Immunology & Serology: Autoimmune & hypersensitivity
80 Immunology & Serology MCQs on Autoimmune & hypersensitivity with answers and explanations.
Which type of hypersensitivity is NOT mediated by antibody?
Types I-III involve IgE, IgG/IgM or immune complexes. Type IV is caused by sensitised T cells and macrophages.
Which is NOT a type of immune disorder?
Tolerance is the normal lack of response to self antigens.
Wheal-and-flare and bronchospasm in type I hypersensitivity are chiefly caused by release of:
Mast cell degranulation releases histamine, which causes vasodilation, increased permeability and smooth muscle contraction.
Which hypersensitivity type is mediated by T cells rather than antibody?
Type IV (delayed) reactions are driven by sensitized T cells and macrophages, as in tuberculin testing and contact dermatitis.
Failure of the immune system to distinguish self from non-self leads to:
Loss of self-tolerance produces autoimmune diseases.
Which of these is NOT an autoimmune disease?
SCID is a primary immunodeficiency. Graves, RA and Addison disease involve autoimmunity.
Inherited defects in innate or adaptive immune components cause:
Primary immunodeficiency results from genetic defects in immune components, causing recurrent infections.
Haemolytic disease of the fetus and newborn due to Rh incompatibility is which type of hypersensitivity?
Maternal anti-D IgG crosses the placenta and destroys fetal red cells.
Delayed hypersensitivity is characterized by an infiltrate mainly of:
Type IV reactions involve T cells and macrophages, as in the tuberculin test.
The Arthus reaction is which type of hypersensitivity?
The Arthus reaction is a local immune complex reaction with vasculitis.
Minutes after a bee sting, a child has wheezing and hypotension. Which antibody mediates this?
Anaphylaxis is type I: allergen cross-links IgE on mast cells, releasing histamine.
Which pair of conditions is driven by IgE bound to mast cells, i.e. immediate (type I) hypersensitivity?
Type I reactions follow allergen cross-linking of mast-cell IgE, as in anaphylaxis and atopy. Serum sickness/Arthus are immune-complex (type III); contact dermatitis and tuberculin reactions are T-cell mediated (type IV).
Within minutes of an intramuscular penicillin dose, a child develops hypotension, wheeze and airway swelling. Which immune mechanism best explains this?
Onset within minutes with shock and bronchospasm indicates mast-cell degranulation via drug-specific IgE. Serum sickness and Arthus reactions take hours to days to develop.
A patient develops an itchy vesicular rash 48 hours after wearing a nickel bracelet. Which arm of immunity mediates this reaction?
Allergic contact dermatitis is a delayed (type IV) reaction; hapten-modified proteins activate memory T cells, which peak at 48-72 h. Antibodies are not required.
A healthcare worker has 15 mm of induration 72 hours after an intradermal tuberculin injection. What does this reaction demonstrate?
The tuberculin reaction is delayed-type hypersensitivity showing T-cell memory to M. tuberculosis antigens from infection or BCG. It does not prove active disease.
A patient with thyroiditis has antibodies against thyroid peroxidase. This illustrates autoimmunity, meaning:
Autoimmunity is loss of self-tolerance, producing autoantibodies or autoreactive T cells against self antigens such as thyroid peroxidase.
A patient on procainamide develops arthralgia and a positive ANA. Which antibody is most typical of this condition?
Drug-induced lupus (procainamide, hydralazine, isoniazid) is characterised by anti-histone antibodies; anti-dsDNA and anti-Sm are usually absent. Symptoms resolve after the drug is stopped.
Anti-Scl-70 (topoisomerase I) antibody is most associated with:
Anti-Scl-70 is specific for diffuse cutaneous systemic sclerosis and is linked to interstitial lung disease. Anti-centromere is more typical of the limited form.
Antimitochondrial antibody (M2 subtype) is a highly specific marker for:
AMA-M2 against the pyruvate dehydrogenase complex is found in about 95% of primary biliary cholangitis. Primary sclerosing cholangitis is associated with atypical p-ANCA.
Antibodies that stimulate the TSH receptor and cause hyperthyroidism are characteristic of:
TSH-receptor stimulating antibodies (TRAb/TSI) mimic TSH and cause Graves disease. This is a type II (antibody-mediated, receptor-stimulating) mechanism. Hashimoto thyroiditis is associated with anti-TPO.