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Immune System & GI tract Flashcards

1
Q

what’s the main component of mucosa immunity?

A

MALT - mucosa associated lymphoid tissue (also have bronchus, nasal and gut (best understood) ALTs)

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2
Q

what are 3 of the challenges of the GALT?

A
  1. Large area to protect (> 400 m2)
  2. exposed to foreign antigens from food
  3. exposure to foreign antigens from colonic bacteria
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3
Q

Pts who have their tonsils removed show a diminished response to what?

A

Diminished IgA response to polio

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4
Q

what 2 unspecific IR things protect the epithelium from damage?

A
  1. mucus (produced as mucin by goblet cells)

2. AMP (antimicrobial proteins; like a-defensins; paneth cells, in base of crypts)

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5
Q

what are 3 structural features of GALT?

A
  1. scattered lymphoid cells (dendritic cells)
  2. isolated organized lymphoid follicles
  3. Peyer’s patches (a part of organized lymphoid follicles)
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6
Q

what are M cells and what do they lack?

A

specialized cells that line the dome region of peyer’s patches and take up antigens by endocytosis and phagocytosis & releases it via transcytosis to present them to the dendritic cells to present it to peyer’s patches T cell region or mesenteric LN.
lack microvilli and mucus

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7
Q

In the GALT where are dendtric cells located?

A

DCs are in organized lymphoid tissue (like Peyer’s patches) and scattered lymphoid cell compartments. They can uptake antigens and migrate to mesenteric LNs to present to T cells

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8
Q

what are the 2 ways to activate the immune system through the gut?

A
  1. antigen presentation in peyer’s patches

2. antigen presentation in mesenteric LNs

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9
Q

where’s the lamina propria in the gut and what’s it made of?

A

Layer of CT (myofibroblasts) directly underneath the mucosal epithelium where immune cells (T cells - CD4 & 8, MO, eosinophils, mast cells, plasma cells - producing IgA) are located.
CD8 cells: effector memory T cells are more active, they have selective chemokine: chemokine receptor interactions in mucosa sites via expression of CCR9

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10
Q

What separates the epithelium from the lamina propria? what cells are located in the epithelium?

A

its separated from the epithelium (CD8aa T cells - central memory T cells: ) by thin layer of basement layer

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11
Q

where is a4B1 T cell integrin induction homed to?

A

periphery

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12
Q

what does a4b7 T cell integrin bind to?

A

mucosal vascular addressin (MAdCAM-1) expressed on the endothelial lining of bvs of the gut

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13
Q

what explains the preference of HIV for GALT?

A

lymphocytes home to the gut by a4B7 integrin molecule which is also a co-receptor for HIV

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14
Q

what in the GALT gets severely and selectively depleted in the 1st weeks post HIV infection?
what does the rates of replenishment determine?

A

CD4 CCR5 T cells

the rates of replenishment determines when AIDS will develop

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15
Q

what’s the main function of B cells in GALT? what mediates this? Where do they home?

A 
class switch to IgA (then become plasma) by cytokine TGF-B
plasma cells home to the lamina propria using CCR9 and a4B7
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16
Q

what’s the function of IgA GALT

A

IgA secreted onto gut surface and binds/neutralizes pathogens/toxins or exports them from lamina propria while be secreted. it also binds/neutralizes anitgens to intenernalize them in via poly-IgA receptor

17
Q

how do DC in GALT becoming activated in response to enteric pathogens?
what kind of response does it create?

A

either directly via DC TLRs or indirectly thru activation of epothelial cells intracellular vesicle TLRs or their NOD1 & 2 cytosolic leading to NF-kB activation to activate DCs
induces Th1 and/or 2 response

18
Q

where are the TLRs and NOD1/2 located in GALT epithelial cells?

A

TLRs are in the vessicles

NOD1/2 are in the cytosol

19
Q

What are the 3 concepts that may explain if the GALT is inappropriately activated in inflammatory disease processes of the gut?

A
  1. mutations in NOD
  2. deregulation of IEL (intraepithlium lymphocytes)
  3. deregulation of regulatory T-cells
20
Q

describe the T cells in the lamina propria

A 
CD4 T cells, effector memory type = activated
Home via CCR9 & a4B7
produce INFy (controls T cells), IL5 (controls worms) & IL10 (involved in producing regulatory cells)
21
Q

describes the T cell in the epithelium

A

CD8 T cells are effector memory type = activated
home via CCR9 and aEB7 to the epithelium
produces INFy
a subset express a:a homodimer of CD8, indicating a higher affinity for non-classical MHC I on epithelial cells (likely causes down regulatory properties rather than activating)

22
Q

what GALT defect can be assoc w/ crohn disease?

A

mutated NOD so can’t make antimicrobial proteins in paneth cells

23
Q

what initates vs sustains crohn disease?

A

Initate: injury to epithelium
Sustained: inappropriate immune response

24
Q

what happens to the # of CD8aa (natural IELs) and CD8ab (induced intraepithelium lymphocytes) as we age?

A

CD8aa (natural IELs): decreases b/c have finite # of them

CD8ab (induced IELs): increases, they activate things

25
Q

what’s the function of natural IELs (CD8aa) & induced IELs (CD8ab)?

A

Nautral IELs CD8aa: recognize self, destroy infected & damaged enterocytes
Induced IELs CD8ab: activated, promote epithelial damage in response to inflammation

26
Q

what’s the process by which deregulation of regulatory T-cells leads to GALT disease?

A

TGF-b, PGE2 and thymic stromal lymphopoietin (TSLP) in the mesenteric LN (maybe induced by commensal bacterial) inhibits DC maturation, immature DC express IL-10 & no co-stimulatory molecule leading to induction of T regulatory cells which supress the immune response by producing TGF-b and IL-10

27
Q

what are the 3 enterotypes across people concerning their microbiome?

A
  1. nationality
  2. age
  3. gender
28
Q

describe autoimmune hepatitis clinical characteristics (who it occurs in, what you’d see in blood, other diseases assoc w/, tx)

A

MC in females
hypergammaglobulinemia & autoantibodies
concurrent w/ other autoimmune dx like autoimmune thyroid disorder (AITD)
Responds to corticosteroids & azathoprine

29
Q

describe primary biliary cirrhosis clinical characteristics (who it occurs in, what you’d see in blood, other diseases assoc w/, tx)

A

MC in females
autoreactive T & B cells responses against mitochondrial self-antigens
Assoc w/ autoimmne dx like AIT, SLE or systemic sclerosis
Tx: ursodeoxycholic acid

30
Q

describe primary sclerosing cholangitis clinical characteristics (who it occurs in, what you’d see in blood, other diseases assoc w/, tx)

A

MC in men
no dx specific auto-antibiodies
Assoc w/ some HLA types & variable beta chains of T cells; also IBD
Tx: ursodeoxycholic acid

GI (8 decks)

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