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Immunology Jenny > 11. Hypersensitivity reactions > Flashcards

11. Hypersensitivity reactions Flashcards

1
Q

Sensitizing antigens

A

1) Environmental
2) Tissue/matrix (self)
3) Persistent microbes
* Can be foreign or self (!) materials

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2
Q

Types of hypersensitivity reactions

A

Type I: classic allergic reaction (IgE)
Type II: immobilized antigen (IgG)
- Immobilized=cell- or matrix associated, cell surface R
Type III: soluble circulating antigens (IgG)
- Immune complexes
Type IV:
- no antibodies
- Th1, Th2, CTL cells (Th for soluble Ag’s, CTL for cell-associated Ag’s)
**Bra tabell i pp!

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3
Q

Clinical expressions of hypersensitivity type I-IV, and times

A

I: “immediate”: allergy, anaphylaxis (minutes)
II: “cytotoxic” (4-6 hrs)
III: “immune complex mediated” (2-8 hrs)
IV: “delayed type” (2-3 days)

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4
Q

FcγRI (CD64)

A
  • IgG
  • High affinity
  • Can bind monomeric IgG
  • Cells: macroph, neutro and eos
  • Function: phagocytosis, activation phagocytes
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5
Q

Type I hypersensitivity reaction

A

First encounter with allergen: symptom free
1) APC present antigen to T cell
2) Naive T cell -> Th2 cells
3) Th2 cell secrete IL-4 and IL-13 -> activate (class-switch) IgE secreting B cell
4) IgE bind naked to mast cell FcεRI
Second encounter:
5) Antigen bind in cross-link to IgE on FcεRI on mast cells -> mast cell activation (release mediators)
- ITAM motif on receptors!

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6
Q

Secretory granule content mast cells, early mediators

A
  • Histamine
  • Enzymes (tryptase, chimase, carboxypeptidase..)
  • From preformed granules, immediate reaction
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7
Q

De novo synthesis products mast cells

A
  • PAF
  • PGD2
  • LTC4 (+LTD4, LTE4)
    *By PLA from arachidonic acid and phosphatidylcholine
    + 5-lipoxygenase and cycloxygenase
    *From membrane
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8
Q

Immediate reaction

A
  • Within 30 min due to histamine from mast cells

- Disappears after 1 hr

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9
Q

Late phase reaction

A
  • Around 8 hrs
  • Eosinophils (activated by IL-5 from Th2 and mast cells)
  • Important to bring patients with severe allergic reaction to hospital even though immediate reaction was resolved!
  • Se tegning i bok!
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10
Q

Inhaled antigen

A
  • Mucosal mast cell
  • Constrict SMC
  • Dilate vessel + increase permeability
  • Consequence: Hayfever and Allergic asthma
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11
Q

Ingested antigen

A
  • Mucosal mast cell
  • Constrict SMC
  • Dilate vessel + increase permeability
  • Consequence: food allergy (increased peristalsis-abdominal cramping)
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12
Q

Connective tissue mast cell

A

Intravenous or subcutaneous allergen

Syst anap++

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13
Q

Systemic anaphylaxis

A
  • Ag directly to blood stream or absorbed rapidly to blood stream
  • Induce connective tissue mast cell degranulation along the capillaries -> severe swelling
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14
Q

Atopy

A

Genetic predisposition to exaggerated IgE production (hyperallergic person)

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15
Q

Example type II hypersensitivity reaction

A
  • Rh-incompatibility -> erythroblastosis fetalis (anti Rh Ab’s attack fetal RBCs in 2nd pregnancy)
  • and drug (penicillin) hypersensitivty?
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16
Q

Type II autoimmune disease

A
  • “Subtype of type II hypersensitivity”
  • No inflammation!!
    1) Basedow disease (Graves disease)
  • Antibody stimulates receptor w/o ligand
  • Agonistic molecule
  • Thyroxine overexpression
    2) Myasthenia gravis
  • Antibody inhibits binding of ligand to receptor
  • Antagonistic molecule
  • Muscle weakness
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17
Q

Examples type III diseases

A

1) Local immune complex disease
- Arthus reaction
- Temporary, in tissues
2) Acute-systemic immune complex disease
- Acute serum disease (7-10 days)
- Temporary, in body fluid
3) Chronic immune complex disease
- SLE (systemic lupus erythematosus)
- Maintained

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18
Q

Example type IV

A

1) Poison ivy contact
- Cathechol molecules (haptens) combined w/ skin proteins -> immunogenic and present MHC I becausethe skin proteins contain self antigen

2) Ni-induced contact dermatitis

3) Coeliac disease
- Gliadin Ag (protein) enter if surface of gut damaged
- Gliadin only immunogenic if tissue transglutaminase changes conformation of it (deaminates)
- HLA-DQ2 (!) can present deaminated gliadin peptide -> patients with this MHC have coeliac disease

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19
Q

Activated Th1 cells secrete:

A

1) Chemokines
- Recruit macrophages
2) TNFα and TNFβ
- Local tissue damage, adhesion molecules on endothel
3) IFNγ
- Activation macrophages, release of proinflammatory mediators
4) IL-3/GMCSF (Granulocyte-macrophage colony-stimulating factor)
- Monocytes in bone marrow

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20
Q

IFNγ effect on epithelial + mesenchymal cells

A

MHC II expression: Makes them able to present antigens with MHC II to CD4 Th1 cells

21
Q

Overfunction of immune system

A
  • Hypersensitivity

- Autoimmunity

22
Q

Underfunction of immune system

A
  • Immunedeficiencies
  • > Congenital (inherited)
  • > Acquired
  • > tumor
23
Q

Immunmodulation

A
  • Stimulation: vaccine

- Inhibition: transplantation

24
Q

FcγRIIA (CD32)

A
  • IgG
  • Low affinity
  • Cells: macroph, neutro, eos and platelets
  • Function: phagocytosis and cell activation
25
Q

FcγRIIB (CD32)

A
  • IgG
  • Low affinity
  • Cells: B cells
  • Function: feedback inhibition! (of B cells)
26
Q

FcγRIIIA (CD16)

A
  • IgG
  • Low affinity
  • Cells: NK
  • Function: ADCC (antibody-dep cellular cytotoxicity)
27
Q

FcεRI

A
  • IgE (monomeric)
  • High affinity
  • Cells: mast cells, eos and basophils
  • Function: Degranulation of mast and baso
28
Q

Class switch mediator IgG

A

INFγ

29
Q

Class switch mediator IgA

A

IL-5

30
Q

Class switch mediator IgE

A

IL-4 and IL-13

31
Q

IgE binding on mast cells

A

Can bind naked (!) to FcεRI on mast cells

- Naked=not bound to antigen

32
Q

Late mediators mast cells

A

Cytokines (IL-3, IL-4, IL-5, IL-6, TNFα)

  • IL-5 most important
  • De novo - trancribed in nucleus
33
Q

Effects of enzymes mast cells

A

Tissue remodeling

34
Q

Effects of cytokines and lipid mediators mast cells

A

Inflammation

*Lipid mediators: PAF, PGD2, LTC4

35
Q

Effects of biogenic amines and lipid mediators mast cells

A
  • Vascular leak
  • Bronchoconstriction
  • Intestinal hypermotility
  • Biogenic amines: histamines
  • Lipid mediators: PAF, PGD2, LTC4
36
Q

Intravenous antigen

A
  • Connective tissue mast cell

- Consequence: systemic anaphylaxis

37
Q

Subcutaneous antigen

A
  • Connective tissue mast cell

- Consequence: urtikaria (“elveblest”)

38
Q

Anaphylactic shock

A
  • Disseminated (spread) increased vascular permeability
  • Decreased blood pressure
  • Constricted airways
39
Q

Allergic triad

A

1) Atopic eczema
2) Hay fever
3) Bronchial asthma
* frequently occur in atopic patients

40
Q

Genetic features of asthma

A
  • Multifactorial: several genes+environment
  • Genetic heterogenecity: diff. allele combinations result in similar phenotypes
  • Many non-genetic components (found by twin-studies)
41
Q

Geographic distribution image hepatitis A and allergy

A

Mirror images

42
Q

Th1 effect and factors favoring Th1 phenotype

A

1) Effect: Protective immunity
2) Factors:
- Older siblings
- Early day care
- Tuberculosis, measles og hep A infection
- Rural environment

43
Q

Th2 effect and factors favoring Th2 phenotype

A

1) Effect: Allergic diseases (incl. asthma)
2) Factors:
- Widespread use of antibiotics
- Western lifestyle
- Urban environment
- Diet
- Sensitization to house-dust mites and cockroaches

44
Q

Type II hypersensitivity reaction characteristics

A
  • Against tissue/circulating cell
  • IgG
  • Ab against foreign Ag or autoantibody
  • Tissue-specific destruction
45
Q

Type II hypersensitivity reaction effects

A

1) Complement activation -> lysis
2) ADCC/FcγR mediated phagocytosis and/or killing
3) Inhibitory Ab’s (anti AchR: myasthenia gravis) + stimulatory antibodies (anti-TSH R: autoimmune thyroiditis)

46
Q

Type III hypersensitivity reaction characteristics

A
  • Soluble immune complexes (small/medium in size)
  • Continuous antigen stimulus
  • Platelet aggregation, local complement activation, chemotaxis, macrophage activation
  • > Inflammation!
  • Systemic tissue damage
47
Q

If too many circulating immune complexes (related to type III hypersensitivity)

A

1) Immune complexes deposited on vessel wall
2) C3a and C5a induce destruction (degran. mast cells + activation neutrophils)
- Diseases
=> Vasculitis (blood vessel walls)
=> Nephritis (renal glomeruli)
=> Arthritis (joint spaces)
*Systemic: f.eks SLE

48
Q

Type IV hypersensitivity reaction characteristics

A
  • Mediated by T cells
  • 2-3 days: “delayed type”
  • Induced mostly by small molecules: proteins, haptens
  • Results: Increased leukocyte adhesion, macrophage activation, chemotaxis, fibroblast activation, angiogenesis, local inflammation
49
Q

Penicillin-induced hypersensitive reactions

A

Type I: IgE => uritcaria, systemic anaphylaxis
Type II: IgM, IgG => hemolytic anemia
Type III: IgG => serum sickness, glomerulonephritis
Type IV: Tdht cells => contact dermatitis

Immunology Jenny (16 decks)

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