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GI Exam 1 > Immunology of the GI Tract > Flashcards

Immunology of the GI Tract Flashcards

1
Q

What is a tertiary lymphoid site?

A

Basically the battlefield - primary is where immune cells are made-thymus and BM, secondary are sites like the spleen, peyers patches, or lymph nodes

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2
Q

peyers patches-

  • what is it?
  • where in gut is it?
  • what does it do?
  • structure of?
A
  • gut associated lymphoid tissue
  • in lamina propria
  • important in promoting IgA production and CTL responses
  • M-cells on apical surface; T-cell area, germinal area, and follicle (B-cells)
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3
Q

purpose of M-cells?

Where are they?

A
  • M-cells are located apically -on top of the peyers patch

- M-cells transfer antigens from gut lumen to lymphoid tissue –> presented by APC to T-helper cells (MHC2)

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4
Q

**What is a germinal center?

A

It is where B-cells are proliferating - on their way to generating an antibody response

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5
Q

T-helper cells do what?

A

Present their antigen to cytotoxic t-cell or B-cell

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6
Q

name for immune cells spread out around the GI mucosa?

A

IELs - mostly T-cells

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7
Q

How many IEL per mucosal epithelial cell?

A

Whole boat load - 1 IEL for every 5-6 epithelial cells

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8
Q

What are the majority type IEL in the mucosal epithelium?

A

alpha-beta

gamma-delta

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9
Q

Cytotoxic t-cell are which cell?

A

CD8 t-cell

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10
Q

What immune cells are in the lamina propria?

A
  • B-cells
  • plasma cells
  • macrophages
  • dendritic cells
  • eosinophils
  • mast cells
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11
Q

process of immune response in GI:

A

1) M cells take up antigen via endocytosis/phagocytosis
2) transport across cell (into peyers patches) and release on basal side
3) antigen binds to dendritic cells
4) dendritic cells activate t-helper cells
5) T-helper cells stimulate antigen specific B cells to form germinal centers
6) b-cells leave peyers patch through lymphatic capillaries
7) move to mesenteric lymph channels
8) gets into blood stream via thoracic duct
9) move to lamina propria in gut (they use addressins to get back to the gut) AND BECOME A PLASMA CELL TO SERETE ITS IgA
10) on basal lamina side = poly Ig receptor made by epithelial cell –> binds all IgA dimers made – internalizes and moves it across and dumps it into gut lumen
11) PART OF THE RECEPTOR - SECRETORY COMPONENT - sticks on the IgA dimer = prevents from degredation

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12
Q

What is requried to activate a t-cell?

A

they MUST be spoon fed an antigen from an antigen presenting cell

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13
Q

What molecules helps immune cells do the “homing mechanism?”

A

-addressins

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14
Q

role of IgA

A
  • major immunoglobulin secretions - ex) saliva, mucus, sweat, gastric fluid, tears, colostrum, and breast milk
  • prevents binding of microbes to epithelia - by binding=expulsion
  • binds bacteria and prevents it from binding epithelium, neutralize toxins, all that shit
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15
Q

one major benefit of breast feeding?

A

IgA in breast milk coats infants gut

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16
Q

Mucosal IgA form?

Serum IgA form?

A

DIMER

MONOMER

17
Q

Two subclasses of IgA?

A

IgA1 = cleaved by bacterial IgA1 protease

IgA2 = not susceptible to cleavage

18
Q

Gamma-delta T-cells: significance?

A
  • antigen non-specific
  • respond to NON-PEPTIDE ANTIGENS
  • DO NOT RESPOND TO MHC presentation
  • rapid responders to common intrusions
19
Q

Mast cells importance:

A
  • beneath epitelia exposed to environment
  • activated by alergic reaction - coated with IgE made for something and then upon exposure again you will get crosslinking of IgE = degranulation
20
Q

Cytotoxic t-cells are super important for..

A

VIRUS INFECTED CELLS

21
Q

Activation of CTLs?

A

same as for B-cells – starts in peyers patch and, leaves via lymphatics and gets back go GI lamina

22
Q

What is oral tolerance?

A

-dont want to make immune response to stuff you want in your food

23
Q

What is oral tolerance used for?

A

experimental treatment for autoimmune diseases

24
Q

2 types of oral tolerance?

A

1) high dose (LOTS OF ANTIGEN)-clonal deletion of antigen specific lymphocytes
2) low dose-clonal anergy (unresponsiveness) + reg T-cells suppress immune responses

25
Q

Selective IgA deficiency
-significance on GI system?
-

A
  • not big deal bc IgM can compensate for absence of IgA

- these people with have greater risk for autoimmune diseases bc some antigens can get across still

26
Q

Food hypersensitivities-

-what antibody is involved here?

A
  • -IgE mediated hypersensitivity reactions=release of histamine!*
  • -nausea, vomiting, abd pain, skin rashes
  • -pharyngeal edema and bronchospasm
  • -fatal anaphylactic rxn
  • -vasoactive amine (principally histamine) - severe changes in vascular permeability = massive protein losing enteropathy and hypoalbuminemia
27
Q

Gluten-sensitive enteropathy

important stuff?

A
  • disease of SMALL INTESTINES = malabsorption due to villous atrophy
  • intestinal epithelial cell lining intact but functionally abnormal
  • Hypersensitivity to gliadin (wheat proteins produce immune reaction)-gliadin is not broken down int amino acids

-celiac sprue and idiopathic sprue

28
Q

What happens to lamina propria in gluten sensitivity?

A

increased CD4 and CD8 t-cells

gamma-delta tcells increase 10 times

29
Q

Main mediator of cell damage in gluten-sensitivity?

A
  • MAIN=damage due to T-cells

- Secondary = anti-gliadin IgA may play additional role

30
Q

Treatment of gluten sensitivity?

A

-gluten diet!

31
Q

Complication of partially or untreated gluten sensitivity?

A

increased incidence of GI lymphoma and carcinoma

32
Q

Ulcerative colitis

  • what is it?
  • where does it affect?
  • therapy?
A
  • superficial inflammation (GRANULOCYTIC =NEUTROPHILS!)
  • LARGE BOWEL
  • anti inflammatory or immunosuppressive therapy IS NOT ENOUGH —-> surgery is better and doesnt affect small intestines
33
Q

Crohns disease:

  • what is it?
  • where does it affect?
  • complications?
A
  • Inflammatory + granulomatous lesions/nodules (WALLING IT OFF)
  • inflammatory macrophages do not die via apoptosis
  • commonly involved the terminal ileum and ascending colon
  • obstructive symptoms, abscess formation, and fistulas leading from bowel to other organs
34
Q

Crohns treatment:

A
  • Infliximab - chimeric anti-TNFalpha monoclonal antbody = reduces signs and symptoms
  • immunosuppression prevents immune response againts chimeric antibody
  • surgery = segmental resection - disease will reoccur in unaffected areas
35
Q

Ulcerative colitis VS Crohns

A
  • UC=secondary invovlement of granulocyte inflammatory cells (INNATE IMMUNITY)
  • CD=classic macrophage-containing granulomatous lesions (ADAPTIVE IMMUNITY)
36
Q

Pernicious anemia?

  • what is it?
  • most common cause?
A
  • def of vit B12 = megaloblastic anemia + neuropathy

- most common cause= autoimmune antibodies against intrinsic factor or gastric parietal cells

37
Q

Treatment of pernicious anemia?

A

Vit B12 supplementation

- can be fatal if it is not treated

GI Exam 1 (11 decks)

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