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

Clarke: Immunology of the GI system Flashcards

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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
What is hte fxn of Th17? cytokines?
defense to extracellular bacteria and parasites IL-17, 21, 22
26
What is the fxn of Treg?
Reg. tolerance IL-10
27
Where are Peyers patches found and what do they contain?
distal ileium | contain 5-500 aggregated lymphoid follicles
28
What are analagen peyers patches?
Hold CD4 DC and are apparent by 11 wks gestation
29
When do discrete B and T cell regions appear in peyers patches? Germinal centers?
19 wks Germinal centers are absent until after breath until exposure to Ag
30
How does the number of Peyers Patches differ throughout life?
50 in the last trimester Rise to 100 at birth Increase to 250 by mid teens Reduce to 75-95 years
31
How do some bacteria and viruses cross the epithelial barrier? What happens then?
Bacteria uses M cell to cross epithelial barrier> GAIN ENTRY TO TISSUES> mphage on BASOLATERAL side engulfs microbes *strong vaccination route
32
What stops food tolerance?
T reg cells and IL-10 are located in Peyers Patches to promote tolerance and prevent activation of other T and B cells.
33
Why do many lymphocytes in the intestinal epithelium range not need Ag presentation?
They are gamma/delta T cells and can recognize Ag w/out MHC help.
34
What are the 7 immune strategies employed to defend the host from invading pathogens?
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
1. BLOCK ENTRY INTO THE ORGANISM What mechanisms are used to BLOCK entry to an organism?
1. Epithelial and mechanical barriers 2. Cilia mediated expulsion 3. Goblet cells> MUCINS 4. Neutralizing Abs 5. Anti-microbial peptides 6. Enzymes
36
1. BLOCK ENTRY INTO THE ORGANISM What are the epithelial and mechanical barriers that BLOCK ENTRY INTO THE ORGANISM?
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
1. BLOCK ENTRY INTO THE ORGANISM What are the neutralizing Abs that that block entry into the organism?
1. natural Abs (IgM and IgG from B1 cells) | 2. sIgA (from adaptive IS)
38
1. BLOCK ENTRY INTO THE ORGANISM What produces AMPs?
leukocytes and Paneth cells> alpha defensins
39
1. BLOCK ENTRY INTO THE ORGANISM What enzymes, secreted by PANETH cells, block entry into the organism?
lysozyme | phospholipase 2
40
What are invasive microbes?
Yersinia pseudotuberculosis, Yersinia enterocolitica, Salmonella typhimurium, Shigella flexneri
41
What are noninvasive microbes?
Vibrio cholera, Escherichia coli
42
2. BLOCK ENTRY INTO THE CELL What is used to block entry into the cell?
Neutralizing Abs STERICALLY BLOCK THE PATHOGEN adhering to the host cell> prevents invasion and causes the bacteria to agglutinate
43
2. BLOCK ENTRY INTO THE CELL What are the three ways that IgA is synthesized?
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
3. PROHIBIT SPREADING What mechanisms are used to prohibit spreading?
``` Coagulation – vascular response Vaso-constriction – vascular response Neutralizing Antibodies Interferons Type 1 (IFNα/β) • Increase MHC class I expression • Induce Cell Mediated Cytotoxicity ```
45
3. PROHIBIT SPREADING Ab produced in germinal centers of the LP goes to.... Ab produced in mesenteric LN goes to....
intestinal lumen open circulation
46
4. DIRECT KILLING What is the role of Paneth cells in direct killing?
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
4. DIRECT KILLING What is used to fight salmonella infections?
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
4. DIRECT KILLING What cells express alpha defensin?
Neutrophils NK cells Paneth cells
49
4. DIRECT KILLING What cells express B defensin?
leukocytes | epithelial cells
50
4. DIRECT KILLING What is used for direct killing of pathgoens?
``` 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
4. DIRECT KILLING What pathologies are assorted with defensins?
chronic inflammatory conditions CRC Crohns disease acne
52
5. KILL INFECTED HOST CELL What is used to kill the infected host cell?
``` 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
6. EXPULSION What is used to get pathogens the hell outa hte cell?
``` IgE Vasoactive substances • Leukotrienes, prostaglandins, histamines) Mucous Smooth muscle contraction Cilia-mediated expulsion ```
54
6. EXPULSION | Where do plasma cells that produce IgE Ab to intestinal helminthes develop?
Starts in the LAMINA PROPRIA where you find immature B cell, where antigen presentation happens. Then moves to MESENTERIC LN to develop further
55
7. NUTRIENT DEPRIVATION What mechanisms are used to deprive bacteria and protozoa of nutrients?
1. Divalent cation sequestration 2. llipid transport using LIPOCALIN 3. Tryptophan removal by indoleamine 2,3-dioxygenase
56
7. NUTRIENT DEPRIVATION What divalent cations are sequestered to deprive bacteria and protozoa of nutrients?
1. Iron 2. Manganese 3. Zinc 3. Ca
57
What removes iron?
lactoerin
58
What removes maganese?
NRAMP (natural resistance associated mphage proteins)
59
What removes Zinc?
ZIP/ZNT families of transporters
60
What is a broad spectrum scavenger of diavlent cations (Ca, Fe, Zn, Mn)?
Calprotectin (s100 protein)
61
Which has a higher tolerance the surface/mucosal immune system or the central IS?
surface/mucosal IS
62
How does the body defend itself after central system Ag exposure?
Central system Ag exposure → inflammatory response → body makes specific antibodies through somatic hypermutation → body defends itself
63
What are the 3 outcomes of surface system Ag Pathogens, commensals and innocuous Ags like food?
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
What cells combat a salmonella infection?
Paneth cells
65
How does salmonella typhimurium interact w/ host cells?
1. Contact using Type III secretion system 2. Subvert host cell cycle, initiate ruffling 3. Restructure cytoskeleton 4. Pronounce ruffling 5. Recovery
66
How does salmonella infect host cells?
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
How does salmonella maintain tight junction attachment?
AvrA

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