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GI- Week 5 > Clarke: Immunology of the GI system > Flashcards

Clarke: Immunology of the GI system Flashcards

1
Q

What are adaptive immune mediators of acute inflammation?

A 
TH1
IFNy
M-1 Mphage
IgG and sIgA
CTL
NK
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2
Q

What diseases are associated w/ acute inflammation?

A

Gut: inflammatory bowel disease, Crohns, Celiac, Ulcerative Colitis

Lung: COPD, Bronchiolitis, Pneumonitis

Skin: Psoriasis

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3
Q

What adaptive immune mediators are associated w/ chronic inflammation?

A 
TH2/TH17 Lymphocytes
IL-4 and IL-17
M-2 Macrophage
IgE (Reaginic Antibody)
Eosinophils
Basophils
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4
Q

What diseases are associated w/ chronic inflammation?

A

Gut: food allergy
Lung: asthma, allergic rhinitis
Skin: atopic dermatitis, urticaria

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5
Q

What influences lymphocyte migration? What is B7 integrin?

A

Lymphocytes are directed by selectins and integrins. Mucosal lymphocytes express B7 INTEGRIN that localizes lymphocytes to MUCOSA.

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6
Q

What is CCL-8?

A

chemokine that tells lymphocytes that there is inflammation in the cell

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7
Q

What happens once an Ag comes through an M cell?

A 
Ag comes in through M cell>
presented to immature B and T cells>
goes to the LN>
classic maturing and class switching>
enters peripheral circulation>
Mature cells circle back to original site of inflammation of GI/mucosa
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8
Q

What is a key difference between the cenrtral and surface immune systems?

A

Ab isotypes

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9
Q

Wha are components of hte central immune system?

A

blood: spleen and liver
Tissues: lymph

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10
Q

What are components of the surface immune system?

A

Skin: cornified epithelial, ducts of exocrine glands

Mucosal: RT, GT, UT

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11
Q

How does the T cell response differ between the central and surface immune systems?

A

central: TH1
surface: TH2

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12
Q

What is the major secretory component of the central immune system?

A

IgG

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13
Q

What is the major secretory component of the surface immune system?

A

IgA

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14
Q

What is GALT?

A

Gut associated lymphoid tissue= part of the barrier system

Primary site for Ag. entry
Largest lymphocyte reservoir in the GI and Respiratory Systems
Lymphoid follicle density increases from mouth to anus

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15
Q

What are other defenses in the GI tract other than the barrier?

A

Extreme pH change

Variable food transit time in diff organs (colon> SI)

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16
Q

What are the three layers of defense in the mucosa?

A
  1. Intraepithelial barrier
  2. Lamina propria
  3. Peyers patch
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17
Q

What lymphocytes are found in the intraepithelial barrier? Does it need MHC to present Ag?

A

γδ lymphocytes- Does NOT need MHC

non-thymic derived

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18
Q

How do the lymphocytes of the intraepithelial barrier defend the mucosa?

A

IELs (intraepithelial lymphocytes):
promote barrier repair
are rapidly recruited
express CD8 (recognize MHC class I Ag)

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19
Q

Where are γδ lymphocytes found and what do they produce?

A

15% of small intestine IEL
40% of colonic IEL
Produce keratinocyte growth factor

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20
Q

What lymphocytes are found in the lamina propria? Does it need MHC to present Ag?

A

classic αβ lymphocytes – needs MHC to present Ag

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21
Q

Where is the rservoir for 70-80% of total lymphocytes?

A

Lamina Propria

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22
Q

What are the predominate T cells in the lamina propria? Where are they derived from?

A

Predominate T cells are CD4, recognize MHC class II Ag

αβ, thymus derived

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23
Q

What is the fxn of TH1? cytokines?

A

Defense to intracellular pathogens
IFNy
TNFa
IL-12

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24
Q

What is the fx of TH2? cytokines?

A

Defense to helminths

IL-10, 13, 5, 4

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25
Q

What is hte fxn of Th17? cytokines?

A

defense to extracellular bacteria and parasites

IL-17, 21, 22

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26
Q

What is the fxn of Treg?

A

Reg. tolerance

IL-10

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27
Q

Where are Peyers patches found and what do they contain?

A

distal ileium

contain 5-500 aggregated lymphoid follicles

28
Q

What are analagen peyers patches?

A

Hold CD4 DC and are apparent by 11 wks gestation

29
Q

When do discrete B and T cell regions appear in peyers patches? Germinal centers?

A

19 wks

Germinal centers are absent until after breath until exposure to Ag

30
Q

How does the number of Peyers Patches differ throughout life?

A

50 in the last trimester
Rise to 100 at birth
Increase to 250 by mid teens
Reduce to 75-95 years

31
Q

How do some bacteria and viruses cross the epithelial barrier? What happens then?

A

Bacteria uses M cell to cross epithelial barrier> GAIN ENTRY TO TISSUES>
mphage on BASOLATERAL side engulfs microbes

*strong vaccination route

32
Q

What stops food tolerance?

A

T reg cells and IL-10 are located in Peyers Patches to promote tolerance and prevent activation of other T and B cells.

33
Q

Why do many lymphocytes in the intestinal epithelium range not need Ag presentation?

A

They are gamma/delta T cells and can recognize Ag w/out MHC help.

34
Q

What are the 7 immune strategies employed to defend the host from invading pathogens?

A
  1. block entry into the ORGANISM (most pathogens)
  2. Block entry into the CELL (bacteria, viruses)
  3. Prohibit spreading (most pathogens)
  4. Direct killing (most pathogens)
  5. Kill infected host cell (virus, intracellular bacteria, protozoa)
  6. Expulsion (multicellular parasites)
  7. Nutrient deprivations (bacteria and protozoa)
35
Q
  1. BLOCK ENTRY INTO THE ORGANISM

What mechanisms are used to BLOCK entry to an organism?

A
  1. Epithelial and mechanical barriers
  2. Cilia mediated expulsion
  3. Goblet cells> MUCINS
  4. Neutralizing Abs
  5. Anti-microbial peptides
  6. Enzymes
36
Q
  1. BLOCK ENTRY INTO THE ORGANISM

What are the epithelial and mechanical barriers that BLOCK ENTRY INTO THE ORGANISM?

A
  1. Tight junctions (< 2 kDa)
  2. Trefoil factors (rapid repair of perforations)
  3. Apical surface of enterocyte forms a selective barrier
    • Dense coating of absorptive microvilli
    • Layer of Filamentous brush border glycocalyx
37
Q
  1. BLOCK ENTRY INTO THE ORGANISM

What are the neutralizing Abs that that block entry into the organism?

A
  1. natural Abs (IgM and IgG from B1 cells)

2. sIgA (from adaptive IS)

38
Q
  1. BLOCK ENTRY INTO THE ORGANISM

What produces AMPs?

A

leukocytes and Paneth cells> alpha defensins

39
Q
  1. BLOCK ENTRY INTO THE ORGANISM

What enzymes, secreted by PANETH cells, block entry into the organism?

A

lysozyme

phospholipase 2

40
Q

What are invasive microbes?

A

Yersinia pseudotuberculosis, Yersinia enterocolitica, Salmonella typhimurium, Shigella flexneri

41
Q

What are noninvasive microbes?

A

Vibrio cholera, Escherichia coli

42
Q
  1. BLOCK ENTRY INTO THE CELL

What is used to block entry into the cell?

A

Neutralizing Abs STERICALLY BLOCK THE PATHOGEN adhering to the host cell>
prevents invasion and causes the bacteria to agglutinate

43
Q
  1. BLOCK ENTRY INTO THE CELL

What are the three ways that IgA is synthesized?

A
  1. Isolated lymphoid follicle: Ag presented to B cell (no T)> IgM recognizes it and binds> DC signals w/ BAFF and B cell differentiates> IgA
  2. Villus T INdependent: Same as above but occurs in the stroma rather than the germinal center
  3. Peyers Patches T DEpendent: APC grabs Ag> presents on MHCII to T cell R> engages CD4> turns out memory and effector T cells> T cell finds B cells to turn into plasma cells through immunological synapse
44
Q
  1. PROHIBIT SPREADING

What mechanisms are used to prohibit spreading?

A 
Coagulation – vascular response 
Vaso-constriction – vascular response 
Neutralizing Antibodies
Interferons Type 1 (IFNα/β)
•	Increase MHC class I expression
•	Induce Cell Mediated Cytotoxicity
45
Q
  1. PROHIBIT SPREADING

Ab produced in germinal centers of the LP goes to….

Ab produced in mesenteric LN goes to….

A

intestinal lumen

open circulation

46
Q
  1. DIRECT KILLING

What is the role of Paneth cells in direct killing?

A

Small intestine is lined with Villi interspersed with Crypts that contain Paneth cells.

Paneth cells harbor pro-defensin 5> Degranulation occurs following bacteria penetration

47
Q
  1. DIRECT KILLING

What is used to fight salmonella infections?

A

Defensins!!

Help to kill phagocytosed bacteria. Most defensins function by binding to the microbial cell membrane, and, once embedded, forming pore-like membrane defects that allow efflux of essential ions and nutrients

48
Q
  1. DIRECT KILLING

What cells express alpha defensin?

A

Neutrophils
NK cells
Paneth cells

49
Q
  1. DIRECT KILLING

What cells express B defensin?

A

leukocytes

epithelial cells

50
Q
  1. DIRECT KILLING

What is used for direct killing of pathgoens?

A 
o	Antimicrobial peptides (AMP)
o	Bacterial permeability increasing proteins (BPI)
o	Lysosomes and Stomach Environment
o	Complement
o	Reactive Oxygen Species (ROS)
o	Reactive Nitrogen Species (RNS)
51
Q
  1. DIRECT KILLING

What pathologies are assorted with defensins?

A

chronic inflammatory conditions
CRC
Crohns disease
acne

52
Q
  1. KILL INFECTED HOST CELL

What is used to kill the infected host cell?

A 
Type 1 Interferons (IFN-α/β)
•	Induces MHC Class I expression
Natural killer cells (NK)
Natural killer T cells (NKT)
Cytotoxic T cell Lymphocytes (CTL)
Antibody dependent cellular cytotoxicity (ADCC)
53
Q
  1. EXPULSION

What is used to get pathogens the hell outa hte cell?

A 
IgE
Vasoactive substances
•	Leukotrienes, prostaglandins, histamines)
Mucous
Smooth muscle contraction
Cilia-mediated expulsion
54
Q
  1. EXPULSION

Where do plasma cells that produce IgE Ab to intestinal helminthes develop?

A

Starts in the LAMINA PROPRIA where you find immature B cell, where antigen presentation happens. Then moves to MESENTERIC LN to develop further

55
Q
  1. NUTRIENT DEPRIVATION

What mechanisms are used to deprive bacteria and protozoa of nutrients?

A
  1. Divalent cation sequestration
  2. llipid transport using LIPOCALIN
  3. Tryptophan removal by indoleamine 2,3-dioxygenase
56
Q
  1. NUTRIENT DEPRIVATION

What divalent cations are sequestered to deprive bacteria and protozoa of nutrients?

A
  1. Iron
  2. Manganese
  3. Zinc
  4. Ca
57
Q

What removes iron?

58
Q

What removes maganese?

A

NRAMP (natural resistance associated mphage proteins)

59
Q

What removes Zinc?

A

ZIP/ZNT families of transporters

60
Q

What is a broad spectrum scavenger of diavlent cations (Ca, Fe, Zn, Mn)?

A

Calprotectin (s100 protein)

61
Q

Which has a higher tolerance the surface/mucosal immune system or the central IS?

A

surface/mucosal IS

62
Q

How does the body defend itself after central system Ag exposure?

A

Central system Ag exposure → inflammatory response →
body makes specific antibodies through somatic hypermutation →
body defends itself

63
Q

What are the 3 outcomes of surface system Ag Pathogens, commensals and innocuous Ags like food?

A
  1. Pathogen–> Deliberate entry→ innate & adaptive immune response → inflammation
  2. Commensal Bacteria–> Accidental entry → innate & adaptive immune response → immune regulation
  3. Food–> Regular entry→ immune tolerance → NO immune response
    • We don’t want to make Ab to our food!!
64
Q

What cells combat a salmonella infection?

A

Paneth cells

65
Q

How does salmonella typhimurium interact w/ host cells?

A
  1. Contact using Type III secretion system
  2. Subvert host cell cycle, initiate ruffling
  3. Restructure cytoskeleton
  4. Pronounce ruffling
  5. Recovery
66
Q

How does salmonella infect host cells?

A

Injects cocktails of poisons to facilitate (Occurs w/ or w/o ruffle formation on host cell)>
Invades then escapes into the cytosol (sub-species of S. enterica)>
Triggers Pro-inflammatory death (Pyroptosis)>
Bacterium release for epithelial invasion>
Released bacteria are targeted for phagocytosis by neutrophils

67
Q

How does salmonella maintain tight junction attachment?

GI- Week 5 (9 decks)

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