MLT GlobeImmunology & Serology: Immune system principles – page 13
257 Immunology & Serology MCQs on Immune system principles with answers and explanations.
A naive T cell binds its specific peptide–MHC complex on a cell that lacks B7 costimulatory molecules. The most likely outcome is:
Signal 1 without signal 2 makes the T cell anergic, a mechanism of peripheral tolerance. Clonal expansion needs both signals; class switching is a B-cell event.
Which enzymes cut DNA at recombination signal sequences to start V(D)J recombination in developing lymphocytes?
RAG1 and RAG2 introduce double-strand breaks for V(D)J joining; their loss causes T-negative, B-negative SCID. TdT only adds random N-nucleotides at the joins.
Class switch recombination and somatic hypermutation in activated B cells both require:
AID deaminates cytidine in switch and variable-region DNA, starting both processes in germinal centres. RAG enzymes act earlier, during V(D)J recombination.
In the MHC class II pathway, the invariant chain (Ii) mainly serves to:
The invariant chain occupies the class II groove in the ER; in the endosome it is degraded to CLIP, which HLA-DM exchanges for exogenous peptide. Transport of cytosolic peptides into the ER is done by TAP.
Before starting abacavir for HIV, the laboratory is asked to test for which allele to prevent a serious hypersensitivity reaction?
HLA-B*57:01 carriers have a high risk of abacavir hypersensitivity, so screening is recommended before treatment. HLA-B27 relates to spondyloarthritis, not drug reactions.
Staphylococcal toxic shock syndrome toxin-1 activates up to 20% of all T cells because it:
Superantigens bridge MHC class II and certain Vβ chains without processing, stimulating many T cells and causing a cytokine storm. A normal peptide activates only rare specific clones.
Dendritic cells can present peptides from ingested (exogenous) antigens on MHC class I to activate CD8 T cells. This process is called:
Cross-presentation lets dendritic cells prime CD8 T cells against viruses or tumours that do not infect the dendritic cell itself. Normally exogenous antigen goes to MHC class II.
Which immunoglobulin classes lack a hinge region and instead have an extra heavy-chain constant domain (CH4)?
μ and ε heavy chains have four constant domains and no true hinge. IgG, IgA and IgD have three constant domains plus a flexible hinge.
Inherited variations in immunoglobulin constant regions between individuals of the same species, such as Gm markers on IgG, are called:
Allotypes are allelic differences within a species (e.g., Gm on γ chains, Km on κ chains). Isotypes are the class and subclass differences shared by all normal members of a species.
In adults, antibodies against bacterial capsular polysaccharides, such as pneumococcal capsule, are mainly of which IgG subclass?
Polysaccharide antigens mostly induce IgG2, so IgG2 deficiency predisposes to encapsulated bacterial infections. Protein antigens mainly induce IgG1 and IgG3.
Which IgG subclass has the longest hinge, the shortest half-life and the strongest ability to activate complement?
IgG3's long hinge makes it flexible and a strong C1q binder, but it has a half-life of only about 7 days. IgG1 is also a good activator but has a normal half-life.
In hybridoma production of monoclonal antibodies, HAT medium kills unfused myeloma cells because they:
Aminopterin blocks de novo nucleotide synthesis, so cells need the HGPRT salvage pathway; HGPRT-deficient myeloma cells die, while hybrids get HGPRT from the B cell. Unfused B cells die because of their limited life span.
A pregnant woman has positive Toxoplasma IgG and IgM. A high IgG avidity result on the same sample mainly indicates that:
IgG avidity rises with affinity maturation; high avidity means the infection was acquired months earlier (usually more than about 4 months). IgM can persist for many months, so it does not prove recent infection.
A child has haemolytic anaemia, thrombocytopenia and acute kidney injury without preceding diarrhoea. C3 is low and C4 is normal. Which defect is most likely?
Atypical haemolytic uraemic syndrome is often due to factor H defects, causing uncontrolled alternative pathway activation on endothelium (low C3, normal C4). C1 inhibitor deficiency causes angioedema with low C4.
In paroxysmal nocturnal haemoglobinuria, red cells lack CD59. The normal function of CD59 is to:
CD59 (membrane inhibitor of reactive lysis) prevents C9 from inserting and polymerising, so its loss allows MAC-mediated lysis. Accelerating convertase decay is the role of CD55 (DAF).
An infant has repeated severe pneumonia and bacteraemia from encapsulated bacteria. CH50 and AH50 are both zero, and C3 is undetectable. The most likely diagnosis is:
C3 is needed by all pathways for opsonisation and MAC formation, so its absence abolishes both CH50 and AH50 and causes severe pyogenic infections. C9 deficiency gives only low (not zero) lytic activity and mild disease.
A patient with glomerulonephritis has persistently very low C3 with normal C4. An autoantibody that stabilises the alternative pathway C3 convertase is found. This autoantibody is:
C3 nephritic factor binds C3bBb and protects it from decay, causing continuous C3 consumption; it is linked to C3 glomerulopathy. Anti-C1q antibodies relate to lupus nephritis and lower C4 as well.