immune balance.
155
Which T-cell subset is predominantly involved in Crohn’s disease pathogenesis?
Th1 and Th17 cells
## Footnote
These subsets are associated with inflammatory responses.
156
Which factor contributes to the breakdown of oral tolerance in IBD?
Loss of immune tolerance to dietary and microbial antigens
## Footnote
This loss leads to inappropriate immune responses.
157
Which genetic factor is strongly associated with Crohn’s disease?
NOD2 mutations
## Footnote
NOD2 is involved in the immune response to bacterial infections.
158
Which environmental factor is considered protective against ulcerative colitis?
Smoking
## Footnote
Surprisingly, smoking has been shown to have a protective effect in ulcerative colitis.
159
What dietary factors are linked to an increased risk of IBD?
Western diet rich in processed foods
## Footnote
Diets high in processed foods are associated with higher IBD risk.
160
How does gut dysbiosis contribute to IBD pathogenesis?
It disrupts microbial balance, leading to overgrowth of pro-inflammatory bacteria
## Footnote
Dysbiosis can exacerbate inflammation and symptoms.
161
What bacterial genera is decreased in IBD?
*Faecalibacterium prausnitzii*
## Footnote
This genus is known for its anti-inflammatory properties.
162
What is a key metabolic function of beneficial gut microbiota that is reduced in IBD?
Production of short-chain fatty acids (SCFAs)
## Footnote
SCFAs are important for colon health and anti-inflammatory effects.
163
Activation of what cytokines lead to chronic inflammation in IBD?
Persistent activation of inflammatory cytokines like TNF-α
## Footnote
TNF-α is a key player in inflammation and tissue damage.
164
What is a major histological feature of chronic IBD?
Fibrosis and tissue remodeling
## Footnote
Fibrosis can lead to strictures and complications.
165
What is a key difference between the immune response in Crohn’s disease and ulcerative colitis?
Crohn’s disease involves granuloma formation, whereas ulcerative colitis does not
## Footnote
This distinction helps in differential diagnosis.
166
Which cytokine is a major therapeutic target in IBD treatment?
TNF-α
## Footnote
Anti-TNF therapies are widely used in IBD management.
167
What treatment is commonly used for moderate to severe IBD?
Anti-TNF therapy (e.g., infliximab)
## Footnote
Infliximab is a well-known anti-TNF agent.
168
What is an emerging therapeutic strategy for IBD?
Fecal microbiota transplantation (FMT)
## Footnote
FMT aims to restore healthy gut microbiota balance.
169
Which cytokine is known to stimulate mucus production by goblet cells, particularly during parasitic infections?
A. IL-6
B. IL-12
C. IL-13
D. TNF-α
c
170
Which stain is most suitable for visualizing goblet cells in histological sections?
A. Hematoxylin alone
B. Gram stain
C. PAS (Periodic Acid-Schiff)
D. Ziehl-Neelsen stain
c
