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MCQs on Rheumatoid Arthritis, Lupus Nephritis, IBD, and Heart Disease


Citrullination is catalyzed by peptidyl arginine deaminase (PAD).Which of the following properties associated with PAD are true:

a. Patients with RA have specific PAD polymorphisms
b. Smoking induces PAD expression in the lungs
c. PAD activity is promoted by NETosis in RA
d. Inflammatory signals (e.g. TNF? or infections) augment its activityInflammatory signals (e.g. TNF alpha or infections) augment its activity
e. All of the above

All of these cytokines induce osteoclast differentiation except:

a. TGF?
b. IL-1
c. RANK-ligand
d. IL-6
e. TNF?

Which of the following is true about SLE nephritis?

a. It generally affects more males
b. There are different levels of severity
c. It is not associated with increased mortality
d. It generally affects only young patients
e. All of the above

Which of these statements is true about complement dysregulation in SLE?

a. It is associated with increased type II interferon signals
b. It may be activated by C3/4 nephritic factors, which are antibodies that inhibit C3 convertase
c. It involves activation of immune complexes resulting in aggregation of C1q complexes and the activation of the classical complement pathway
d. It can be activated by only the alternative complement pathway
e. All of the above

Rheumatoid arthritis results in:

a. Increased mortality via cardiovascular disease
b. Inflammation in the lungs, and synovial joints
c. Citrullination of proteins by peptidyl arginine deaminases
d. Elevated TNF? and IL-1? levels
e. All of the above

The inflammatory pannus in rheumatoid arthritis has all of the following except:

a. Increased M2 macrophage polarization
b. Decreased Treg function
c. Increased osteoclast activation
d. Increased RANK ligand activation by IL-6 signalling
e. Increased IL-12-/23


Early in the disease, lymphopenia in SLE is characterized by...

a. Decreased cellularity in the bone marrow
b. Increased autoantibodies targeting CD4 T cells
c. Increased Treg function
d. Increased apoptosis of neutrophils


Which of the following defects could lead to chronic inflammation in patients with inflammatory bowel disease?

a. Decreased mucus secretion
b. A lack of microbial-produced short chain fatty acids
c. Decreased anti-microbial peptide secretion
d. Ineffective autophagy by epithelial cells
e. All of the above


Which of the following statement is correct?

a. Inactivation of IFN? results in a pro-inflammatory state and the development of inflammatory bowel disease
b. A link between specific genetic markers and the development of Crohn's disease has not yet been identified
c. Inflammation in patients with inflammatory bowel disease is thought to be secondary to an infection by a gut pathogen
d. Mutations in the NOD/CARD 15 gene result in failure of NF-?B activation and a dysfunctional innate immune response

Which of the following statements is incorrect?

a. Gut microbes can invoke either a pro-inflammatory or anti-inflammatory immune response
b. Inflammatory mediators released into the gut lumen will cause a bloom of pathobionts and kill resident anaerobic bacteria
c. A tolerant immune response in the gut is characterized by increased levels of IL-6 and IL-12
d. Maintenance of gut homeostasis involves interactions between epithelial cells, dendritic cells, and T cells


Which of these statements is not true:

a. Modified LDL results from a mutation
b .Modified LDL is a DAMP that activates TLRs
c. A peptide from modified LDL is an autoantigen
d. Modified LDL activates endothelial cells via LOX-1 binding


Plaque rupture is due to:

a. Vascular smooth muscle cell (VSCM) apoptosis
b. Sustained inflammation
c. Production of proteases by immune cells
d. All of the above


Which statement is not true: After MI,

a. Resident macrophages help clean up debris and promote repair
b. Leukotrienes are important for resolving inflammation
c. Neutrophils contribute to the generation of ROS
d. Fibroblasts form a collagen scar


Which of the following process is not a target for post-MI treatment?
a. Blocking efferocytosis
b. Blocking ROS and DAMPs
c. Blocking adaptive immunity
d. Blocking proinflammatory cytokines

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