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19 BMD 430 lecture 19

1.

Define hypersensitivity.

An exaggerated or inappropriate immune response to an antigen that causes tissue damage; classified into Types I–IV

2.

Which type of immunity primarily functions against parasitic infections?
A. Type 1
B. Type 2
C. Type 3
D. Type 4

B. Type 2

3.

Which of the following is not a characteristic of parasites?
A. Large multicellular organisms
B. Easily phagocytosed
C. Complex eukaryotic structure
D. Evasive immune strategies

B. Easily phagocytosed

4.

What is the body’s general strategy to eliminate a parasite?

Type 2 immunity involving IgE, mast cells, and eosinophils that promote parasite expulsion through mucus, coughing, or peristalsis.

5.

Which cytokines are key mediators of Type 2 immunity?
A. IL-2, IFN-γ, TNF
B. IL-4, IL-5, IL-13
C. IL-6, IL-8, IL-12
D. IL-10, IL-17, IL-23

B. IL-4, IL-5, IL-13

6.

Why is switching from IgE to IgG important during allergic responses?

IgG4 blocks allergens from binding IgE, preventing mast cell activation and chronic inflammation.

7.

Which antibody binds most tightly to FcεRI receptors on mast cells?
A. IgA
B. IgE
C. IgG4
D. IgM

B. IgE

8.

What is Ozalimumab, and how does it work?

A monoclonal antibody that binds free IgE to prevent mast cell activation; slightly increases infection risk due to lower parasite exposure.

9.

Which of the following cells release major basic protein to kill parasites?
A. Mast cells
B. Basophils
C. Eosinophils
D. Dendritic cells

C. Eosinophils

10.

Describe how mast cells contribute to defense against parasites.

Tissue-resident cells with granules of histamine and proteases; when IgE is cross-linked, they degranulate and trigger inflammation and expulsion responses.

11.

Which histamine receptor is primarily responsible for inflammation and smooth muscle contraction?
A. H1
B. H2
C. H3
D. H4

A. H1

12.

What are secondary mediators, and how does aspirin affect them?

Lipid mediators like prostaglandins and leukotrienes produced after degranulation; aspirin blocks COX enzymes, reducing prostaglandin synthesis.

13.

What type of molecule is most likely to act as an allergen?
A. Large insoluble protein
B. Small soluble protein structurally similar to parasite antigen
C. Nucleic acid fragment
D. Lipid antigen

B. Small soluble protein structurally similar to parasite antigen

14.

Explain the process of sensitization.

Initial exposure to allergen → Th2 differentiation → B cell class switching to IgE → IgE binds mast cells, priming them for re-exposure

15.

Which environmental factor decreases allergy risk?
A. Antibiotic use
B. Excessive hygiene
C. Early parasite exposure
D. Urban pollution

C. Early parasite exposure

16.

Name three genes or proteins that, when altered, can affect allergy susceptibility.

IL-4R, STAT6, Filaggrin, HLA, or FCER1A

17.

The “wheal and flare” reaction in skin testing is caused by:
A. Complement activation
B. Mast cell degranulation
C. Cytotoxic T cells
D. Neutrophil infiltration

B. Mast cell degranulation

18.

Differentiate between the early and late phases of an allergic response.

Early phase = histamine release within minutes; Late phase = cytokine-mediated inflammation hours later

19.

A patient eats peanuts and experiences hypotension, airway constriction, and swelling.

  • What type of hypersensitivity is this?
  • What treatment should be given?

Type I hypersensitivity (anaphylaxis); treated with epinephrine, which constricts vessels and relaxes airways.

20.

Which of the following is not a symptom of allergic asthma?
A. Airway constriction
B. Mucus production
C. IL-13 activity
D. Complement deposition

D. Complement deposition

21.

Describe how desensitization immunotherapy works

Gradual allergen exposure increases IgG4 and reduces IgE, leading to immune tolerance

22.

Type II hypersensitivity is primarily mediated by:
A. T cells
B. IgE
C. IgG or IgM
D. Immune complexes

C. IgG or IgM

23.

A newborn develops anemia due to maternal antibodies crossing the placenta.

  • What is this condition?
  • What type of hypersensitivity is it?

Erythroblastosis fetalis; Type II hypersensitivity.

24.

Which mechanism mediates Type III hypersensitivity?
A. Antibody-dependent cellular cytotoxicity
B. Immune complex deposition
C. Mast cell degranulation
D. Delayed T cell response

B. Immune complex deposition

25.

What is serum sickness, and what causes it?

A Type III reaction caused by immune complex deposition after exposure to foreign serum; symptoms include vasculitis, arthritis, and nephritis

26.

Which of the following is not associated with Type IV hypersensitivity?
A. Tuberculin skin test
B. Contact dermatitis
C. Serum sickness
D. Poison ivy rash

C. Serum sickness

27.

Explain the difference between the sensitization and effector phases of DTH.

Sensitization = memory Th1 cells form; Effector = re-exposure causes cytokine release and macrophage recruitment.

28.

Define chronic inflammation and explain why it is problematic.

Persistent immune activation causes tissue damage, fibrosis, and potential organ failure.