Unit 5: Cytokines; The complement system - Practice Quiz

BTS511 — Immunology 60 Questions
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1 What are cytokines?

overview of cytokines Easy
A. Enzymes that digest food in the stomach
B. Lipid molecules that store energy in cells
C. Large structural proteins found only in muscle tissue
D. Small secreted proteins that mediate and regulate immunity and inflammation

2 Cytokines produced by lymphocytes are often specifically called:

overview of cytokines Easy
A. Hormones
B. Antibodies
C. Antigens
D. Interleukins if they act between leukocytes

3 When a cytokine acts on the same cell that secreted it, this action is called:

properties and functions of cytokines Easy
A. Exocrine
B. Paracrine
C. Autocrine
D. Endocrine

4 The property of a single cytokine having many different biological effects is known as:

properties and functions of cytokines Easy
A. Redundancy
B. Synergy
C. Antagonism
D. Pleiotropy

5 When two or more cytokines produce the same effect, this is termed:

properties and functions of cytokines Easy
A. Cascade induction
B. Pleiotropy
C. Specificity
D. Redundancy

6 Which term describes the combined effect of two cytokines being greater than the sum of their individual effects?

properties and functions of cytokines Easy
A. Antagonism
B. Autocrine action
C. Synergy
D. Redundancy

7 In the JAK-STAT pathway, what does the abbreviation JAK stand for?

JAK-STAT pathway Easy
A. Juxta-active kinase
B. Junction-associated kinase
C. Joint activation kinase
D. Janus kinase

8 In the JAK-STAT signaling pathway, STAT proteins ultimately act as:

JAK-STAT pathway Easy
A. Cell surface receptors
B. Transcription factors that regulate gene expression in the nucleus
C. Membrane lipids
D. Extracellular enzymes

9 What is the first event that triggers the JAK-STAT pathway?

JAK-STAT pathway Easy
A. Formation of the membrane attack complex
B. Degradation of DNA in the nucleus
C. Binding of a cytokine to its cell surface receptor
D. Release of antibodies into the blood

10 JAK proteins activate STAT proteins by adding which chemical group to them?

JAK-STAT pathway Easy
A. A sugar group
B. A phosphate group
C. An acetyl group
D. A methyl group

11 The complement system is primarily a part of which type of immunity?

overview of the complement system Easy
A. None of the immune system
B. Innate immunity
C. Passive immunity only
D. Only adaptive immunity

12 The complement system is composed mainly of:

overview of the complement system Easy
A. Red blood cells
B. A group of plasma proteins that act in a cascade
C. DNA molecules
D. Lipid membranes

13 Which organ is the primary site of synthesis for most complement proteins?

overview of the complement system Easy
A. The liver
B. The spleen
C. The kidney
D. The pancreas

14 Which of the following is NOT one of the three main pathways of complement activation?

complement system pathways Easy
A. The alternative pathway
B. The digestive pathway
C. The classical pathway
D. The lectin pathway

15 The classical complement pathway is typically initiated by:

complement system pathways Easy
A. Binding of mannose by MBL
B. Direct contact with sunlight
C. Antigen-antibody complexes binding C1
D. Spontaneous hydrolysis of C3

16 The lectin pathway is activated by which protein recognizing carbohydrates on microbes?

complement system pathways Easy
A. Factor H
B. Mannose-binding lectin (MBL)
C. Properdin
D. C1q

17 Which complement component is central to all three activation pathways?

complement system pathways Easy
A. Factor B
B. C3
C. C1q
D. C9

18 Why does the complement system require tight regulation?

regulation of the complement system Easy
A. To increase blood sugar levels
B. To digest dietary proteins
C. To produce red blood cells
D. To prevent damage to the body's own healthy cells

19 Which regulatory protein helps protect host cells by acting as a cofactor for the inactivation of C3b?

regulation of the complement system Easy
A. C5
B. MBL
C. Factor H
D. Properdin

20 The final assembled complement structure that creates pores in target cell membranes is called the:

biological consequences of the complement system Easy
A. Major histocompatibility complex
B. Membrane attack complex (MAC)
C. Antigen-binding site
D. T-cell receptor complex

21 A researcher observes that a single cytokine, when secreted, induces different biological effects in two different target cell types. Which property of cytokines best explains this observation?

overview of cytokines Medium
A. Pleiotropy
B. Redundancy
C. Antagonism
D. Synergy

22 A cytokine acts on the same cell that secreted it, altering that cell's own behavior. This mode of action is described as:

overview of cytokines Medium
A. Juxtacrine
B. Endocrine
C. Autocrine
D. Paracrine

23 Two cytokines are administered together and produce a combined effect greater than the sum of their individual effects. This phenomenon is termed:

properties and functions of cytokines Medium
A. Redundancy
B. Cascade induction
C. Synergy
D. Pleiotropy

24 A patient's Th1 response is being suppressed by cytokines from Th2 cells. IL-10 produced by Th2 cells inhibits cytokine production by Th1 cells. This inhibitory relationship illustrates cytokine:

properties and functions of cytokines Medium
A. Antagonism
B. Synergy
C. Autocrine signaling
D. Pleiotropy

25 Which functional class of cytokines is chiefly responsible for directing the migration of leukocytes to sites of infection along a concentration gradient?

properties and functions of cytokines Medium
A. Interferons
B. Tumor necrosis factors
C. Chemokines
D. Colony-stimulating factors

26 In the JAK-STAT pathway, what is the immediate event that follows cytokine binding to its receptor and receptor dimerization?

JAK-STAT pathway Medium
A. Direct phosphorylation of DNA
B. Transphosphorylation of associated JAK kinases
C. Degradation of STAT proteins
D. Release of second messengers like cAMP

27 After STAT proteins are phosphorylated by JAKs, what enables them to bind DNA and regulate transcription?

JAK-STAT pathway Medium
A. Binding to G-protein coupled receptors
B. Ubiquitination and proteasomal processing
C. Cleavage by caspases into active fragments
D. Dimerization via SH2 domains and translocation to the nucleus

28 A mutation abolishes SOCS (Suppressor of Cytokine Signaling) protein function. What is the most likely consequence for JAK-STAT signaling?

JAK-STAT pathway Medium
A. Prolonged, uncontrolled signaling due to loss of negative feedback
B. Complete inability to activate STAT proteins
C. Constitutive dephosphorylation of all JAKs
D. Failure of cytokines to bind their receptors

29 The complement system is described as a group of proteins that circulate mostly in an inactive form. What best describes how these proteins become functionally active?

overview of the complement system Medium
A. Sequential proteolytic cleavage in a cascade
B. Simultaneous binding of all components to antigen
C. Conformational change without cleavage
D. Reversible phosphorylation by kinases

30 Which liver-derived complement component is present in the highest concentration in serum and is central to all three activation pathways?

overview of the complement system Medium
A. C1q
B. C3
C. Factor B
D. C9

31 The classical pathway is typically initiated when C1q binds to which structure?

complement system pathways Medium
A. Mannose residues on microbial surfaces
B. Lipopolysaccharide directly
C. Antigen-bound IgG or IgM antibodies
D. Spontaneously hydrolyzed C3

32 The lectin pathway is distinguished from the classical pathway primarily by its:

complement system pathways Medium
A. Requirement for antigen-antibody complexes
B. Initiation by mannose-binding lectin recognizing microbial carbohydrates
C. Use of Factor D as its initiating protease
D. Independence from C3 activation

33 Which enzyme complex functions as the C3 convertase of the classical and lectin pathways?

complement system pathways Medium
A. C5b6789
B. C4b2a
C. C4b2a3b
D. C3bBb

34 In the alternative pathway, the C3 convertase C3bBb is stabilized against rapid decay by which protein?

complement system pathways Medium
A. Decay-accelerating factor
B. Properdin (Factor P)
C. C1 inhibitor
D. Factor I

35 The membrane attack complex (MAC) forms a lytic pore in target cells. Which component polymerizes to complete the transmembrane channel?

complement system pathways Medium
A. C3b
B. Factor B
C. C9
D. C4a

36 A deficiency in C1 inhibitor (C1-INH) leads to hereditary angioedema. This reflects that C1-INH normally functions to:

regulation of the complement system Medium
A. Bind and neutralize C5a
B. Cleave C3b into inactive fragments
C. Inactivate C1r and C1s proteases
D. Accelerate decay of C3bBb

37 Patients with paroxysmal nocturnal hemoglobinuria (PNH) lack GPI-anchored regulators such as CD59 on red cells. Which consequence directly results from loss of CD59?

regulation of the complement system Medium
A. Inability to form C3 convertase
B. Overproduction of anaphylatoxins
C. Failure to activate the classical pathway
D. Uncontrolled MAC formation causing red cell lysis

38 Factor I requires cofactors such as Factor H or MCP to perform which regulatory function?

regulation of the complement system Medium
A. Polymerization of C9 into pores
B. Binding of C1q to antibodies
C. Proteolytic cleavage and inactivation of C3b
D. Stabilization of the C5 convertase

39 The complement fragments C3a, C4a, and C5a are collectively known as anaphylatoxins because they:

biological consequences of the complement system Medium
A. Neutralize bacterial toxins directly
B. Form the membrane attack complex
C. Opsonize pathogens for phagocytosis
D. Trigger mast cell degranulation and increase vascular permeability

40 Coating of a pathogen with C3b to enhance its uptake by phagocytes bearing complement receptors is an example of:

biological consequences of the complement system Medium
A. Cytolysis
B. Chemotaxis
C. Neutralization
D. Opsonization

41 A cytokine binds its receptor with a in the picomolar range and exerts biological effects at concentrations far below those needed to saturate all receptors on a cell. Which property of cytokines best explains why such low occupancy can trigger a full response?

overview of cytokines Hard
A. Cytokines bind irreversibly, so occupancy is permanent once initiated
B. Receptor number is fixed and non-inducible, preventing any amplification of signal
C. Cytokines act only in an endocrine manner, ensuring uniform systemic concentrations
D. High-affinity receptors coupled to signal amplification cascades allow near-maximal responses at low fractional occupancy

42 The terms pleiotropy and redundancy describe overlapping cytokine behaviors. Which experimental result most directly demonstrates redundancy rather than pleiotropy?

properties and functions of cytokines Hard
A. One cytokine blocks the action of another cytokine on the same target
B. One cytokine induces the synthesis of a second cytokine in a cascade
C. A single cytokine induces class switching in B cells and growth arrest in a different cell type
D. Knockout of a single cytokine produces no phenotype because another cytokine induces the same effect on the target cell

43 IL-2 receptor exists as a low-affinity ( chain alone), intermediate-affinity (), and high-affinity () form. A resting T cell expressing only chains is exposed to physiological IL-2. What is the most likely outcome?

properties and functions of cytokines Hard
A. Maximal proliferation, because the complex is the true signaling unit
B. No signaling at all, because the chain is the sole signal transducer
C. Immediate apoptosis, because IL-2 without chain is toxic
D. Minimal response, because the intermediate-affinity receptor requires higher IL-2 concentrations than are physiologically present

44 A patient has a loss-of-function mutation in the common gamma chain () shared by IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21 receptors. Which downstream molecular consequence best explains the resulting X-linked SCID phenotype?

JAK-STAT pathway Hard
A. Loss of JAK2 recruitment blocking erythropoietin signaling only
B. Inability of STAT5 to be dephosphorylated, causing prolonged signaling
C. Constitutive activation of JAK3 leading to uncontrolled lymphocyte proliferation
D. Failure to activate JAK3, which docks on , abolishing STAT signaling for multiple lymphopoietic cytokines

45 In the canonical JAK-STAT pathway, which sequence correctly orders the molecular events after ligand binding?

JAK-STAT pathway Hard
A. Receptor dimerization → STAT docking → STAT phosphorylation → JAK activation → nuclear translocation → receptor phosphorylation
B. STAT dimerization → receptor dimerization → JAK activation → STAT docking → nuclear translocation → gene transcription
C. JAK transphosphorylation → receptor dimerization → STAT dimerization → STAT docking → nuclear translocation → receptor phosphorylation
D. Receptor dimerization → JAK transphosphorylation → receptor tyrosine phosphorylation → STAT docking via SH2 → STAT phosphorylation → STAT dimerization → nuclear translocation

46 SOCS (suppressor of cytokine signaling) proteins provide negative feedback in JAK-STAT signaling. Which mechanism is NOT a recognized action of SOCS proteins?

JAK-STAT pathway Hard
A. Dephosphorylating STAT dimers directly in the nucleus via intrinsic phosphatase activity
B. Binding phosphorylated JAKs to inhibit their kinase activity
C. Competing with STATs for receptor phosphotyrosine docking sites
D. Targeting signaling components for proteasomal degradation via their SOCS box

47 The complement system comprises over 30 proteins. A defining feature that distinguishes complement 'activation' from constitutive presence in serum is best described as:

overview of the complement system Hard
A. Antibody-dependent transcriptional upregulation of all components
B. Reversible non-covalent assembly that dissociates without proteolysis
C. Continuous secretion of preformed active enzymes by hepatocytes
D. Sequential proteolytic cleavage generating active fragments in an amplifying cascade

48 The classical, lectin, and alternative pathways converge at C3. Which statement correctly identifies the C3 convertase of each initiating pathway?

complement system pathways Hard
A. All three pathways use C3bBb as the C3 convertase
B. Classical: C4b2a; Lectin: C3bBb; Alternative: C4b2a
C. Classical/lectin: C4b2a; Alternative: C3bBb
D. Classical/lectin: C3bBb; Alternative: C4b2a

49 The alternative pathway is described as being in a state of continuous low-level activation ('tick-over'). What molecular event initiates this tick-over independent of any pathogen?

complement system pathways Hard
A. Spontaneous hydrolysis of C3 to C3(O), which binds factor B allowing factor D to generate a fluid-phase convertase
B. MBL binding to mannose residues on host cells
C. Direct cleavage of C4 by factor D in plasma
D. C1q binding to circulating IgM pentamers

50 The lectin pathway is activated when MBL or ficolins bind carbohydrate patterns on microbes. Which pair of enzymes associated with MBL is functionally analogous to C1r and C1s of the classical pathway?

complement system pathways Hard
A. Factor B and factor D, which cleave C3 directly
B. Properdin and factor H, which stabilize the convertase
C. C1q and C1r, which are shared between both pathways
D. MASP-1 and MASP-2, which cleave C4 and C2 to form C4b2a

51 Formation of the C5 convertase requires addition of an extra C3b to the existing C3 convertase. Which correctly pairs the pathway with its C5 convertase?

complement system pathways Hard
A. Classical/lectin: C4b2a3b; Alternative: C3bBb3b
B. Both pathways: C5b6789 directly, without a convertase
C. Classical/lectin: C3bBb3b; Alternative: C4b2a3b
D. Both pathways: C4b2a3b only

52 Paroxysmal nocturnal hemoglobinuria (PNH) results from a somatic mutation in the PIGA gene. Why does this cause complement-mediated hemolysis of red cells?

regulation of the complement system Hard
A. Mutation of C3 makes it resistant to factor I cleavage
B. Increased C1 inhibitor causes uncontrolled classical pathway activity
C. Loss of GPI anchors prevents surface expression of DAF (CD55) and CD59, removing protection from the convertases and MAC
D. Overexpression of factor B accelerates alternative pathway activation on all cells

53 Hereditary angioedema is caused by C1 inhibitor (C1-INH) deficiency. Beyond complement, why does this produce the characteristic swelling attacks?

regulation of the complement system Hard
A. C1-INH also inhibits the kallikrein-kinin system, so its deficiency allows excess bradykinin generation causing vascular permeability
B. C1-INH deficiency leads to overproduction of C5a, the sole mediator of the swelling
C. C1-INH normally blocks histamine release from mast cells, so its loss causes an allergic reaction
D. C1-INH deficiency prevents MAC assembly, causing fluid leakage from lysed endothelium

54 Factor I is a plasma protease that cleaves C3b and C4b, but it requires cofactors. Which combination correctly matches a regulator with its principal mechanism?

regulation of the complement system Hard
A. Factor H acts as a cofactor for factor I and accelerates decay of the alternative C3 convertase
B. CD59 acts as a cofactor for factor I cleavage of C3b
C. Properdin accelerates decay of the alternative convertase
D. DAF (CD55) is the essential cofactor for factor I proteolysis of C4b

55 Some pathogens, and host cells, recruit factor H using sialic acid or specific surface polysaccharides. What is the functional advantage of factor H binding for these surfaces?

regulation of the complement system Hard
A. It stabilizes C3bBb, increasing local C3b generation
B. It marks the surface as 'self,' promoting inactivation of deposited C3b and preventing amplification of the alternative pathway
C. It accelerates deposition of the MAC, enhancing clearance
D. It converts the surface into a stronger activator of the classical pathway

56 The anaphylatoxins C3a, C4a, and C5a differ in potency. Which ranking of potency and corresponding regulatory point is correct?

biological consequences of the complement system Hard
A. C3a > C5a > C4a; inactivation requires DAF binding
B. C4a > C5a > C3a; inactivation occurs only via factor I cleavage
C. All are equipotent; none are enzymatically regulated once released
D. C5a > C3a > C4a; all are inactivated by serum carboxypeptidase N removing a C-terminal arginine

57 Opsonization by C3b enhances phagocytosis. A patient with recurrent pyogenic (encapsulated bacterial) infections but intact MAC function most likely has a defect in which step?

biological consequences of the complement system Hard
A. Factor D, causing exclusively viral infections
B. C1q, causing only lupus-like autoimmunity without infection
C. C3, impairing opsonization and immune complex clearance while sparing later MAC assembly in some cases
D. C8, preventing MAC assembly and causing Neisseria infections specifically

58 A patient has recurrent, disseminated Neisseria meningitidis infections but normal responses to other bacteria and normal C3 levels. Which deficiency best explains this specific susceptibility?

biological consequences of the complement system Hard
A. Deficiency of C3, abolishing all opsonization
B. Deficiency of C1-INH, causing uncontrolled classical activation
C. Deficiency of a terminal complement component (C5–C9), impairing MAC-mediated lysis of Neisseria
D. Deficiency of factor H, causing spontaneous hemolysis

59 Complement receptor CR1 (CD35) on erythrocytes plays a key role in immune complex handling. What is its principal function in this process?

biological consequences of the complement system Hard
A. Directly lysing immune complexes via intrinsic protease activity
B. Assembling the MAC on the immune complex surface
C. Binding C3b-coated immune complexes and transporting them to the liver and spleen for removal by phagocytes
D. Neutralizing anaphylatoxins by cleaving their C-terminal arginine

60 Cytokines can act in autocrine, paracrine, and endocrine modes. Considering their typically short half-life and high receptor affinity, why is most cytokine action normally restricted to autocrine/paracrine ranges?

overview of cytokines Hard
A. Cytokines are too large to diffuse beyond the immediate cell surface
B. Short half-life and rapid receptor capture limit diffusion, confining most effects locally except for a few like IL-6 and TNF
C. Endocrine action is impossible because cytokines are destroyed instantly in blood
D. All cytokines are membrane-bound and never secreted, preventing distant action