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Immunology Exam 2 > Type 1-3 Hypersensitivity Reactions > Flashcards

Type 1-3 Hypersensitivity Reactions Flashcards

1
Q

T1HS reaction mediated by

A

IgE

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2
Q

Atopic triad for T1HS

What are the other two?

A
  1. Asthma
  2. Atopic Dermatitis
  3. Allergic Rhinitis

*Food allergy, Insect bites/stings

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3
Q

Describe the two phases of allergic reactions and their components

A
  1. Sensitization phase
    1. Production of Th2 and IgE
    2. IgE binds to FcERI on mast cells and basophils
  2. Effector phase
    1. Acute reaction = degranulation
    2. Late phase reaction = chronic (also influx of Th2 Cd4 cells
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4
Q

What is causing the increased prevalence of allergies?

(three reasons)

A

​Hygeine Hypothesis

  • Th1–> Th2 shift
  • decreased Treg cell number and activity

(Also changes in indoor air quality and changes in lifestyle)

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5
Q

Mast cells differentiate in response to _____ and ______

What is their main receptor?

A

CD117 (c-kit) & **SCF **(stem cell factor)

  • FcERI (high affinity)
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6
Q

___ is the high affinity mast cell receptor, and ___ is the low affinity one

A

High = FcERI – Mast cells and basophils

Low = FcERII – BC, TC, monocytes, FDC’s

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7
Q

FcER1 receptors have __ domains and must ___ in order to activate mast cells

A

4 domains

crosslink

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8
Q

Preformed and de novo inflammatory molecules released by mast cells

A

Preformed

  • Enzymes (tryptase, chymase, etc)
  • Toxic Mediators (histamine, heparin)

De novo

  • Cytokines (TNFa, IL, GM-CSF)
  • Chemokine (CCL3)
  • Lipid mediator (Leukotrienes and PAF)
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9
Q

Histamine is formed from ____

It works by binding to _____

It is inhibited by _____

A

Histidine

H1 receptors

H1 antagonists

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10
Q

H1 receptors are present on…

A

endothelial cells

smooth muscle

nerve cells

hematopoetic cells

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11
Q

Basophils have a similar function to _____ (they express ____ )

They have a role in _______

A

Mast cells (express FceR1)

role in TH2 differentiation

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12
Q

Monteleukast (a.k.a. _____) inhibits what thing?

A

Monteleukast = Singulair®

Inhibits Leukotriene LTC4

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13
Q

Eosinophil granules rich in _________

Examples?

What stimulates the production of these granules?

A

Basic proteins

  • Major Basic Protein
  • Eosin. cationic protein
  • Neurotoxin

Stimulated by IL-5

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14
Q

Activated eosinophils express

A

FceR1

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15
Q

Degranulation of eosinophils is induced by…

A
  • Eotaxin
  • C5a
  • Antigens (via IgE…crosslinking of FceR1)
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16
Q

IL-12 drives differentiation of what?

What is produced after it differentiates?

A

Th0 -> Th1

Produces IFNg

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17
Q

IL-4 drives differentiation of what?

What is produced after differentiation?

A

Th0 –> TH2 cell

IL - 4, 5, 13

(involved in allergies)

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18
Q

Main driver for the isotype switch that causes:

IgM/IgD naive B cell –> IgE B cell

A

IL4

(IL13 plays a role too?)

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19
Q

How does IgE B cell decide if it wants to be a memory cell or plasma cell?

A

The path of differentiation depends on the cytokines present

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20
Q

What happens when TH0 cell isn’t really exposed to any of the previously mentioned factors (IL-12, IL-4)?

A

It becomes a Th17 cell and produces IL-17

21
Q

What is atopy/atopic syndrome?

A

Genetic predisposition to IgE production

(allergies tend to be familial, predisposition varies from person to person)

22
Q

5 properties if inhaled allergens

3 examples?

A
  1. Proteins (induce T cells)
  2. Proteases (distupt epith.)
  3. High solubility/stability
  4. Low molecular weight
  5. Low dose
  6. Contains peptides that bind MHC2

Pollen, dust mites, cockroach antigens

23
Q

Chronic manifestations of allergies

A
  1. Systemic anaphylaxis:
    1. IV entry
    2. Drugs, serum, venom, peanuts
    3. Edema, increased vascular perm., tracheal occlusion, shock
  2. Wheal and flare:
    1. SubQ
    2. Insect bites or during an allergy test
    3. Local increase in blood flow and vascular permeability
  3. Allergic rhinitis (hay fever)
    1. Inhaled
    2. Edema and irritation of the nasal mucosa
  4. Bronchial asthma
    1. Inhaled
    2. Bronchial constriction, increased mucous production, airway inflammation
  5. Food allergy
    1. Oral
    2. V/D, pruritis, urticaria, anaphylaxis
24
Q

When does a late phase reaction occur?

What is the chart measuring on the slide that shows early/late phase reactions?

A

after 6-8 hours

PEFR (peak expiratory flow rate)

25
Q

4 steps for sensitization to inhaled allergens

A
  1. First exposure
  2. Extraction of antigen
  3. Presentation to T-cell -> activation of Ag-specific T-cell
  4. Production of IgE (via IgE B-cells), and binding to mast cell
26
Q

Diagnostic measures for Allergies

A
  1. Skin testing (gold standard)
  2. Avoidance
  3. Ag-specific IgE
    1. RAST = Radioallergosorbent test
    2. ELISA
  4. Total serum IgE (not as reliable?)
27
Q

Allergy to penicillin can cause ___ or ___ reactions

A

Type 1 or Type 2 hypersensitivity reactions

28
Q

Allergy to penicillin steps

A
  1. Complement-coated penicillin modified RBCs are phagocytosed by MQ
  2. MQ present peptides and activate CD4 T cells to become Th2 cells
  3. B cells activated by antigen and Th2 cells
  4. plasma cells secrete penicillin-specific IgE (which arms mast cell)
  5. Penicillin-modified RBCs activate the armed mast cell = anaphylaxis
29
Q

Systemic anaphylaxis: Allergens and response pathway

A

Insect venom, drugs, food, IV route stuff

  1. Antigen gets into bloodstream
  2. Enters tissue
  3. Activates Connective tissue Mast cells
  4. Mast cell degranulation and release of inflammatory mediators
30
Q

Allergic rhinitis steps (4)

A
  1. Inhale Ag
  2. Activates local mast cells
  3. BV permeability and activation of epithelium
  4. Eosinophil recruitment
31
Q

Pathogenesis-es of asthma

A
  • Acute = Type 1 hypersensitivity
    • Mucosal mast cell captures antigen
    • releases inflammatory mediators (contract SM, increase mucous and BVP)
  • Chronic = Type 4 hypersensitivity
    • Chronic response mediated by cytokines + eosinophil products
32
Q

Extrinsic Asthma is mediated by ____

A

Extrinsic = IgE

= A classical Type 1 Hypersensitivity response

(Intrinsic = no IgE)

33
Q

Clinical Sx of asthma

A
  • Coughing, Weezing
  • Hypersensitive airways
  • Increased number of Goblet cells
34
Q

Tx of allergic reactions

A
  • Avoidance (best)
  • Desensitization
    • ​Increase Ag dose – shift to Th1 response or induce IL10/TGFb secreting Treg cells
  • Drugs
    • Inhibitors of inflammation (CS’s, Anti-LTC4, Chromolyn Sodium)
    • Bronchodilators
    • Antihistamines
    • Anti-IgE (omalizumab)
35
Q

Drug-induced blood cell dyscrasias-

related to _____

Idiosyncratic: often immune-mediated ( _____ most common)

A

Related to pharmacologic action of the drug

Thrombocytopenia most common

36
Q

Mechanism of antibody-mediated Blood cell destruction:

  1. Reaction type?
  2. Antibodies?
A
  1. Type 2 HS
  2. AB’s
    • Drug (hapten) specific
    • Antibody binds to cells in presence of drug or drug metabolite
    • True autoantibodies
    • Fibrinogen receptor (GP2b3a) antagonists
37
Q

Penicillin modifies proteins on ____ to create _____

A

human RBCs

foreign epitopes

38
Q

Production of anti-penicillin AB’s (4 steps)

A
  1. Complement coated penicillin-modified RBC’s are phagocytosed by MQ
  2. MQ present to CD4 cells to become Th2
  3. Th2 cells + antigen both result in B cell activation
  4. Plasma cells secrete anti-penicillin IgG (that then binds to the RBC)
39
Q

Lysis and phagocytosis of penicillin-modified RBC

A

Penicillin-specific IgG binds to proteins on RBC, which leads to:

  • Activation of complement factors C1-C9 = MAC formation
  • Activation of C1-C3 = covalent bonding of C3b = phagocytosis of the whole thing into a MQ cell
40
Q

erythroblastosis fetalis - first pregnancy

A
  1. Rh negative mom with RH+ baby
  2. Primary response, Low affinity IgM (and a little IgG) is made
  3. just a little RBC destruction from anti-Rh IgG (mom’s)
  4. Baby is born healthy
41
Q

Erythroblastosis fetalis - second pregnancy

A
  1. Rh negative mom with Rh positive baby (again.)
  2. Secondary immune response = high affinity IgG traverses the placenta into fetal circulation
  3. Massive RBC destruction by mom’s anti-Rh IgG
  4. Anemia in the baby
42
Q

Tx for Erythroblastosis Fetalis

A

anti-Rh IgG’s

(Just enough to bind to fetal RBC that are entering maternal circulation and trick’s mothers system into thinking it already has IgG’s against it so she doesn’t make more when the next baby comes)

43
Q

Coombs test

A

_Direct _

  • Use washed fetal RBC **coated with maternal antibody **
  • add coombs reagent (anti-human AB)

Indirect

  • Add Rh+ cells to maternal serum
  • add coombs reagent
44
Q

What is Coomb’s reagent

A

Rabbit anti-human antibody

45
Q

Arthus rxn is a ____ response

Induced by….

Example?

A

Localized response

…induced by injection of soluble antigen in pt. with pre-existing AB’s

Example = desensitization of IgE-mediated allergies

46
Q

Arthus reaction steps (4)

What is the end (tissue) result?

Over what amount of time does this occur?

A
  1. Local injected antigen in a patient with existing IgG
  2. Immune complex activates complement
  3. C5a binds to C5 receptor on mast cell
  4. Binding of immune complex to FcrIII receptor on Mast cell = degranulation

Result = Local inflammation, BV occlusion, fluid and protein release

*occurs over 1-2 hours

47
Q

T3HS reaction caused by _____

Clinical Sx depend on ____ and ____

Inflammation is induced by ____ and ______

A

Immune complexes (IgG + Ag)

Size and localization of IC’s

Complement activation and PMN’s

48
Q

3 Types and examples of systemic immune complex diseases (T3HS)

A

Serum sickness (repeated foreign protein injection)

Chronic infections (subacute bacterial endocarditis)

Chronic Autoimmune disease (RA, SLE)

49
Q

Results of IV, subQ, inhaled routes of T3HS reactions

A

IV = vasculitis, nephritis, arthritis

SubQ = arthus reaction in the perivascular area

Inhaled = Farmer’s lung

Immunology Exam 2 (11 decks)

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