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MI2.1-8 | Immunology: Basic, Applied & Immunological Disorders — Graded Quiz

Graded 12 questions · Untimed · 2 attempts

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Q1 MI2.1 1 pt

A 38-year-old man with poorly controlled type 2 diabetes presents with a spreading cellulitis and soft-tissue gas on X-ray, consistent with necrotising fasciitis caused by Streptococcus pyogenes. His WBC is 2.1 × 10⁹/L (neutropenia). The impaired innate immune response in this patient most likely leads to failure of which early antimicrobial mechanism?

A Lack of antigen presentation by dendritic cells to naïve T cells
B Failure of rapid phagocytosis and oxidative burst against bacteria at the infection site
C Absent IgG class switching due to loss of T helper cell co-stimulation
D Impaired NK cell recognition of MHC-I upregulation on infected fibroblasts

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Q2 MI2.2 1 pt

A 70-year-old man with myeloma is treated with daratumumab (anti-CD38 monoclonal antibody). Three months later, his anti-SARS-CoV-2 vaccine antibody titres are undetectable despite two doses. Which mechanism best explains this vaccine failure?

A Daratumumab blocks T cell receptor signalling by depleting CD38+ T regulatory cells
B CD38+ plasma cells, including long-lived antibody-secreting cells, are depleted by daratumumab
C Anti-CD38 antibodies cross-react with spike protein epitopes, neutralising vaccine antigen
D Myeloma proteins (paraprotein) competitively inhibit antigen-antibody binding in ELISA assay

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Q3 MI2.4 1 pt

A 19-year-old student from Nagaland returns from a 3-month NGO placement in sub-Saharan Africa with fever, splenomegaly, and haemolytic anaemia. Blood smear shows Plasmodium falciparum. Why do repeated malaria infections fail to establish sterile immunity, unlike measles where one infection gives lifelong protection?

A Malaria infects B cells and destroys them, preventing memory formation
B P. falciparum undergoes antigenic variation (PfEMP1 switching) that evades existing antibody responses
C Malaria parasites suppress complement activation by producing serine proteases
D Malaria exclusively causes Type III hypersensitivity, which does not generate immunological memory

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Q4 MI2.4 1 pt

A 45-year-old woman with rheumatoid arthritis (RA) starts therapy with a TNF-α inhibitor (etanercept). Within 6 months, she develops miliary tuberculosis. The drug's mechanism that predisposed her to reactivation TB is BEST described as:

A TNF-α blockade impairs neutrophil recruitment to the lung alveoli
B TNF-α is required for granuloma formation and maintenance; its blockade leads to granuloma dissolution and mycobacterial dissemination
C Etanercept causes IgG class switching away from opsonising antibodies against M. tuberculosis
D TNF-α blockade prevents CD8+ T cell recognition of M. tuberculosis antigens on MHC-I

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Q5 MI2.7 1 pt

A 28-year-old woman with SLE (anti-dsDNA positive, low C3/C4) develops a new purpuric rash, arthritis, and glomerulonephritis. The pathology demonstrates immune complex deposition in glomeruli and vessel walls. Which complement component should be measured to assess ongoing consumption by the classical pathway in this flare?

A Factor B and Factor D (properdin pathway components)
B C1q, C4, and C3 (classical pathway components sequentially consumed)
C Mannose-binding lectin (MBL) and MASP-1
D C5 to C9 (membrane attack complex components only)

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Q6 MI2.7 1 pt

A 3-month-old girl with recurrent oral candidiasis, Pneumocystis jirovecii pneumonia, and persistent rotavirus diarrhoea has no detectable lymphocytes on blood smear. Adenosine deaminase (ADA) enzyme activity is absent. What is the pathophysiological mechanism of immunodeficiency?

A ADA deficiency causes IgG subclass deficiency by blocking B cell class switching
B ADA deficiency leads to accumulation of deoxyadenosine toxic to both T and B lymphocytes
C ADA deficiency causes neutrophil chemotaxis failure via impaired cAMP signalling
D ADA deficiency prevents class II MHC expression on thymic epithelium

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Q7 MI2.8 1 pt

A 55-year-old man with end-stage renal disease receives a cadaveric renal transplant. Pre-transplant cross-match (recipient serum + donor lymphocytes) shows positive T-cell cross-match. Despite calcineurin inhibitor therapy, the kidney is rejected within 2 weeks. What is the immunological basis for this rapid hyperacute or accelerated rejection?

A New generation of alloreactive CD4+ T cells that recognise donor MHC-II antigens via indirect pathway
B Pre-formed donor-specific antibodies (DSAs) binding to donor endothelium and activating complement and ADCC
C NK cell-mediated killing of donor cells due to mismatch at killer immunoglobulin-like receptors (KIRs)
D Regulatory T cell depletion by calcineurin inhibitor allowing uncontrolled allo-reactive response

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Q8 MI2.5 1 pt

A laboratory technician performs a Widal test on a sample from a patient with 10 days of fever. Results: O antigen titre 1:160, H antigen titre 1:160. A sample from the same patient taken 7 days earlier showed O titre 1:20, H titre 1:80. How should these results be interpreted?

A The H titre rise is significant; the O titre rise is non-specific and can be ignored
B A fourfold or greater rise in O antigen titre over 7 days is significant and supports current active typhoid infection
C Both titres are non-significant; repeat testing at 1:320 threshold is required
D Rising H titre confirms recent enteric fever; a static O titre suggests prior vaccination

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Q9 MI2.2 1 pt

A 22-year-old man develops urticaria and facial angioedema 30 minutes after eating prawns at a beach restaurant in Goa. His serum IgE level is markedly elevated and a skin prick test is positive for shrimp tropomyosin. The class of antibody mediating this response is produced by which B-cell differentiation event?

A T-independent antigen stimulation of marginal zone B cells producing IgE directly
B IL-4 and IL-13 driven class-switch recombination from IgM to IgE in Th2-polarised germinal centres
C Somatic hypermutation increasing IgE affinity without class switching
D Antigen-independent pre-commitment of B cells in bone marrow to IgE secretion

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Q10 MI2.6 1 pt

Maharashtra has achieved 95% measles vaccination coverage over 10 years. Although some unvaccinated individuals remain, measles outbreaks have not occurred in the region. Which concept best explains protection of the unvaccinated individuals?

A Cross-reactive immunity from other paramyxovirus infections
B Herd immunity reducing pathogen transmission below the threshold needed to sustain an outbreak
C Passive antibody transfer from vaccinated mothers protecting adult unvaccinated individuals
D Natural attenuation of measles virus to lower virulence over time

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Q11 MI2.8 1 pt

A 50-year-old man with hepatocellular carcinoma (HCC) has tumour tissue examined by immunohistochemistry. α-fetoprotein (AFP) is strongly expressed. Which category of tumour antigen does AFP represent, and what is its significance for immune surveillance and clinical use?

A Tumour-specific antigen (TSA) found only in HCC, recognised by cytotoxic T cells as a neoantigenic mutation product
B Tumour-associated antigen (TAA) — a foetal protein re-expressed in HCC, useful as a serum biomarker but poorly immunogenic due to central tolerance
C Cancer-germline antigen expressed in HCC through demethylation of silenced germline genes
D Oncoviral antigen expressed because HCC is caused exclusively by HBV integration into AFP gene

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Q12 MI2.7 1 pt

A 16-year-old girl develops a malar rash, joint pain, and haematuria. ANA and anti-dsDNA antibodies are positive. Renal biopsy shows mesangial and subendothelial immune deposits. The laboratory confirms complement C3 level is 42 mg/dL (normal 90-180 mg/dL). Which type of hypersensitivity reaction is primarily responsible for the renal pathology?

A Type I — IgE-mediated mast cell degranulation causing mesangial inflammation
B Type II — IgG antibodies directly binding glomerular basement membrane antigens
C Type III — circulating immune complex deposition activating complement and recruiting neutrophils
D Type IV — Th1 CD4+ T cells and macrophages directly infiltrating glomeruli

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