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Immunology > Mucosal Immunity > Flashcards

Mucosal Immunity Flashcards

1
Q

To where do effector B and T cells home after activation with specific antigen?

A

Site of infection

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2
Q

True or False: The Mucosal immune system can work independently of the systemic immune system.

A

True

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3
Q

What is sterile protection?

A

Complete blockade of pathogen entry into the host

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4
Q

True or False: Mucosal tissues are more vulnerable to attack than skin.

A

True

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5
Q

What is Waldeyer’s ring?

A

The ring of tonsils and adenoids around the entrance to the gut and airway

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6
Q

What are the first mucosal lymphoid aggregates contacted by inhaled or swallowed antigens?

A

Waldeyer’s ring

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7
Q

Why is it important for the mucosal immune system to modulate inflammation?

A

Most mucosal tissues have a critical physiological function which can be affected by inflammation

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8
Q

How is inflammation modulated in the mucosal immune system?

A

Mucosal surfaces are enriched in TGF-b, have toleragenic dendritic cells, noninflammatory macrophages, lots of Treg cells, and more IgA producing plasma cells

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9
Q

How does the mucosal epithelium contribute to the pre-existing defenses of the mucosal immune system?

A

Simple columnar epithelial cells are impermeable due to tight junctions between the cells; stratified squamous epithelium has no tight junctions allowing diffusion of IgG Ab

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10
Q

True or False: Mucus and antimicrobials are only produced by mucosal epithelial cells in response to a pathogen challenge

A

False- constitutive production

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11
Q

What intestinal cells are especially good at producing antimicrobials?

A

Paneth cells

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12
Q

How does mucus contribute to innate defense?

A

The inner mucus layer is very dense and difficult to penetrate and contains high concentrations of antimicrobials and IgA

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13
Q

Are TLRs expressed on the apical (lumenal) surface of mucosal epithelium cells? What is the importance of this?

A

They are not otherwise they would constantly be activated by commensal bacteria

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14
Q

How are noninflammatory macrophages produced and how do they contribute to the innate immune defense?

A

In the presence of of high TGF-b, macrophages down-regulate surface receptors that trigger respiratory burst/ production of proinflammatory cytokines, but they do avidly phagocytose microbes

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15
Q

What makes a dendritic cell toleragenic? What type of T cells do they stimulate development of?

A

TGF-b and downregulation of costimulatory molecules maintain mucosal dendritic cells in a quiescent state; when they present antigen to CD4+ T cells they generate Treg cells

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16
Q

What is the general utility of toleragenic dendritic cells?

A

Maintain tolerance to harmless antigens

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17
Q

Which TLRs are adept at recognizing viral infections?

A

TLR 7-9

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18
Q

What are NOD proteins?

A

Nucleotide-binding oligomerization domain proteins

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19
Q

What is detected by NOD-1? NOD-2? What transcription factor is stimulated?

A

NOD-1 detects Gram- negative bacteria; NOD-2 detects both Gram positive and Gram negative; Causes NF-kB signaling

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20
Q

What would result from a mutation in NOD2?

A

Reduced amount of defensins and other antimicrobials in secretions mean that invasive bacteria and commensals cannot be kept in check

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21
Q

What is microbial translocation?

A

Prolonged inflammatory responses reduce epithelial barrier integrity such that large amounts of commensal bacteria and microbial products enter the host

22
Q

How can microbial translocation trigger a systemic immune response?

A

Infiltrating bacteria and shed LPS chronically stimulate BL TLRs, and LPS drains into the bloodstream

23
Q

What is Crohn’s disease?

A

An autoinflammatory bowel disease caused by chronic inflammation due to intestinal immune dysregulation, resulting in loss of epithelial integrity and microbial translocation

24
Q

How is Crohn’s disease characterized?

A

Loss of epithelium at inflamed sites

25
Q

What are the typical symptoms of Crohn’s disease?

A

Belly pain, diarrhea, loss of appetite. weight loss, fever, anemia

26
Q

What are the possible causes of Crohn’s?

A

NOD2 gene, NEMO deficiency, Treg deficiency, or defects in autophagy?

27
Q

What are the treatment options for Crohn’s disease?

A

Anti-inflammatory drugs, immune system suppressors, antibiotics

28
Q

Where are inductive sites located within the mucosa?

A

Just below the epithelial layer

29
Q

Where can Peyer’s patches be found? Where are they located in the highest concentrations?

A

Small intestines- most in the ileum

30
Q

What inductive sites are found within the large intestine?

A

Many small lymphoid follicles throughout the colon and rectum

31
Q

If a mucosal surface (e.g., vagina, nose) does not have inductive sites just below the epithelium, were is the inductive site located?

A

Nearest draining lymph nodes

32
Q

What are M cells?

A

Specialized epithelial cells above follicles in intestines that have processes which project into the lumen and capture antigen to present to dendritic cells

33
Q

True or False: M cells are covered by thick mucus

A

False- no mucus

34
Q

How do M cells take up, process, and transport antigen?

A

M cells phagocytose antigens and transports it across the cell into intracellular ‘pockets’ which contain B, T, dendritic cells, and macrophages

35
Q

How can M cells be taken advantage of by pathogens?

A

Because M cells do not degrade or digest pathogens, some microbes can use M cell phagocytosis to gain entry into the host

36
Q

True or False: M cells are only present in the intestine and palatine tonsils

A

True

37
Q

What cells are responsible for antigen binding and uptake in mucosal tissues without M cells?

A

Dendritic cells

38
Q

What antibody is produced by most mucosal plasma cells? What stimulates this production?

A

IgA; class switching mediated by TGF-b signalling

39
Q

What makes IgA noninflammatory?

A

It doesn’t have a C1q binding site and so it cannot fix complement

40
Q

How is IgA transcytosed across mucosal epithelial cells?

A

Dimeric or tetrameric IgA is bound by a J chain, which binds to polymeric Ig receptor stimulating transport and secretion into the lumen

41
Q

What is secretory IgA?

A

IgA bound to part of the PIgR cleaved

42
Q

What is the benefit of having a J chain and secretory component on IgA?

A

Makes it more resistant to proteolysis

43
Q

What are four important functions of mucosal IgA?

A

Immune exclusion, intracellular neutralization, clearance, and neutralization of virus or toxin in lamina propria

44
Q

What is immune exclusion?

A

IgA can bind to a pathogen or toxin and trap it in the mucus to be swept out via peristalsis

45
Q

How is selective IgA deficiency compensated for?

A

Increased production of more defensins, S-IgM and IgG

46
Q

How can serum IgG contribute to mucosal tissue defense?

A

Serum IgG can gain access to the mucosal tissues via leaky (fenestrated) capillaries

47
Q

What adhesion molecules’ expression is stimulated in T cells activated in the small intestines? Large intestines?

A

Small- alpha4beta7 and CCR9; Large- alpha4beta7 and CCR10

48
Q

To what does alpha4beta7 bind?

A

Binds to MADCAM addressin on intestinal HEVs

49
Q

What molecules draws CCR9+ cells into the small intestines? CCR10+ into the large?

A

CCL25; CCL28

50
Q

How do mucosal lymphocytes know which homing molecules they should express?

A

During activation, DC secrete products that up-regulate tissue-specific homing receptors on the lymphocytes

51
Q

How is Vitamin A and D used by the mucosal immune system?

A

Retinoic acid is secreted by intestinal dendritic cells and up-regulates expression of alpha4beta7 on intestinal lymphocytes; Vitamin D metabolites are similarly used by skin DC to direct homing of lymphocytes to wounds

Immunology (13 decks)

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