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GI Exam 1 > GI immunology > Flashcards

GI immunology Flashcards

1
Q

Homeostasis in the gut is normally preserved by two mechanisms:

A
  1. IgA blocking antigens from interacting with mucosa of the gut.
  2. Supression of pro-imflammatory responses d/t oral tolerance
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2
Q

How do we get oral tolerance?

A

eating undigested fibers, vitamin A, lipids, breastfeeding for 4 months and mixed feeding afterwards

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3
Q

how do we get food allergies?

A

failure of oral tolerance d/t genes and environment

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4
Q

What can underlie food allergen sensitization?

A

defect in epithelial barrier

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5
Q

The gut flora or microbiota is influenced by early-life exposures such as maternal microbes, infant diet, antibiotics, probiotics and the physical environment. What does the gut microbiota lead to?

A
  1. development of the immune system,
  2. intestinal homeostasis and
  3. host metabolism.

(disruption of the gut flora can lead to diseases)

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6
Q

___________ of the gut microbiota can result in immune disease, intestinal disease, and metabolic disease.

___________ leads to immune tolerance, homeostasis, and healthy metabolism.

A

Dysbiosis of the gut microbiota can result in immune disease, intestinal disease, and metabolic disease. On the other hand, symbiosis leads to immune tolerance, homeostasis, and healthy metabolism.

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7
Q

Cesearean births are sterile. What does this mean?

A

they are less likely to make a healthy immune response in bb

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8
Q

GALT (gut-assx lymphoid tissue) consists

A
  1. tonsils,
  2. adenoids,
  3. Peyer’s patches,
  4. isolated lymphoid tissues (ILT),
  5. and the appendix
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9
Q

______________ is necessary for the proper development of Peyer’s patches and mature isolated lymphoid follicles.

A

Exposure to bacteria in the early life

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10
Q

The isolated lymphoid follicles act as lymph nodes for the gut. Dendritic cells within Peyer’s patches, after being exposed to an antigen, can present to the mesenteric lymph node OR to the isolated lymphoid follicle in the gut itself.

Every isolated lymphoid follicle in the gut is a product of a single B cell.

Peyer’s patches contain naïve B and T cells.

Most T cell responses for the gut are generated in the ____________

A

mesenteric LN

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11
Q

After birth, bacteria colonize the bbs intestines immediately; caysing events that events that will help to develop the [GALT and mucosa].

  1. What is the PRIMARY route we are exposed to antigens?
  2. How do [peyers patches and GALT] receive antigens, because they do not have afferent lymphatic vesses.
A
  1. GALT.
  2. Antigen-transporting DC transport the antigen to them
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12
Q

How do isolated lymphoid follicles (ILFs) mature?

A
  1. MAMPS (microbe assx molecular patterns) are recogized by PRR (patterm recognition receptors) on epithelial cell in the intestines and DCS, located next to cryptopatches.
  2. B and T cells are then recruited.
  3. Cryptopatches develop into mature ILFs
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13
Q

What is an isolated lymphoid follicle?

A

A single B cell follicle that acts as an site for IgA production. They develop after birth in the SI and LI, but only after being exposed to microbiota.

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14
Q

Microbes can also enter into peyers patches through M cells, where they are endocytosed by DCs. Ag loaded DCs will cause T cell differentiation and B cell maturation –>Which induce what?

A

IgA producing plasma cells

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15
Q

What does exposure to microbiota (MAMPS) do to assist the intestine in its development?

A
  • Intestinal epithelial cells proliferate–>
  • increase depth of crypts–>
  • increase density of Paneth cells in the SI
  • & cause the intestinal cells to release AMPs (antimicrobial peptides).
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16
Q

Commensal bacteria are present in high density. They are usually outside the mucus layer that covers the epithelium. What are our immune responses to them?

A
  1. Some killed by antimicrobial molecules made by epithelial cells.
  2. If they penetrate epithelium, rapidly killed by mØ in the lamina propria.
  3. If they penetrated the specialized-follicle assz epithelium (M-cells), rapidly killed by mØ, but some can live in DC days.
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17
Q

Commensal bacteria are present in high density. They are usually outside the mucus layer that covers the epithelium.

  1. Some killed by antimicrobial molecules made by epithelial cells.
  2. If they penetrate epithelium, rapidly killed by mØ in the lamina propria.
  3. If they penetrated the specialized-follicle assz epithelium (M-cells), rapidly killed by mØ, but some can live in DC days. What happens then?
A
  1. DCs interact with T and B cells in Peyers patches OR DCs go to the mesenteric LN
  2. Induce IgA producing plasma cells
  3. B and T cells leave the mesenteric LN–> efferent lymph–> enter blood at the thoracic duct–> HOME BACK to intestinal mucosa
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18
Q

How do activated T and B cells in the mesenteric lymph node arrive in the lamina propria / mucosa?

A

They enter the mesenteric lymph node, enter the bloodstream through the thoracic duct, travel throughout the entire bloodstream, and then home in and enter the lamina propria / mucosa.

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19
Q

Mucus and epithelial AMPs (antimicrobial peptides) prevent microbes from going into the intestines. When they do get past the epithelium, they are rapidly elimnated by macrophages which induce which cytokine?

A

IL10

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20
Q

The outcome of the interaction between APC and T-cells is modulated by what?

A

MAMPs from the microflora

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21
Q

Which T cells would interact with an APC carrying an MAMP if the result was Crohn’s disease?

What would their product be?

A

Th1 / Th-17 would release

–> IFN-y, TNF, IL-17 (all pro-inflammatory)

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22
Q

What T cells would interact with an APC carrying an MAMP if the result was homeostasis?

What would the products be?

A

T reg cells–>

IL-10 and TGF-beta

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23
Q

What T cells would interact with an APC carrying an MAMP if the result was allergy and Ig-E dependent parasite defense?

What would the products be?

A

Th2–>

IL-4, IL-5, IL-13

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24
Q

how is homeostasis maintained between the host and the commensal flora?

A
  1. Mucus in the intestines is a barrier between the microbiota and the host tissue that prevents microbes from going through epithelium
  2. AMPS will also protect against these pathogens.
  3. If they tranlocated through, MO will kill them and release IL10–> makes T reg
  4. DCs can also capture the antigens–> mesenteric LN from lamina propria, but do not penetrate it. THey release IL6 and TGF B.
  5. In the MLN, T-reg cells to differentiate.
  6. DCs will also activate Th17–> IL17 and IL22, which makes AMPs and controls gut microbiota.
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25
Q

What makes up the mucosal firewall?

A
  1. Epithelial barrier
  2. Mucus layer
  3. AMPs
  4. IgA and DC
  5. Treg cells
  6. Th17
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26
Q

What is the mucosal firewall?

A

prevents good bacteria (commensals) from activating GALT

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27
Q

Symbiosis (or two organisms benefiting from eachother) occurs when there is a balanced microbial composition, maintaining homeostasis. Dysbiosis occurs d/t environment factors which would lead to?

A

dysregulation (lack of homeostasis) of the immunt system and

lead to inflammation in susceptible host (genetics)

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28
Q

Microbiota and immune system co-evolve. Malnutrition affects both and disrupt barrier to enteropathogen infection. What would reccurent enteric infections lead to?

A
  1. Nutrient deficiencies
  2. Impaired intestinal barreir fx

Both increase susceptility to infections.

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29
Q

How do undigested dietary carbohydrates, in the presence of commensal bacteria, decrease host response to the same commensal bacteria?

A
  1. Undigested dietary carbohydrates can be fermented –> short chain FA (acetate).
  2. Acetate –> increase presence of IL-10 + T regs.
  3. T regs decrease host response to commensal bacteria.
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30
Q

What are the functions of short-chain fatty acids (like acetate) produced by commensal bacteria on the G.I.?

A
  1. Increased T reg presentation.
  2. Increased IgA effectiveness.
  3. Increased production of mucus.
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31
Q

What three things are all of critical importance to the formation of induced Tregs for use in the guts to inhibit inflammatory responses?

A
  1. TGF-beta.
  2. Retinoic acid.
  3. An enzyme called “IDO.”
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32
Q

Immune tolerance is sustained immune unresponsiveness to self-Ags, beneficial Ags and commensal bacteria.

Oral tolerance is suppression of immune responses to Ags that have been administered by oral route

. What occurs when there is failure to induce tolerance to food protein?

A

Food allergy and celiac disease

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33
Q

What is peripheral tolerance?

A

When [mature self-reactive lymphocytes] in peripheral tissue are: inactivated (anergy), deleted (apoptosis), suppressed by T-cell?

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34
Q

What is central tolerance

A

Immature lymphocytes that attack self-antigens in the lymph organs are

  1. deleted
  2. change BCR specificity
  3. become Treg cells
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35
Q

Peripheral tolerance is when there are mature self reactive lymphocytes in peripheral tissues which are either inactivated, killed, or supressed. In the intestines, what is needed?

A

additional layers of peripheral tolerance are needed to make sure we have tolerance to Ags such as food and commensal organisms

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36
Q

What immune cells are important in ORAL TOLERANCE and where?

A

macrophaves

DC

TREG cells

in the lamina propria and mesenteric LN.

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37
Q

Oral tolerance is lead by mø, DCs, and Treg cells in the lamina propria and mesenteric LNs. Mø grab Abs from lumen and bring to DCs in LP via gap junctions. What happens next?

A
  1. Mo take up ags from the lumen
  2. Transfer acquired Ag –> DCs in the lamina propria via gap junctions.
  3. DCs stimulate naive CD4+ T cells –> FoxP3-expressing- Treg cells by released RA, TBF-B and IDO.
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38
Q

Once the Naive T cells are stimulated, they are made into FoxP3 T reg cells via the release of ***RETINOIC ACID (RA), TGF-B and indoleamine23dioxygenase (IDO)****. Why?

A
  1. RA –> makes CD4 t cells,
  2. IDO–> drives FoxP3 t reg development
  3. TGF-B–> determines the expression
39
Q

There are two main types of adverse food reactions, toxic and non-toxic.

Non toxic are both immune mediated and non immume mediated.

Nonimmune mediate mechanisms include?

A
  1. pharmacological,
  2. enzymatic,
  3. irritants,
  4. psychosomatic
40
Q

Immune mediated adverse reactions can be what?

A
  1. IgE mediated (Type 1 hypersensitivity)
  2. Non-IgE mediated (Type 3 if IgG or IgM is involved or 4)
41
Q

Food allergy is when an immune reason is responsible. Thus, there are two types of immune reactions, either IgE or non-IgE.

How are the two divided?

A
  1. IgE mediated (Type 1) are divided into immediate onset reactions or late-phase reactions, those that are prolonged.
  2. Non-IgE mediated reactions are regulated by T-cells and occur 4- 28 hours ADTER you ingest the food.
42
Q

What mediates non-IgE mediated adverse food reactions?

A

T cells

43
Q

Are T cell mediated adverse food reactions immediate onset or delayed in onset?

A

delayed in onset

4-28 hours

44
Q

If someone has an immediate allergic reaction to food, what is probably mediating that reaction?

A

IgE

45
Q

In terms of a food intolerance, what is considered “late phase / delayed in onset?”

A

4 to 28 hours after ingestion.

46
Q

What is the basic process by which a type I allergy to food is initiated?

A
  • Allergens are eaten by a DC–> presented to a naïve T cell.
  • IL-4 induces the naïve T cell –> Th2 cell
  • Produces more IL-4 to induce B cells to produce IgE.
  • The Th2 cell also produces other cytokines to recruit the other effector cells of allergy: basophils, eosinophils, and mast cells.
47
Q

Clinically, a child might be exposed to an allergen without symptoms. Then, on next exposure, the child presents symptoms. One may not think of an allergic diagnosis immediately, but it must still be considered as the initial contact to an allergen will not produce an immune response for_______

A

7 days

48
Q

What is allergic sensitization?

A

Allergen sensitization is the process where IgE-associated food allergies appear early in childhood.

    1. Allergen contacts GI tract
    1. Produced IgE (primary sensitization) in those genetically predisposed
    1. 2nd allergen contact actives [T cells] and induced IgE response in a secondary immune reaction.
    1. inflammation in the intestines, skin and respiratory tract occurs soon after
49
Q

Activation of ______ cells is CENTRAL in food allergy. Why?

A

MAST CELLS (via IgA).

Releases proteases, histamine and cytokines, increasing the permeability of the epithelium and allowing proteins to leave.

50
Q

When mast cells release histamine it also causes increase in vascular permeability, resulting in C3 and C5. When tryptase is released from mast cells, what occurs to the C3 and C5?

A

generates C3a and C5a which further activates mast cells and increases symptoms such as inflammation

51
Q

In normal conditions, Treg cells are exposed to the allergen and work to decrease our immune response. how do they do this?

A
  1. Prevent B cells from making IgE
  2. Stop goblet cells from overproducing mucous
  3. Densitize mast cells and basophils
  4. Supres Th2 cell homing
52
Q

Diet can have a major in fact on allergic sensitization. For example:

  • ________ (4) all decrease inflammation from allergic responses by stimulating Treg activity.
  • On the other hand, a ________ increases Th2 responses.
  • Healthy gut microbiota increase induction of Treg cells
  • Healthy microbiota can also suppress basophils and mast cells essential for the allergic response.
A

Diet can have a major in fact on allergic sensitization. For example:

Vitamin A, vitamin D, fiber, and folate

high-fat diet

53
Q

You have a lesser chance of food allergy if you have high vitamin D,A and long chain FA, inc. in T reg and dec. in basophils and IgE. What puts you at a high risk of food allergy?

A
  1. high fat diet,
  2. medium chain triglycerides,
  3. increased Th2
54
Q

What are the most common food allergies in the US?

A
  1. Milk
  2. Egg
  3. Peanut
  4. Soy
  5. Wheat
  6. Tree nuts
  7. Fish
  8. Shellfish
55
Q

Peanut allergy is IgE mediated. How does it occur?

A

Eat peanuts–> taken up by DC–> peanut specific T-cells are made–> become Th2

IL4, 5 and 13 are released–> B cells–> make Peanut speific IgE–> activate mast cells –> release histamine, leukotrienes, cytokines and prostaglandins and there is itching, swelling, airway obstruction, hives.

56
Q

How do nuts (including peanuts) contribute to a more severe than usual allergic reaction?

A
  • Nuts and peanuts can activate compliment and convert C3 into C3a, stimulating macrophages basophils and mast cells to produce PAF and histamine.
    • PAF will increase vascular permeability and smooth muscle contraction–> anaphylaxis.
  • C3a will stimulate the cells even as the allergic antigen is stimulating them, resulting in a more severe affect.
57
Q

It is important to take a detailed history (PRIMARY TOOL) when diagnosing IgE mediated allergy. Along with this, blood tests and skin prick tests need to be ordered. What may be completed which is considered to be the gold standard?

A

oral food challange

58
Q

Allergies are tested using prick or puncture tests. They are not very invasive and cause results within 15 minutes. If the test is negative, how can we follow up?

A

Intradermal tests

59
Q

__________ are the key to both local and systemic food allergy symptoms.

A

mast cells

60
Q

Systemic Ig-E mediated food alleries can cause reactions OUTside of the gut. They are dependent on what?

A

histamine and platelet-activating factor released from MAST CELLS

61
Q

Gastrointestinal (LOCAL) manifestations of food allergy are also dependent upon on what?

A

TH2 and their release of

  • il4
  • il13
  • il9
62
Q

Therefore, ______and _____ cells are both necessary for local G.I. allergic symptoms.

A

Th2

Mast

63
Q

The local acute gastrointestinal response to allergens (diarrhea) is mediated by …

A

platelet activating factor and serotonin.

64
Q

Mast cells are central to both local and systemic manifestations of food allergy. Ag disseminated systemically can trigger distal reactions through mechanisms dependent on?

A

histamine and platelet activating factor (PAF) **** systemic

65
Q

GI manifestations of food allergy are dependent on Th2 cytokines like IL4 IL13 and IL9. Mastocytosis is necessary for the local symptoms. What mediates local acute GI response (diarrhea)?

A

PAF and serotonin

66
Q

What is anaphalaxis and what is it due to?

A

Most severe SYSTEMIC reaction where different parts of the body have a reaction at the same time d/t IgE releasing mediators.

67
Q

what can occur in analyphaxis to the body

A

GI tract: can increase fluid secretion and peristalsis, causing diarreah and vomiting.

Airways: decrease diameter and increase mucous secretionàphlegm and coughing

BV: increase blood flow and permeability: edema, increased lymph flow and carry ANT to LN

68
Q

Non-IgE mediated reactions are delayed and take up to _____

A

48 hours

69
Q

Type 4 hypersensivity: mediated by T cells. They are commonly commonly triggered by autoimmunity and?

How is tissue damaged?

A

persisitent responses to environmental Ags and microbial Ags.

Tissue is then damaged by macroghages and cytokines made by TH1/TH17 cells or when CD8 kill cells

70
Q

What is the basic mechanism of type III hypersensitivity?

A
  1. An antigen attaches to an antibody, then the Fc region attaches to an Fc receptor on an endothelial cell.
  2. · Ab come in, bind to the antigen and form an immune complex
  3. This immune complex activates the classical complement system, which releases anaphylotoxins C3a, C5a, and C4a
71
Q

CMA (cows milk allergy) can be d/t what?

A

to IgE or non-IgE mediated mechanisms

72
Q

Cows milk allergy can be due to IgE or non-IgE mediated mechanisms. This means children can have delayed type reactions to cows milk, even having a negative skin prick test. These patients are thought to have what kind of hypersensitivity?

A

delayed type IV

73
Q

If a patient does not have IgE antibodies for cows milk, but has a history of allergic reaction to it, what type of hypersensitivity do they have?

A

Type IV hypersensitivity.

74
Q

What are the two mechanisms for peanut allergy?

A

IgE mediated–> activates PAF and histamine

IgG mediated (non-IgE)–> activates macrophages to make PAF, causing smooth muscle contraction.

75
Q

Summary of how food-induced allergy and anaphalxis can occur. 2 mechanisms:

A
  1. B cells
  2. Can activate IgG or IgE
  • IgE--> directly activate the mast cells
  • IgG–>
    • Activates compliment–> C3a/C5a–> activates mast cells
    • Activates macrophages–> makes PAF–> activates mast cells
76
Q

What is food intolerance?

A

You lack the enzyme needed to digest the food

77
Q

IBSà–>

A

IBSàchronic condition that can cause cramping, constipation and diarrhea.

78
Q

Food intolerance ranges from sensistivity to additives such as sulfites to recurring stress/psychological factors about eating food can make you sic and celiac disease.

What is celiac disease?

A

Immune-mediated SYSTEMIC disorder triggered by eating gluten. Symptoms are mainly gastrointestinal, not at risk of anaphylaxis

79
Q

In what two locations has celiac disease not been identified?

A

Sub-Saharan Africa.

East Asia.

80
Q

What are the main genetic predisposing factors for celiac disease?

A

HLA-DQ2 and HLA-DQ8; gluten dependent manifestations

81
Q

What autoantibody is specifically associated with celiac disease?

A

Anti-tissue transglutaminase 2 (anti-tTG2) antibodies

(thus, aB against the TG2 are assx with the dz).

82
Q

The main predisposing factors for celiac disease are HLA-DQ2 and HLA-DQ8. HLA-DQ2 is present in 95% of people with celiac disease, the other 5% express HLA-DQ8.However a big proportion of the population have the HLA-DQ2 gene but do not have celiac.

what does this imply?

A

Having the gene is not enough to have the dz

83
Q

What is the hallmark o CD?

A

Immune-mediated enteropathy that involves the innate and adaptive immunity.

84
Q

how is gluten is taken up and presented to T cells, which causes CD

A
  1. Class II MHC molecules are found on professional APCs.
  2. Microbial Ags are taken up via phagocytosis or endocytosis.
  3. Ags break into peptides
  4. Peptides are loaded into class II MHC and presented to CD4 T helper cells.
85
Q

Why is gluten so difficult for humans to digest?

A

Gluten is proline-rich, and humans lack prolyl endopeptidases. It is also rich in glutamine.

86
Q

Some of these glutamines are deaminated by TG2 resulting in?

A

negatively charged glutamic acid residues

87
Q

What are the two antibodies found in celiac disease against tissue transglutaminase 2?

Which one is most commonly assayed for?

A

IgA and IgG

anti-tTG2 IgA

88
Q

What might cause a false negative in an anti-tTG2 antibody assay?

A

IgA deficiency.

An anti-tTG2 antibody assay is testing for specifically anti-tTG2 IgA. Some patients have low IgA overall, and in these patients, the assay would come back low – a false negative.

89
Q

What test is necessary to confirm celiac diagnosis?

A

Intestinal biopsy

90
Q

What test can exclude the diagnosis of celiac disease?

A

HLA-DQ2 and HLA-DQ8 testing.

91
Q

local acute reaction in the GI is d/t what?

A

PAF and serotonine

92
Q

anaphalyxis is due to

A

PAF and histamine

93
Q
A

GI Exam 1 (13 decks)

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