This page contains the Answers to the weekly MCQ posted on the Home Page. To generate a list of all MCQ to date go Categories in the right column and click on MCQ.
Explanation: Unlike B- and T-cell receptors of the adaptive immune system, the innate TLR are germline encoded and do not undergo genetic rearrangement.
a) iii (inflammation); b) v (anti-helminth/ allergic response); c) iv (mucosal inflammation) d) i (promotion of B-cell antibody production e)ii (regulatory effects).
Explanation: C1 esterase inhibitor results in bradykinin accumulation in hereditary angiodema (HAE)
Explanation: Patients with Sjogren’s Syndrome have a 5-50X increased rate of lymphoma (2-9% of patients). These lymphomas are often generated in the mucosal associated lymphoid tissue (MALT) effected by the disease.
Explanation: The recent START RCT demonstrated reduced morbidity and mortality in patients with CD4+ T-cells >500 cells/micoL who commenced ART compared with patients who differed treatment.
Explanation: The MEFV gene encodes the Pyrin protein which is normally a regulator of the inflammasome. Mutations in MEFV leads to dysregulated activation of this pathway.
Explanation: Subcutaneous immunotherpay for peanut has been associated with patient mortality. All other features are part of a safe management plan. Peanut specific IgE can be measured by skin prick testing or ImmunoCAP assay (updated version of RAST).
Explanation: Type III hypersensitivity is characterised by pathology caused by Ag-Ab complexes that deposit in tissue. In SLE this classically occurs in skin, joints and kidneys.
Explanation: Deficiencies in C1q,C2 and C3 are associated with a Lupus-like syndrome, deficiencies in the complement MAC are associated with recurrent N. menigitis. Deficiencies in B-cells an Ab are associated with H. influenzae. Deficiency in C1 esterase inhibitor is associated with hereditary angiodema.
Explanation: Integrase inhibitors inhibit HIV DNA from integrating into the host genome by inhibiting the “integrase” enzyme.
Explanation: NK cells are part of the innate immune system. They detect virally infected cells that have down-regulated MHCI as an immune evasion mechanism. `NK cells activation by toll-like receptors is not well established. NK cells do not express T-cell receptors to bind MHCI/II+Ag or IgE.
Explanation: IVIG is an indicated treatment in ITP, Guillain-Barre Syndrome and Myasthenia Gravis, but not SLE.
Explanation: Natalizumab targets alpha-4 integrin preventing lymphocyte migration into the CNS. Alemtuzumab targets CD52 (CAMPATH) and is a pan-lymphocyte depleting agent more commonly used in solid organ transplant patients. Rituximab targets CD20+ B-cells and has proven efficacy in MS although is less effective than other first line agents. Infliximab targets TNF-alpha and is used in inflammatory conditions such as Rhematoid arthritis, it has no known role in the treatment of MS.
Explanation: GPA is associated with C-ANCA shown below:
Explanation: 10% of patients have low TPMT activity and use of Azathioprine here risks significant toxicity
Explanation: Corticosteroids downreg adhesion molecules on immature (band form) neutrophils in the marginal compartment, releasing them into the circulation.
Explanation: These “checkpoint inhibitors” target T-cell inhibitory receptors CTLA-4 (Ipilimumab) and Program Death-1 (PD-1; Pembrolizumab and Nivolumab). This results in promoting unbridled T-cell activation and anti-tumour immunity.
Explanation: Omalizumab was first licensed for use in allergic asthma, however it also has efficacy in first-line treatment-refractory chronic idiopathic urticaria and will likely be PBS-listed for this in 2017. There is no current evidence for its use in anaphylaxis or allergic rhinitis.