NUR 555 QUIZ 2: IMMUNOLOGY AND INFLAMMATION
QUESTIONS AND CORRECT ANSWERS PLUS
RATIONALE NEW UPDATE 2026-2027 SNHU
46 QUESTIONS
TABLE OF CONTENTS
# TOPIC
1 Differentiate the cellular and molecular mechanisms of innate versus adaptive immunity and predict
consequences of specific defects
2 Classify hypersensitivity reactions by immunopathogenesis and correlate each with representative clinical
disorders and diagnostic findings
3 Analyze laboratory immunologic panels to identify primary immunodeficiencies, autoimmune processes,
and transplant rejection patterns
4 Apply current immunomodulatory and anti-inflammatory pharmacotherapeutics with rationale grounded in
mechanism of action and cytokine biology
5 Evaluate the role of chronic inflammation in oncogenesis, cardiovascular disease, and metabolic
dysfunction
6 NUR 555 Quiz 2
7 Immunology and Inflammation Questions and Correct Answers plus Rationale New Update 2026
8 2027 SNHU
9 Foundations of Advanced Pathophysiology: Immunology and Inflammation
10 Applied Advanced Pathophysiology: Immunology and Inflammation
11 Advanced Advanced Pathophysiology: Immunology and Inflammation
12 Advanced Pathophysiology: Immunology and Inflammation Review
ABSTRACT
Page 1
,This study document brings together 46 carefully worded exam questions drawn from NUR 555
Quiz 2: Immunology and Inflammation Questions and Correct Answers plus Rationale New Update
2026-2027 SNHU, with the strongest emphasis placed on Differentiate the cellular and molecular
mechanisms of innate versus adaptive immunity and predict consequences of specific defects,
Classify hypersensitivity reactions by immunopathogenesis and correlate each with representative
clinical disorders and diagnostic findings, Analyze laboratory immunologic panels to identify
primary immunodeficiencies, autoimmune processes and and transplant rejection patterns. Every
item follows the wording style and level of reasoning you meet in the real paper, and each one is
paired with a clear rationale so the correct choice is never a guess. Work through the set at your
own pace, mark the questions that slow you down, then come back to them until the reasoning
feels automatic. Learners who revise this way walk into the exam room recognising the pattern
behind the questions instead of meeting them for the first time. Keep going - steady, honest
practice is what turns a difficult paper into a comfortable pass.
Q1 DIFFERENTIATE THE CELLULAR AND MOLECULAR MECHANISMS OF INNATE VERSUS
ADAPTIVE IMMUNITY AND PREDICT CONSEQUENCES OF SPECIFIC DEFECTS
A patient with recurrent pyogenic infections and poor wound healing is found to
have normal T-cell function but absent respiratory burst activity on
dihydrorhodamine testing. Which molecular defect best explains this pattern?
A. Deficiency of adenosine deaminase causing toxic purine accumulation in lymphocytes
B. Mutation in the gp91phox subunit of NADPH oxidase impairing superoxide generation
CORRECT
C. Defective CD40 ligand expression preventing immunoglobulin class switching
D. Absence of C5-C9 complement components blocking membrane attack complex formation
RATIONALE: Chronic granulomatous disease results from NADPH oxidase defects (commonly
gp91phox), preventing superoxide production and causing recurrent catalase-positive infections;
the normal DHR test is abnormal in CGD. Adenosine deaminase deficiency causes SCID (T-cell
defect), CD40L defect causes hyper-IgM syndrome, and C5-C9 defects cause recurrent
Neisseria infections, none matching the respiratory burst pattern.
Page 2
, Q2 DIFFERENTIATE THE CELLULAR AND MOLECULAR MECHANISMS OF INNATE VERSUS
ADAPTIVE IMMUNITY AND PREDICT CONSEQUENCES OF SPECIFIC DEFECTS
Which statement most accurately distinguishes the immunopathogenesis of type II
from type III hypersensitivity reactions?
A. Type II is IgE-mediated mast cell degranulation; type III is T-cell mediated cytotoxicity
B. Type II involves IgG/IgM binding to fixed tissue antigens; type III involves deposition of
circulating antigen-antibody immune complexes CORRECT
C. Type II is delayed and cell-mediated; type III is immediate and complement-independent
D. Type II requires sensitized T lymphocytes; type III requires only complement activation without
antibody
RATIONALE: Type II hypersensitivity is antibody-mediated against antigens fixed on cell surfaces
or matrix (e.g., Goodpasture, hemolytic transfusion reactions), whereas type III results from
soluble circulating immune complexes depositing in tissues (e.g., SLE, serum sickness). Options
A, C, and D misassign IgE (type I), T-cell mechanisms (type IV), or omit antibody entirely, which
is incorrect.
Q3 DIFFERENTIATE THE CELLULAR AND MOLECULAR MECHANISMS OF INNATE VERSUS
ADAPTIVE IMMUNITY AND PREDICT CONSEQUENCES OF SPECIFIC DEFECTS
A kidney transplant recipient develops rising creatinine and a biopsy showing
mononuclear interstitial infiltrate with tubulitis two weeks post-transplant. Which
mechanism predominates?
A. Preformed donor-specific antibodies causing hyperacute rejection
B. T-cell mediated recognition of donor MHC alloantigens initiating acute cellular rejection
CORRECT
C. Immune complex deposition from chronic antigenemia causing membranous nephropathy
D. Ischemia-reperfusion injury with neutrophil infiltration independent of alloimmunity
RATIONALE: Acute cellular rejection is driven by recipient T cells recognizing donor MHC (direct
allorecognition), producing interstitial lymphocytic infiltrate and tubulitis, typically days to weeks
post-transplant. Hyperacute rejection is antibody-mediated and occurs within minutes to hours,
immune complex disease is not the primary mechanism here, and ischemia-reperfusion injury
presents earlier with neutrophil predominance.
Page 3
QUESTIONS AND CORRECT ANSWERS PLUS
RATIONALE NEW UPDATE 2026-2027 SNHU
46 QUESTIONS
TABLE OF CONTENTS
# TOPIC
1 Differentiate the cellular and molecular mechanisms of innate versus adaptive immunity and predict
consequences of specific defects
2 Classify hypersensitivity reactions by immunopathogenesis and correlate each with representative clinical
disorders and diagnostic findings
3 Analyze laboratory immunologic panels to identify primary immunodeficiencies, autoimmune processes,
and transplant rejection patterns
4 Apply current immunomodulatory and anti-inflammatory pharmacotherapeutics with rationale grounded in
mechanism of action and cytokine biology
5 Evaluate the role of chronic inflammation in oncogenesis, cardiovascular disease, and metabolic
dysfunction
6 NUR 555 Quiz 2
7 Immunology and Inflammation Questions and Correct Answers plus Rationale New Update 2026
8 2027 SNHU
9 Foundations of Advanced Pathophysiology: Immunology and Inflammation
10 Applied Advanced Pathophysiology: Immunology and Inflammation
11 Advanced Advanced Pathophysiology: Immunology and Inflammation
12 Advanced Pathophysiology: Immunology and Inflammation Review
ABSTRACT
Page 1
,This study document brings together 46 carefully worded exam questions drawn from NUR 555
Quiz 2: Immunology and Inflammation Questions and Correct Answers plus Rationale New Update
2026-2027 SNHU, with the strongest emphasis placed on Differentiate the cellular and molecular
mechanisms of innate versus adaptive immunity and predict consequences of specific defects,
Classify hypersensitivity reactions by immunopathogenesis and correlate each with representative
clinical disorders and diagnostic findings, Analyze laboratory immunologic panels to identify
primary immunodeficiencies, autoimmune processes and and transplant rejection patterns. Every
item follows the wording style and level of reasoning you meet in the real paper, and each one is
paired with a clear rationale so the correct choice is never a guess. Work through the set at your
own pace, mark the questions that slow you down, then come back to them until the reasoning
feels automatic. Learners who revise this way walk into the exam room recognising the pattern
behind the questions instead of meeting them for the first time. Keep going - steady, honest
practice is what turns a difficult paper into a comfortable pass.
Q1 DIFFERENTIATE THE CELLULAR AND MOLECULAR MECHANISMS OF INNATE VERSUS
ADAPTIVE IMMUNITY AND PREDICT CONSEQUENCES OF SPECIFIC DEFECTS
A patient with recurrent pyogenic infections and poor wound healing is found to
have normal T-cell function but absent respiratory burst activity on
dihydrorhodamine testing. Which molecular defect best explains this pattern?
A. Deficiency of adenosine deaminase causing toxic purine accumulation in lymphocytes
B. Mutation in the gp91phox subunit of NADPH oxidase impairing superoxide generation
CORRECT
C. Defective CD40 ligand expression preventing immunoglobulin class switching
D. Absence of C5-C9 complement components blocking membrane attack complex formation
RATIONALE: Chronic granulomatous disease results from NADPH oxidase defects (commonly
gp91phox), preventing superoxide production and causing recurrent catalase-positive infections;
the normal DHR test is abnormal in CGD. Adenosine deaminase deficiency causes SCID (T-cell
defect), CD40L defect causes hyper-IgM syndrome, and C5-C9 defects cause recurrent
Neisseria infections, none matching the respiratory burst pattern.
Page 2
, Q2 DIFFERENTIATE THE CELLULAR AND MOLECULAR MECHANISMS OF INNATE VERSUS
ADAPTIVE IMMUNITY AND PREDICT CONSEQUENCES OF SPECIFIC DEFECTS
Which statement most accurately distinguishes the immunopathogenesis of type II
from type III hypersensitivity reactions?
A. Type II is IgE-mediated mast cell degranulation; type III is T-cell mediated cytotoxicity
B. Type II involves IgG/IgM binding to fixed tissue antigens; type III involves deposition of
circulating antigen-antibody immune complexes CORRECT
C. Type II is delayed and cell-mediated; type III is immediate and complement-independent
D. Type II requires sensitized T lymphocytes; type III requires only complement activation without
antibody
RATIONALE: Type II hypersensitivity is antibody-mediated against antigens fixed on cell surfaces
or matrix (e.g., Goodpasture, hemolytic transfusion reactions), whereas type III results from
soluble circulating immune complexes depositing in tissues (e.g., SLE, serum sickness). Options
A, C, and D misassign IgE (type I), T-cell mechanisms (type IV), or omit antibody entirely, which
is incorrect.
Q3 DIFFERENTIATE THE CELLULAR AND MOLECULAR MECHANISMS OF INNATE VERSUS
ADAPTIVE IMMUNITY AND PREDICT CONSEQUENCES OF SPECIFIC DEFECTS
A kidney transplant recipient develops rising creatinine and a biopsy showing
mononuclear interstitial infiltrate with tubulitis two weeks post-transplant. Which
mechanism predominates?
A. Preformed donor-specific antibodies causing hyperacute rejection
B. T-cell mediated recognition of donor MHC alloantigens initiating acute cellular rejection
CORRECT
C. Immune complex deposition from chronic antigenemia causing membranous nephropathy
D. Ischemia-reperfusion injury with neutrophil infiltration independent of alloimmunity
RATIONALE: Acute cellular rejection is driven by recipient T cells recognizing donor MHC (direct
allorecognition), producing interstitial lymphocytic infiltrate and tubulitis, typically days to weeks
post-transplant. Hyperacute rejection is antibody-mediated and occurs within minutes to hours,
immune complex disease is not the primary mechanism here, and ischemia-reperfusion injury
presents earlier with neutrophil predominance.
Page 3
