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Immuno block 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What type of hypersensitivity is Type I?

A

immediate type

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2
Q

What type of hypersensitivity is Type II?

A

modified self

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3
Q

What type of hypersensitivity is Type III?

A

immune complex

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4
Q

What type of hypersensitivity is Type IV?

A

delayed-type

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5
Q

What can be sources of allergens?

A
  • inhaled materials
  • injected materials
  • ingested materials
  • contacted materials
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6
Q

What is the immune reactant, antigen, and effector mechanism of Type I hypersensitivity?

A

Immune reactant=> IgE

Antigen=> soluble

effector mechanism=> mast cell activation

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7
Q

What is the immune reactant, antigen, and effector mechanism of Type II hypersensitivity?

A

Immune reactant=> IgG

  • If antigen is cell- or matrix associated antigen then effector is complement, FcR+ cells (phagocytes, NK cells)

antigen is cell-surface receptor then effector is that Ab alters signaling

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8
Q

What is the immune reactant, antigen, and effector mechanism of Type III hypersensitivity?

A

immune reactant => IgG

antigen => soluble antigen

effector mechanism => complement, phagocytes

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9
Q

What is the immune reactant, antigen, and effector mechanism of Type IV hypersensitivity?

A

immune reactant=> T cells => Th1, Th2, CTL

  • Th1 and Th2 are will recognize soluble antigens
  • Th1 will provide macrophage activation as effector mechansism
  • Th2 will provide eosinophil activation as effector

CTL will recognize cell-associated antigen and use cytotoxicity as its effector mechanism

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10
Q

What are some examples of type I hypersensitivities?

A

allergic rhinitis, asthma, systemic anaphylaxis

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11
Q

With drug allergies such as penicillin, what type of hypersensitivity would you expect?

A

type II => IgG

cell or matrix associated antigen so effector mechanism is complement binding, FcR+ cells (phagocytes, NK cells)

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12
Q

Chronic uticaria would elicit what type of hypersensitivity?

A

Type II => IgG

the antigen is the cell surface receptor and the effector Ab altering the signaling

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13
Q

What type of hypersensitivity reaction will be present due to serum sickness or arthrus reaction?

A

Type III => that releases complement, phagocytes

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14
Q

What can cause type IV hypersensitivities?

A

Th1=> contact dermatitis, tuberculin reaction

Th2 => chronic asthma, chronic allergic rhinitis

CTL=> graft rejection

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15
Q

Name the features of inhaled allergens that may promote priming of Th2 cels that drive IgE responses.

A
  • proteins (they induce T cell responses)
  • proteases
  • low dose of allergen will promote Th2
  • low molecular weight so can diffuse
  • high solubility and stability
  • contains peptides that bind MHC II that is required for T cell priming
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16
Q

Describe the relationship of allergans and Th4 wrt type I hypersensitivity

A

TH2 CD4 cells can induce class switching from IgM to IgE;

antigens that selectively stimulate TH2 cells that drive an IgE response are known as allergens

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17
Q

Hypersensitivity:

A
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18
Q

Hypersensitivity reactions:

A
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19
Q

Hypersensitivity disease:

A
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20
Q

since humans inhale many proteins that do not induce allergic responses, there must be something unusual about allergens that leads to stimulation of IgE production. What are the features that may cause Th2 cells to class switch to IgE to get a response?

A
  • most allergens are small proteins
  • proteases
  • most are highly soluble and low molecular weight
  • most are carried on desiccated particles so must be stable (pollen, mite feces)
  • upon contact with mucosa of airways, soluble antigens elute from the delivery particles and diffuse into the mucosa
  • low dose of allergen will promote Th2
  • contains peptides that bind MHC II that is required for T cell priming
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21
Q

What do parasites secrete that allows them to move around in the host but also calls in a Th2 response?

A

many parasites produce and secrete proteolytic enzymes that break down connective tissues

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22
Q

How do Th2 cells stimulate class switching to IgE?

A
  • produces and secretes IL-4, IL-5 and IL-13
  • upregulates CD40L and CD23 (low affinity receptor for IgE); these costimulatory molecules can bind to their counter receptors (CD40 and CR2) on the presenting B cell
  • combination provides B cell stimulation
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23
Q

Type I hypersensitivity reactions are initiated primarily by mast cells (eosinophils and basophils are also involved). What is expressed on all 3 of these cells types?

A

all 3 of these cell types express the high affinity IgE receptor (Fc RI)

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24
Q

What causes the cells associated with type I hypersensitivity to carry out their effector function?

A

mast cells (also eosinophils, basophils) degranulate when IgE is cross-linked

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25
Q

When do eosinophils and basophils join in the type I hypersensitivity reactions?

A

the mediators released by mast cells initiate inflammation, and recruit eosinophils and basophils to the site of inflammation; eosinophils and basophils contribute to the inflammatory response by releasing the contents of their granules

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26
Q

What is significant about atopic individuals and hypersensitivity reactions?

A

there is a genetic basis with 40% whites producing more responses to IgE

atopic individuals have higher levels of soluble IgE and more circulating eosinophils than non-atopic individuals

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27
Q

elevated IL-4 levels are seen in atopic individuals. What chromosome could be affected? why is this chromosome important?

A

chromosome 5

chromosome 5 encodes a cluster of genes that encode IL-3, IL-4, IL-5, IL-9, IL-13, and GM-CSF

(all of these are involved in isotype switching, eosinophil survival, mast cell proliferation)

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28
Q

HLA class II polymorphism also affects the IgE response to certain allergens. How?

A

HLA class II:peptide combination predisposes to stimulation of a TH2 response

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29
Q

An individual’s sensitivity to a particular allergen can be easily tested. How?

A

1st step of response: injection of an allergen into the skin of a sensitive individual produces a characteristic inflammatory reaction known as a wheal and flare at the injection site

2nd step of response: 6-8 hours post injection, a second reaction (the late phase reaction)
occurs at the site of injection

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30
Q

How does the 1st response of a allergen sensitivity test work?

A

Mast cell degranulation causes the wheal and flare reaction is called an immediate reaction because it appears within a few minutes;

released histamine and other mediators cause increased permeability of local blood vessels (fluid enters tissue causing swelling or edema);

the swelling produces the wheal;

increased blood flow in the area causes redness (flare)

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31
Q

Describe the 2nd response to when a person is tested for sensitivity to an allergan

A

consists of more widespread swelling and is mediated by leukotrienes, chemokines, and cytokines produced by mast cells following IgE-mediated activation

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32
Q

The effects of IgE-mediated allergic reactions vary with the site of mast cell activation. Why is this true?

A

re-exposed to an allergen, the resulting reaction depends on the tissues that come in contact with the allergen;

only the mast cells that reside at the site of allergen contact will be induced to degranulate (via IgE crosslinking by allergen)

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33
Q

What is systemic anaphylaxis?

A

wide-spread activation of mast cell degranulation causing both an increase in vascular permeability and a widespread constriction of smooth muscle

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34
Q

What causes systemic anaphylaxis? What are the results?

A

allergens in the blood

  • fluid leaving the blood causes dramatic reduction of blood pressure (anaphylactic shock)
  • connective tissues swell due to influx of fluid
  • damage can be sustained by many organ systems, impairing their function
  • constriction of airways and swelling of the epiglottis can result in asphyxiation leading to death
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35
Q

What is the difference in anaphylaxis and prophylaxis?

A

anaphylaxis (anti-protection)

prophylaxis (protection)

36
Q

In what ways could potential harmful allergens be introduced directly to the blood?

A

insect sting

drug injections

orally absorbed food that distributes from gut into blood

37
Q

What is the difference in anaphalactoid reactions vs anaphylactic reactions?

A

anaphalactoid reactions: resemble anaphylactic reactions, but do not involve interaction between allergen and IgE

38
Q

treatment of anaphylactic and anaphylactoid reactions is what?

A

injection of epinephrine

39
Q

Why is epinephrine a good treatment for anaphylactic shock?

A

epinephrine stimulates reformation of tight junctions between endothelial cells, thus reducing permeability of blood vessels, diminishing tissue swelling, and raising blood pressure

relaxes constricted bronchial smooth muscle and stimulates the heart

40
Q

Describe an allergic asthma attack

A
  • triggered when submucosal mast cells in the lower respiratory tract are stimulated by allergen/IgE interaction
  • characterized by increase in fluid and mucous secretions into respiratory tract, and bronchial constriction due to contraction of smooth muscle surrounding airways
  • chronic inflammation of the airways involving persistent infiltration of leukocytes (TH2 cells, eosinophils, and neutrophils)
41
Q

chronic asthma is considered what type of hypersensitivity reaction?

A

type IV hypersensitivity

asthmatic disease can be exacerbated by immune responses to bacterial or viral infection of
the respiratory tract (especially infections that elicit TH2 responses)

42
Q

What is urticaria (hives)?

A

itchy swellings caused by release of histamine by mast cells in the skin (following activation by allergen)

43
Q

What is an angioedema?

A

inflammation caused by activation of mast cells in deep subcutaneous tissue

44
Q

What does the reactin of a uticaria look like?

A

reaction is essentially a wheal and flare reaction

45
Q

both urticaria and angioedema result from what? When can both occur?

A

food or drug allergens that get carried to the skin via the bloodstream;

both can occur during an anaphylactic reaction

46
Q

Food allergies can cause systemic effects and gut reactions. once an individual is sensitized to a food allergen, any subsequent intake of that allergen leads to an immediate reaction in the gastrointestinal tract. What is the process?

A
  1. allergen passes thru the wall of the gut, binds to IgE on mast cells (GI tract) triggering degranulation
  2. histamine causes increase in permeability of blood vessels, leading to accumulation of fluid in the gut lumen
  3. contraction of smooth muscles of the stomach walls produces cramps and vomiting, while the same reaction occurs in the intestine to cause diarrhea
47
Q

There are 3 distinct strategies used to reduce the effects of allergic disease. Name them

A

1) modification
2) pharmacological approach: to use drugs that reduce the impact of contact with an allergen
* corticosteroids, antihistamines, cromolyn sulfate, epinephrine
3) immunological treatment:

48
Q

In the immunologic treatment to prevent production of allergen specific IgE. How does it work?

A

modulate the immune response so that it shifts from an IgE response to an IgG response

49
Q

In immunologic treatment, describe desensitization and what does it do?

A

a series of injections of increasing doses of the allergen;

gradually changes a TH2 (IgE) response to a TH1 response in which no IgE is produced;

can result in anaphylaxis

50
Q

How would you attempt to induce anergy wrt to allergies and Th2 CD4 cells

A

vaccinate patients with allergen-derived peptides that are known to be presented by HLA class II molecules to TH2 CD4 cells in an attempt to induce anergy

51
Q

How can the parasite evade IgE immune response?

A

only a small number of the IgE is parasite-specific so the non-specific IgE out-competes the parasite-specific IgE for binding to the Fc RI on mast cells, basophils, and eosinophils;

this strategy prevents the parasite from triggering IgE- mediated effector mechanisms; this allows the parasite to evade immune responses

52
Q

type II hypersensitivity reactions are caused by what?

A

antibodies specific for altered components of
human cells

53
Q

In each case of Type II hypersensitivity, the chemically active drug does what?

A

chemically active drug binds to the surface of red blood cells or platelets and creates new epitopes to which the immune system is not tolerant

54
Q

What is the first step in a penicillin type II induced hypersensitivity?

A 
the new epitopes generated by penicillin stimulate the production of IgM and IgG antibody specific
 for the new epitope(s)
55
Q

When penicillin creates new epitopes for IgG, how does the RBC end up being destroyed?

A
  1. penicillin-modified RBCs must be coated with complement => facilitates phagocytosis by macrophages via complement receptors
  2. macrophages present the newly formed epitopes to naïve CD4+ T cells to produce armed effector TH2 cells
  3. effector TH2 cells specific for new epitopes supply help to antigen-specific B cells; ultimately, IgG specific for new epitopes is produced
  4. IgG antibodies bind to the altered RBCs and stimulate either complement activation or phagocytosis by macrophages
  5. end result, altered RBCs are destroyed
56
Q

type III hypersensitivity reactions are caused by what?

A
57
Q

What is an immune complex?

A

antigen:antibody complexes (immune complexes) are generated in almost all immune responses

most cases, these immune complexes are removed without causing tissue damage

58
Q

Why are smaller immune complexes more dangerous to the host?

A

less efficient at complement fixing

they tend to remain in circulation and become deposited along blood vessel walls

59
Q

during a type III hypersensitivity reaction and the immune complexes have accumulated, how is an inflammatory response created?

A

circulating leukocytes recognize the immune complexes thru their Fc and complement receptors, activating their inflammatory activities

60
Q

systemic type III hypersensitivity reactions can be caused how?

A

by intravenous administration of large
quantities of antigen

61
Q

A type III hypersensitivity can be induced where the immune complexes activate complement and initiate an inflammatory response known as what? What is the route it enters?

A

Arthrus reaction

subQ

62
Q

What is serum sickness? what causes it? How would a person present?

A

results from immune responses to non-self material administered into the bloodstream as a treatment for a variety of illnesses;

serum sickness is caused by a systemic accumulation of immune complexes (and eventual systemic inflammatory responses),

characterized by chills, fever, rash, arthritis, vasculitis, and sometimes glomerulonephritis

63
Q

type III hypersensitivity can also result from continual inhalation of antigens that elicit what Ig instead of the proper one? What will the result be over time to the continually inhaled allergens?

A

IgG instead of IgE antibody responses;

continued inhalation of these antigens results in the accumulation of immune complexes in the walls of lung alveoli which leads to inflammatory immune responses

64
Q

Bird Feeder’s and Farmer’s lung are most common diseases associated with which hypersensitivity?

A

Type III

65
Q

When do Type IV hypersensitivites present and what mediates them?

A

mediated by antigen-specific effector T cells

usually occur 1-3 days after contact with antigen and called delayed-type hypersensitivity (DTH)

66
Q

How does the amount of antigen needed for Type IV compare to those of other types? why?

A

DTH reactions require 100-1000 fold larger quantities of antigen due to the relative inefficiency of antigen processing/presentation

67
Q

Describe the M. tuberculosis test for a positive test

A
  1. small amount of protein extracted from M. tuberculosis is injected subcutaneously
  2. individual that has produced immune responses to M. tuberculosis produces an inflammatory reaction around the site of injection 24-72 hrs post-injection
68
Q

What mediates the M. tuberculosis test and what is the result?

A

mediated by effector TH1 cells that recognize peptides (presented by MHC class II molecules on macrophages) derived from the injected protein;

these cells produce cytokines that activate and recruit macrophages to the site

69
Q

Why is poison ivy considered a contact sensitivity?

A

contact of the allergen with the skin is required to initiate the allergic response

70
Q

Describe an initial poison ivy response

A
  1. initial contact => penadecacatechol penetrates and forms covalent bonds with extracellular proteins and epithelial proteins, forming new antigens that are recognized as non-self;
  2. local antigen presenting cells (macrophages and Langerhans’ cells) take up the new antigens, return to 2* lymph tissues, and present peptide antigens on MHC class II to naïve CD4 cells
  3. penadecacatechol penetrates cell membranes and modifies intracellular proteins, the modified proteins can be processed and presented via MHC class I molecules to naive CD8+ cells
  4. production of effector T cells and immunological memory, but little if any inflammatory response
71
Q

What occurs in each subsequent contact with poison ivy?

A

each subsequent contact with poison ivy plants results in an unpleasant rash of the skin that is mediated by antigen-specific effector CTLs (which kill cells exposed to penadecacatechol), and antigen-specific effector TH1 cells that produce cytokines that activate macrophages and induce inflammation

72
Q

What are some of the effector molecules of Mast cells?

A
  • histamine, heparin
  • TNF-a
  • carboxypeptidase
73
Q

Why is TNF-a released from Mast cells?

A

promotes inflammation

stimulates cytokine production by many cell types

activates endothelium

74
Q

why effect does histamine and heparin released from mast cells cause?

A

toxic to parasites

increase vascular permeability

cause smooth muscle contraction

75
Q

The enzymes released by mast cells (carboxypeptidase, tryptase, chymase, cathepsin G) have what effect?

A

remodeling of connective tissue matrix

76
Q

IL-4 and IL-13 secreted from mast cells caused what type of response?

A

Th2 response

77
Q

Leukotrienes released from mast cells have what function?

A

cause smooth muscle contraction

increase vascular permeability

cause mucus secretion

78
Q

What is the role of PAF when secreted from mast cells?

A

chemotactic for leukocytes

amplifies production of lipid mediators

activates neutrophils, eosinophils, platelets

79
Q

If mast cell activation and granule release occurs in the GI tract, What happens locally followed by the end result?

A

increased fluid secretion and increased peristalsis

results in expulsion of GI tract contents

80
Q

If mast cell activation and granule release occurs in airways, what is the initial and final results?

A

decreased diameter, increased mucus secretion

expulsion of airway contents

81
Q

If Mast cell activation and granule release occurs in the blood vessels, what is the initial and final result?

A

increaded blood flow and permeability

final result is edema, inflammation, increased lymph flow and carriage of antigen to lymph nodes

82
Q

systemic mast cell activation is anaphalaxis and occurs when antigen in bloodstream enters tissues and activates tissue mast cells throughout the body. What happens respectively in the heart and vascular system? respiratory tract? GI tract?

A

H&V system=> increased permeability, swelling, loss of BP, decrease in O2, irregular heartbeat, loss of consciousness, anaphylactic shock

respiratory tract=> smooth muscle contracts, constrict throat & airways, difficulty swalling, breathing, wheezing

GI tract=> contraction of smooth muscle, stomach cramps, vomit, fluid outflow into gut, diarrhea

83
Q

In what 2 ways can type II hypersensitivity from penicillin cause RBC removal?

A
  • activation of complement components C1-C9 and formation of MAC causing lysis
  • activation of complement C1-C3 leading to opsonization of C3b on RBC for phagocytosis
84
Q

In type IV hypersensitivity, Th1 cells release chemokines. What is their action?

A

macrophage recruitment to site of antigen

85
Q

Also during Type IV reactions, cytokines are released. Name them and their associated function

A

IFN-y => activates macrophages, increasing release of inflammatory mediators

IL-3, GM-CSF => monocyte production by bone marrow stem cells

86
Q

During Type IV, Th1 cells release cytotoxins. Name them and their function

A

TNF-a and LT =>

  • local tissue destruction
  • increased expression of adhesion molecules on local blood vessels

Immuno block 2 (9 decks)

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