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OU Immunology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Anatomy of GALT

A
  • Waldeyer’s Ring
  • Peyer’s patches- T and B cells and follicular dendritic cells- small intestine
  • Isolated lymphoid follicles – in small and large intestines
  • Lamina propria- many IgA-producing B cells
  • Intraepithelial lymphocytes- lymphocytes reside between lumenal epithelial cells beneath the tight junctions.
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2
Q

What is claudin and occludin?

A

proteins whose strands band the epithelial plasma membranes together

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3
Q

examples of diseases caused by oral tolerance

A
  • Crohn’s disease

- Ulcerative coliltis

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4
Q

How does IgG gets passed onto the fetus?

A

FcRn binds to maternal IgG and transcytoses to the fetal circulation

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5
Q

How does IgA gets passed in breast milk?

A

sIgA secreting B cells migrate to breast in response to hormones; sIgA is transported to milk via the SC transport process.

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6
Q

Characteristic of gut at birth

A
  • little to no bacterial colonization
  • little to no mucus secretion
  • no IgA producing plasma cells
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7
Q

Composition of immune cells in human breast milk

A
  • Macrophages (55-60%)
  • Neutrophils (30-40%)
  • Lymphocytes (5-10%)
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8
Q

Other protective components in breast milk

A
  • lysozyme
  • lactoferrin
  • oligosaccharides
  • antiviral lipids
  • glycosylated proteins
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9
Q

When you’re clearing a bacterial infection, the termination of the response happens when bacteria is cleared. How do you terminate an autoimmune, alloimmune, or allergic [AAA] response?

A

You can’t terminate the response because you cannot get rid of the antigen

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10
Q

How does diversity / heterogeneity happen in the AAA response?

A

breakdown of tolerance at a primary level that didn’t keep cells in circulation

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11
Q

What is the major cause of damage in the actual immune response (most of the time)?

A

inflammation or immune response to etiologic agent

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12
Q

What can happen if you have a pathogen antigen that look like auto-antigens?

A
  • pathogen will be more effective
  • once your body find the pathogen as a foreign substance, it will try to get rid of it and your self-antigens that looks like the pathogen
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13
Q

Can you distinguish between protective immunity and immunologically-mediated diseases?

A

No because they are often part of the same process; immune response work like abnormal ones

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14
Q

How can you classify the immunologically-mediated responses?

A

by source of antigen or mechanism

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15
Q

How can you classify immunologically-mediated responses via source of antigen?

A
  • autoimmune - your own cells
  • alloimmune - within a species
  • allergy - environment
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16
Q

How can you classify immunologically-mediated responses via mechanism?

A

Coombs and Gell type I-IV (CaG)

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17
Q

Define tolerance as it relates to immunology

A

you don’t reject yourself

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18
Q

Properties of tolerance

A
  • acquired
  • active process
  • developed during fetal life
  • required continued presence of immunogen
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19
Q

How can you lose tolerance?

A

if you stop becoming exposed to it or if you stop expressing it

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20
Q

Define central tolerance

A

tolerance that occurs in a central area where cells are going through development; ex. negative selection

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21
Q

Give an example of peripheral tolerance

A
  • immunogen-induced anergy in absence of co-stimulation

- suppressive cells

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22
Q

What is responsible for oral tolerance to proteins?

A
  • Treg

- CD103+ dendritic cells in the gut

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23
Q

Describe how tolerance can happen in the gut

A
  • M cells process antigen (ex. food)
  • taken up by dendritic cells
  • travel to mesenteric lymph nodes to make IL-10
  • favors Treg development
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24
Q

What are anti-idiotypic antibodies?

A
  • Ab against antigen binding portion of another Ab

- neutralize the antigen binding portion of auto Ab

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25
Q

What is Galluci’s definition of “disease”?

A

when rate of damage exceeds rate of healing

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26
Q

Explain TH1 and TH2 type persons

A
  • kids - middle age tend to lean towards TH1
  • passed middle age tend to lean towards TH2
  • TH1 -> TH2 => antiviral -> anti-parasitic
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27
Q

What are the ways in which you can have a loss of tolerance?

A
  • failure to delete autoreactive clone by thymus
  • breakdown of peripheral tolerance
  • nonspecific activation; eg superantigens
  • molecular mimicry
  • abnormal lymphocyte interaction
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28
Q

What is molecular mimicry?

A

pathogens pick up the surfaces of cell membranes and stick it on their own surface so that body recognizes them as self

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29
Q

What are examples of autoimmune diseases involving T cells?

A
  • DMI
  • RA
  • MS
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30
Q

What is the key to autoimmunity?

A

TH17

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31
Q

What are the three main alloantigen systems?

A
  • ABO blood types
  • Rh factor
  • HLA
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32
Q

Why does alloimmunity happen?

A

the genome between each person is different; even though there are conserved proteins between people, HLA change with each person because it accommodates each person’s T cell/receptors

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33
Q

What are other terms for alloantigens?

A
  • isoantigens

- isoimmunity

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34
Q

Why is the first baby most likely not affected by erythroblastosis fetalis?

A

because the barrier has never been broken before; it CAN happen if the placenta tears

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35
Q

RhoGAM

A
  • drug used to prevent erythroblastosis fetalis

- antibodies against Rh factor

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36
Q

What are drugs that have reduced the need for transfusions and how do they work?

A
  • epogen
  • oprelvekin
  • stimulates your bone marrow to make more erythrocytes
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37
Q

If you’ve never had a transfusion before, what is one possible way in which you can get a reaction to that?

A

a bacterial infection via molecular mimicry which has an antigen similar to the blood that you’re getting a transfusion from

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38
Q

What are reasons that you may need transfusion (either blood or derivatives of)?

A
  • replacement
  • passive immunization
  • immunosuppression
  • diagnostic products
39
Q

If the organ is perfused before transplant, why does the blood type matter?

A

because blood grouping antigens can be expressed on capillary endothelial cells

40
Q

Acute organ rejection

A
  • T cell mediated

- even if peptide is the same, sees MHC as foreign

41
Q

Describe the mechanism of acute organ rejection

A
  • patient’s CD4/8 sees the donor’s DC MHC classes as foreign
  • patient’s DC processes donor’s dead cells and expresses donor’s MHC classes on their surface
42
Q

Mechanism of chronic transplant rejection

A
  • antibodies against MHC on the capillary endothelium
  • leads to thickening -> substances no longer able to diffuse through capillary
  • will kill the organ over time
43
Q

Graft-vs-host disease

A

when transplanted immune cells attacks the recipient

44
Q

If immune cells are transplanted into you an go through your thymic education and go through your negative selection, why is it not 100% effective against inducing tolerance?

A

because some cells will/can escape the thymus

45
Q

Define sensitization

A

like immunization with respect to allergy

46
Q

T/F: Symptoms of allergies depend on the allergen.

A

FALSE; they depend on the immunologic mechanism involved

47
Q

If you’ve never been exposed to a drug before, how can you amount an immune response to that drug?

A

you’ve been exposed to something similar and therefor you may have T or B cells that recognize that antigen

48
Q

CaG I

A
  • IgE mediated
  • allergen crosslinks two IgE molecules on mast cells -> degranulation
  • mediators released (ex. histamine, leukotrienes)
  • inflammation
49
Q

CaG III

A
  • complement mediated

- allergen + IgG -> immune complex -> complement -> toxins -> inflammation

50
Q

CaG IV

A
  • cell mediated

- t cells pick up allergen -> produce cytokines -> inflammation

51
Q

CaG II

A
  • cytotoxic
  • allergen sticks to surface of target cell
  • target cell looks foreign
  • complement or ADCC -> cell death or anti-receptor antibodies
52
Q

What does anti-receptor antibodies do?

A

reduce or alter function of cell

53
Q

What are other names for IgE-mediated allergy?

A

immediate or anaphylactic hypersensitivity

54
Q

Besides allergy, what else is IgE mediated?

A

atopy; rhinitis

55
Q

What are the ways in which CaG I cannot happen even if you are exposed to the allergen?

A
  • insufficient antibodies for crosslinking
  • too much antibodies that they bind up the allergen, keeping it away from the mast cells
  • small monovalent antigen that cannot crosslink
56
Q

Mast cell degran. in GI

A
  • ↑ fluid secretion, ↑ peristalsis

- expulsion of GI content via N/V/D

57
Q

Mast cell degran. in airways

A
  • ⇩↓ diameter, ↑ mucus secretion

- expulsion of airway content via cough, sneeze

58
Q

Mast cell degran. in blood vessels

A
  • ↑ blood flow, ↑ permeability

- edema, inflammation, ↑ antigen to lymph nodes

59
Q

Besides mast cells, what else can bind to IgE?

A
  • eosinophils and basophils
  • also have Fcε receptors
  • important in allergic asthma
  • populate lungs in asthma patients
  • more toxic than mast cells
60
Q

Cell destruction in spleen is associated with which CaG classification?

A

CaG II

61
Q

What are examples of diseases that CaG lead to?

A
  • Grave’s disease
  • Masthenia Gravis
  • via anti-receptor antibodies
62
Q

What is the time course of CaG II?

A
  • within hours

- varies on how sensitive a person is ex. more Ab = more severe, how much allergen patient is exposed to

63
Q

Which CaG classification is vasculitis, arthus reaction, and serum sickness associated with?

A

CaG III

64
Q

What are conditions for CaG to occur?

A

highly immune person expose to high level of immunogen

65
Q

What is the time course of CaG II?

A

within 2-12 hours

66
Q

What does DTH refer to?

A
  • delayed type hypersensitivity

- CaG IV

67
Q

What are the immune effectors for CaG IV?

A
  • CD4 Tcells promote inflam. reponse via TH1 and TH17

- CD8 Tcells cause tissue rejection

68
Q

What is the time course of CaG IV?

A
  • 8-12 hours to 48-72
  • vary with allergen
  • can wear nickel for months before response developed
69
Q

Define atopy

A

inherited tendency for IgE mediated allergy to common environmental allergens

70
Q

T/F; Not all IgE-mediated diseases are atopic

A

True

71
Q

What are your probability of having atopy with respect to inheritance from your parents?

A
  • 50% = one parent

- 75% = both parents

72
Q

Describe the mechanism of allergy

A
  • allergen exposure
  • allergen extracted, passes mucous membrane to an APC
  • APC processes it on the surface of their cell
  • shown to T cell -> TH2 response
  • IL4 production -> IgE -> mast cells
73
Q

What is another name for allergic rhinitis?

A

hay fever

74
Q

What are the differences between extrinsic vs. intrinsic

A
  • extrinsic: TH2

- intrinsic: does not know initial cause but usually follows infection

75
Q

What are nonspecific triggers of atopic diseases?

A
  • exercise
  • stress
  • cold
  • irritants
  • drugs
76
Q

What are the differences in FEV1 values between non-asthmatics and asthmatics?

A
  • non-asthmatics’ lungs will expand with max. inspiratory -> bigger FEV1
  • asthmatics will not have that expansion; albuterol will help with that
77
Q

atopic diseases

A
  • allergic rhinitis
  • allergic asthma
  • atopic dermatitis
  • allergic gastroenteropathy
78
Q

Non-atopic allergens

A
  • ingestants

- injectants

79
Q

What happens during sensitization?

A

when you’re exposed to the allergen for the first time, instead of making neutralizing antibodies (IgG), you start to make IgE

80
Q

What are the symptoms associated with anaphylaxis?

A
  • tongue swelling
  • constricted airways
  • wheezing
  • hypovolemia
  • vascular collapse
  • urticaria / angioedema
81
Q

anaphylactoid reactions

A

mast cells mediated; no IgE or T cells involved

82
Q

What are ways in which you can get mast cells to degran. to produce an anaphylactoid reaction?

A
  • receptor or drug interaction with mast cells
  • radiocontrast dyes changing osmotic pressure
  • drying out of bronchial tissues by breathing hard
83
Q

Which cells are involved in early phase inflammation?

A
  • mast cells

- basophils

84
Q

Which cells are involved in late phase inflammation?

A
  • these aren’t really involved in an acute response
  • eosinophil (usually traffic into place of prolonged inflammation)
  • neutrophil
85
Q

What are conditions that need to be met in order for CaG III to occur?

A
  • patient must have high levels of IgG

- patient must be exposed to high dose of antigen

86
Q

Explain why you need a perfect ratio for CaG III to happen

A
  • not enough antibodies or antigen -> complexes aren’t big enough
  • big complexes get cleared
  • need slight antigen excess
87
Q

Describe the events that occur in serum sickness

A
  • primary happens within 1 week after exposure of foreign protein; resolves in 4 weeks
  • secondary happens within 2-4 days after exposure
88
Q

What symptoms can serum sickness lead to?

A
  • at site on injection: rash, swelling, pain
  • fever
  • headache
  • nausea
  • vomiting
  • malaise
  • arthralgia
  • myalgia
89
Q

What results if the site of immune-complex deposition is in the joint spaces?

A

arthritis

90
Q

Injected serum can lead to immune complex disease. What else can cause it?

A
  • any disease that results in a circulating antigen ex. RA, lupus, etc.
  • infectious diseases ex. viremia
  • Farmer’s lung
  • Aspergillosis mold
91
Q

Which CaG is allograft rejection?

A

CaG IV

92
Q

Which CaG is graft-vs-host disease?

A

CaG IV

93
Q

chemokine functions

A

recruit immune cells into area of interest

OU Immunology (7 decks)

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