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SMP - MIM Part 1 > Lecture 13 - Immune Tissue Injury > Flashcards

Lecture 13 - Immune Tissue Injury Flashcards

1
Q

Allergies vs autoimmunity?

A

Allergies are immune response against innocuous non-self antigens

Autoimmunity is an immune response against a self particle

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2
Q

What are the 4 types of immune tissue injuries based on the Gell and Coombs classification?

A
  1. Type I: IgE mediated
  2. Type II: IgG mediated
  3. Type III: IgG mediated
  4. Type IV: T cell mediated
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3
Q

Other name for Type III tissue injury?

A

Immune complex disease

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4
Q

Type I tissue injury:

  1. Antigen?
  2. Effector mechanism?
  3. 3 examples of hypersensitivity reaction?
A
  1. Soluble protein antigens that are small, stable (often enzymes)
  2. Mast cell, eosinophil, and basophil activation by IgE cross-linking
  3. Allergic rhinitis, asthma, systemic anaphylaxis
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5
Q

Original purpose of the effector mechanism of Type I tissue injury?

A

Immune response against multicellular organisms that was underutilized

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6
Q

Type II tissue injury SUBTYPE 1:

  1. Antigen?
  2. Effector mechanism?
  3. Example of hypersensitivity reaction?
A
  1. Cell or matrix associated antigen
  2. Complement FcR+ cells => lysis
  3. Some drug allergies
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7
Q

Type II tissue injury SUBTYPE 2:

  1. Antigen?
  2. Effector mechanism?
  3. Example of hypersensitivity reaction?
A
  1. Cell-surface antigens (receptors or not)
  2. AB alters signaling either by causing uncontrollable activation or by blocking receptor function OR ADCC
  3. Chronic urticaria
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8
Q

Type III tissue injury:

  1. Antigen?
  2. Effector mechanism?
  3. 2 types of hypersensitivity reaction?
A
  1. Soluble antigen
  2. Formation of immune complexes => complement and phagocytes
  3. Serum sickness (generalized), Arthus reaction (localized)
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9
Q

Type IV tissue injury SUBTYPE 1:

  1. Immune reactant?
  2. Antigen?
  3. Effector mechanism?
  4. 2 examples of hypersensitivity reaction?
A
  1. TH1 cells
  2. Soluble antigen
  3. Macrophage activation
  4. Contact dermititis, tuberculin reaction
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10
Q

Type IV tissue injury SUBTYPE 2:

  1. Immune reactant?
  2. Antigen?
  3. Effector mechanism?
  4. 2 examples of hypersensitivity reaction?
A
  1. TH2 cells
  2. Soluble antigen
  3. IgE production with eosinophil activation and mastocytosis
  4. Chronic asthma, chronic allergies
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11
Q

Type IV tissue injury SUBTYPE 4:

  1. Immune reactant?
  2. Antigen?
  3. Effector mechanism?
  4. Example of hypersensitivity reaction?
A
  1. Cytotoxic T cells
  2. Cell-associated antigen
  3. Cytotoxicity
  4. Graft rejection
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12
Q

Skin lesion associated with Type I tissue injury?

A

Wheal and flare

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13
Q

Skin lesion associated with Type IV tissue injury?

A

Induration: nodular swelling

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14
Q

Timing of Type I tissue injuries?

A

Within 30 min of encountering the AG

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15
Q

Timing of Type IV tissue injuries?

A

24-48 hrs

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16
Q

Systemic anaphylaxis (Type I tissue injury):

  1. Common allergens?
  2. Route of entry
  3. Response?
A
  1. Drugs, venoms, foods (peanuts), serum
  2. IV: either directly or following oral absorption
  3. Edema, increased vascular permeability, laryngeal edema, shock => DEATH
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17
Q

Acute urticaria (Type I tissue injury):

  1. Common allergens?
  2. Route of entry
  3. Response?
A
  1. Animal hair, insect bites, allergy testing
  2. Through skin or systemic
  3. Local increase in Q and vascular permeability => edema
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18
Q

Seasonal rhinoconjunctivitis (Type I tissue injury):

  1. Common allergens?
  2. Route of entry
  3. Response?
A
  1. Pollens, dust-mite feces
  2. Contact with conjuctiva of eyes and nasal mucosa
  3. Edema of conjunctiva and nasal mucosa and sneezing
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19
Q

Asthma (Type I tissue injury):

  1. Common allergens?
  2. Route of entry
  3. Response?
A
  1. Danders on cats, pollens, dust-mite feces
  2. Inhalation => contact with mucosal lining of lower airways
  3. Bronchial constriction, increased mucus production, airway inflammation
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20
Q

Food allergy (Type I tissue injury):

  1. Common allergens?
  2. Route of entry
  3. Response?
A
  1. Peanuts, tree nuts, shellfish, fish, milk, eggs, soy, wheat
  2. Oral
  3. Vomiting, diarrhea, pruritis, urticaria, anaphylaxis (rare)
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21
Q

Antigen dose in Type 1 tissue injury?

A

LOW

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22
Q

What is special about the antigens in Type 1 tissue injury?

A

They favor TH2 polarization (instead of the normal Treg), which help B cells isotype switch to make IgE ABs via the IL-4 cytokine

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23
Q

Route of presentation of signals that favor TH2 polarization in Type I tissue injury?

A

Barrier epithelia

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24
Q

What 3 cytokines are involved in Type I tissue injury? What is the role(s) of each?

A
  1. IL-4 drives class switching to IgE and stimulates smooth muscle contraction
  2. IL-5 stimulate the differentiation of eosinophils
  3. IL-13 stimulates smooth muscle contraction
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25
Q

3 mucosal receptors that bind allergens?

A
  1. Protease-Activated Receptors (PARs)
  2. C-type lectins
  3. TLR-4
26
Q

What do many allergens contain?

A

DAMPs

27
Q

What are some allergens complexed with?

A

Bacterial components (e.g. LPS and animal danders)

28
Q

Describe the mechanism behind TH2 polarization in Type I tissue injury. 3 steps

A
  1. Allergens bind the epithelium
  2. Epithelial cells secrete immuno-modulatory molecules => IL-25 and IL-33 stimulate DCs to upregulate co-stimulatory molecules: OX40L, CD40 and ST2 + IL-1 alpha and beta which not only activate DCs but also have a positive autocrine feedback on epithelial cells and futher stimulate them to produce TSLP and GM-CSF to license the DC
  3. DCs migrate to mesenteric LN and activate naive T cells to become TH2 cells
29
Q

What particular DC phenotype may play a role in Type 1 tissue injury?

A

CD103+ DCs

30
Q

Why don’t Type I tissue injuries occur in ALL individuals?

A

Allergens do not license the DCs in the submucosa and naive T cells will become Treg (like in normal pathway)

31
Q

Other than degranulation, what other effect is induced by IgE cross-linking on mast cells?

A

Mast cells express CD40L and secrete IL-4 => binds to CD40 and IL-4 receptors on the plasma cells => stimulates class switching by B cells and the production of more IgE

32
Q

Determinants of the likelihood of developing atopic allergic disease?

A

Both inherited and environmental factors are important determinants:

33
Q

What is the hygiene hypothesis?

A

The postulate of the ‘hygiene hypothesis’ or ‘counter-regulation hypothesis’ is that exposure to some infections and to common environmental microorganisms in infancy and childhood (e.g. Helminth infection, HEP A virus, commensal microbiota) drives the immune system toward a general state of non-atopy

In contrast, children with genetic susceptibility to atopy and who live in an environment with low exposure to infectious disease and environmental microorganisms are thought not to develop efficient immunoregulatory mechanisms and to be most susceptible to the development of atopic allergic disease

34
Q

What do mast cell effects depend on? Explain.

A

Depends on what tissue it is acting on:

  1. GIT: increased secretions and peristalsis => can lead to diarrhea and vomiting
  2. Eyes, nasal passages, airways: decreased diameter, increased mucus secretions => can lead to congestion and blockage of airways and swelling and mucus in nasal passages
  3. BVs: increased Q and permeability => can lead to increased effector immune response and hypotension => potentially can lead to shock
35
Q

Example of purpose of mast cells on GIT?

A

Expel worms from GIT

36
Q

4 receptors of eosinophils?

A
  1. IL-5
  2. Fcα
  3. Fcγ (low affinity)
  4. Fcε (high affinity)
37
Q

What do eosinophils release? 4

A
  1. Th2 type cytokines
  2. Antimicrobial agents
  3. Prostaglandins and leukotrienes
  4. IDO: production toxic for TH1 cells
38
Q

Acute vs chronic response in allergic asthma?

A
  1. Acute (within 30 min): inflammatory mediators causing mucus secretion, SM contraction => obstruction + recruitment of cells
  2. Chronic (4 to 8hrs later): cytokines from TH2 cells and eosinophil products cause this
39
Q

Type II tissue injury SUBTYPE 2: effect if the antigen is a receptor?

A

Cell is not killed, but the receptor may be inactivated or activated

40
Q

Describe Type II tissue injury involving RBCs/platelets. Reason?

A

Innocuous antigens bind to the surface of RBCs or platelets causing the reaction

DRUGS: penicillin, methydopa, quinidine, cephalosporins, and some anti-inflammatories

For unknown reasons a minority of persons make IgG antibodies to these drugs

41
Q

What type of tissue injury are hemolytic anemias?

A

Type II

42
Q

4 types of hemolytic anemias?

A
  1. Transfusion reactions (most commonly directed against ABO blood type antigens)
  2. Erythroblastosis fetalis (in Rh+ offspring of Rh- mother)
  3. Drug-induced hemolytic anemia (hapten-carrier relationship)
  4. Autoimmune hemolytic anemia
43
Q

Describe hemolytic disease of the newborn.

A

Develops when maternal IgG antibodies specific for fetal blood-group antigens cross the placenta and destroy fetal RBCs

The consequences of such transfer can be minor, serious, or lethal

Severe hemolytic disease of the newborn, called erythroblastosis fetalis, most commonly develops when an Rh+ fetus expresses an Rh antigen on its RBCs that the Rh- mother does not express (due to father allele) => during pregnancy, fetal RBCs are separated from the mother’s circulation by the trophoblast and during her first pregnancy with an Rh+ fetus, an Rh- woman is usually not exposed to enough fetal RBCs to activate her Rh-specific B cells => at the time of delivery, however, separation of the placenta from the uterine wall allows larger amounts of fetal umbilical-cord blood to enter the mother’s circulation => this activates Rh-specific B cells, resulting in production of Rh-specific plasma cells and memory B cells in the mother => secreted IgMs clears the Rh+ fetal red cells from the mother’s circulation, but the memory cells remain => activation of these memory cells in a subsequent pregnancy results in the formation of IgG anti-Rh antibodies, which cross the placenta and damage the fetal RBCs => mild to severe anemia can develop in the fetus, sometimes with fatal consequences

44
Q

Treatment for hemolytic disease of the newborn?

A

Can be almost entirely prevented by administering human anti-Rh IgG antibodies against the Rh antigen to the mother within 24-48 h after the first delivery

These antibodies, called Rhogam, bind to any fetal RBCs that enter the mother’s circulation at the time of delivery and facilitate their clearance before B-cell activation and ensuing memory-cell production can take place

45
Q

How does conversion of Hb to bilirubin play a role in hemolytic disease of the newborn?

A

It can present an additional threat to the newborn because the lipid-soluble bilirubin may accumulate in the brain and cause brain damage

46
Q

What are the 2 Coombs test? What are they used for?

A
  1. Indirect: maternal serum + Rh+ RBCs => wash out unbound IgGs => add rabbit anti-human AB => agglutination?
  2. Direct: washed fetal RBCs coated with maternal IgGs => add rabbit anti-human AB => agglutination?

The direct Coombs’ test is used in the evaluation of a jaundiced neonate when Rh incompatibility is suspected

47
Q

Can maternal anti-ABO ABs cause harm to the fetus?

A

No because they are of the IgM isotype and cannot cross the placenta, and so do not cause harm (only IgGs can cross)

48
Q

4 phases of an Arthus reaction (localized Type III tissue injury)?

A
  1. Locally injected antigen in immune individual with IgGs
  2. Local immune complex formation
  3. Activation of mast cells => degranulation
  4. Local inflammation, increased fluid and protein release, phagocytosis, and BV occlusion
49
Q

2 examples of Arthus reactions?

A
  1. Bee sting
  2. Hypersensitivity pneumonitis after inhalation of bacterial spores, fungi, or dried fecal proteins (e.g. farmer’s lung, Bagassosis from moly sugar cane, bird fancier’s lung)
50
Q

Can one same antigen cause different types of tissue injuries in different people?

A

YUP

51
Q

What is serum sickness (generalized Type III tissue injury)?

A
  1. Injection of a foreign protein or proteins leads to an antibody response
  2. Antigen excess situation before AB response is FULLY mounted => small soluble immune complexes formed that are difficult for the immune system to clear
  3. These antibodies form immune complexes with the circulating foreign proteins
  4. The complexes are deposited in small vessels and activate complement and phagocytes, inducing fever and the symptoms of vasculitis, nephritis, and arthritis => effects are transient and resolve when the foreign protein is cleared once the full AB response is mounted (=EQUIVALENCE)
52
Q

Examples of causes of serum sickness?

A

Drug reactions, e.g., penicillin, sulfa drugs, barbiturates, anticonvulsants, insulin, iodine (found in many X-ray contrast dyes), anti-lymphocyte globulin, streptokinase

53
Q

Other name for Type IV tissue injuries?

A

Cell-mediated hypersensitivity

54
Q

3 syndromes caused by type IV tissue injuries? What differentiates these?

A

Differentiated by route of administration:

  1. Delayed-type hypersensitivity: antigen is injected into the skin
  2. Contact hypersensitivity: antigen is absorbed into the skin
  3. Gluten-sensitive enterophathy = Celiac disease: antigen is absorbed by the gut
55
Q

Main example of delayed-type hypersensitivity?

A

Tuberculin test

56
Q

Antigens for contact hypersensitivity?

A

Small metal ions and haptens

57
Q

Antigen for Celiac disease?

A

Gliadin

58
Q

stages of a delayed-type hypersensitivity type IV tissue injury?

A
  1. Uptake, processing, and presentation of the antigen by local antigen-presenting cells
  2. TH1 cells that have been primed by a previous exposure to the antigen migrate into the site of injection and become activated
  3. These cells release mediators that activate local endothelial cells, recruiting an inflammatory cell infiltrate dominated by macrophages and causing the accumulation of fluid and protein => lesion becomes apparent
59
Q

What are skin DCs called?

A

Langerhans cells

60
Q

What do the antigens in delayed-type hypersensitivity type IV tissue injury have in common?

A

Contact sensitizing agents are often lipid soluble or reactive divalent cations

61
Q

Important concept to remember with type IV tissue injuries?

A

First encounter is often asymptommatic and it is the second one (the challenge) that causes symptoms

SMP - MIM Part 1 (14 decks)

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