KUBY IMMUNOLOGY CORE EXAMS SET 2025/2026
QUESTIONS AND ANSWERS RATED A+
✔✔Alternative C' pathway - the Tickover Pathway - ✔✔a)
• C3 is constantly made & inactivated - "ticking over"
• Spontaneous hydrolysis of C3 -> C3(H2O)
• C3(H2O) binds Factor B
• Factor B cleaved by Factor D
• C3(H2O)Bb is "fluid phase convertase" - cleaves C3
b)
• Some cleaved C3b bind to microbial cell surface
• C3b binds Factor B -> cleaved by factor D -> forms C3bBb - Membrane-bound C3
convertase
c)
• Membrane-bound C3 convertase is stabilized by Properdin
• Another C3b binds -> C3bBbC3b formed - C5 convertase
✔✔Alternative pathway - the Tickover Pathway (cont'd) - ✔✔After properdin stabilizes
the C3 convertase, it cleaves many more C3 proteins
• Newly active C3b binds to C3bBb to form C3bBbC3b, or the C5 convertase
• C5 convertase cleaves many C5 proteins
✔✔Alternative C' pathway - the Properdin pathway - ✔✔• Properdin can directly bind to
a surface
• This can then recruit C3b and Factor B
• Factor D is recruited and cleaves Factor B into Bb
• The resultant C3bPBb is an active C3 convertase
• Subsequent steps identical to alternative tickover pathway
✔✔Alternative C' Pathways - Protease-activated pathway - ✔✔• Initiation of clotting
cascades has also been shown to stimulate cleavage of complement proteins
• Thrombin cleaves C3 and C5 in vitro
• Platelet activation releases ATP, calcium ions, and serine/threonine kinases that could
stabilize C3b in fluid phase • This indicates that strong inflammatory reactions could
potentially activate complement systems
✔✔The major pathways of complement activation - ✔✔• All three complement pathways
converge at the formation of the C5 convertase (C3b2a4b or C3bBbC3b)
• C5 initiates the generation of the Membrane Attack Complex (MAC)
• Membrane attack complex is the result of deposition of C5b, C6, C7, C8, and C9 in
target cell membranes
• This pore structure disrupts osmotic integrity, resulting in cell death
✔✔Innate defense against infection:
Lysis of bacterial and cell membranes? - ✔✔Responsible complement component:
, Membrane attack complex (C5b-C9)
✔✔Innate defense against infection:
Opsonization - ✔✔Responsible complement component:
Covalently bound C3b, C4b
✔✔Innate defense against infection:
Induction of inflammation and chemotaxis by anaphylatoxins - ✔✔Responsible
complement component:
C3a and C5a (anaphylatoxins) and their receptors on leukocytes
✔✔Interface between innate and adaptive immunity:
Augmentation of antibody responses - ✔✔Responsible complement component:
C3b and C4b and their proteolyzed fragments bound to immune complexes and
antigen; C3 receptors on immune cells
✔✔Interface between innate and adaptive immunity:
Enhancement of immunologic memory - ✔✔Responsible complement component:
C3b and C4b and their fragments bound to antigen and immune complexes; receptors
for complement components on follicular dendritic cells
✔✔Interface between innate and adaptive immunity:
Enhancement of antigen presentation - ✔✔Responsible complement component:
MBL, C1q, C3b, C4b, and C5a
✔✔Interface between innate and adaptive immunity:
Potential effects on T cells - ✔✔Responsible complement component:
C3, C3a, C3b, C5a
✔✔Complement in the contraction phase of the immune response:
Clearance of immune complexes from tissues - ✔✔Responsible complement
component:
C1, C2, C4; covalently bound fragments of C3 and C4
✔✔Complement in the contraction phase of the immune response:
Clearance of apoptotic cells - ✔✔Responsible complement component:
C1q; covalently bound fragments of C3 and C4. Loss of CD46 triggers immune
clearance
✔✔Complement in the contraction phase of the immune response:
Induction of regulatory T cells - ✔✔Responsible complement component:
CD46
QUESTIONS AND ANSWERS RATED A+
✔✔Alternative C' pathway - the Tickover Pathway - ✔✔a)
• C3 is constantly made & inactivated - "ticking over"
• Spontaneous hydrolysis of C3 -> C3(H2O)
• C3(H2O) binds Factor B
• Factor B cleaved by Factor D
• C3(H2O)Bb is "fluid phase convertase" - cleaves C3
b)
• Some cleaved C3b bind to microbial cell surface
• C3b binds Factor B -> cleaved by factor D -> forms C3bBb - Membrane-bound C3
convertase
c)
• Membrane-bound C3 convertase is stabilized by Properdin
• Another C3b binds -> C3bBbC3b formed - C5 convertase
✔✔Alternative pathway - the Tickover Pathway (cont'd) - ✔✔After properdin stabilizes
the C3 convertase, it cleaves many more C3 proteins
• Newly active C3b binds to C3bBb to form C3bBbC3b, or the C5 convertase
• C5 convertase cleaves many C5 proteins
✔✔Alternative C' pathway - the Properdin pathway - ✔✔• Properdin can directly bind to
a surface
• This can then recruit C3b and Factor B
• Factor D is recruited and cleaves Factor B into Bb
• The resultant C3bPBb is an active C3 convertase
• Subsequent steps identical to alternative tickover pathway
✔✔Alternative C' Pathways - Protease-activated pathway - ✔✔• Initiation of clotting
cascades has also been shown to stimulate cleavage of complement proteins
• Thrombin cleaves C3 and C5 in vitro
• Platelet activation releases ATP, calcium ions, and serine/threonine kinases that could
stabilize C3b in fluid phase • This indicates that strong inflammatory reactions could
potentially activate complement systems
✔✔The major pathways of complement activation - ✔✔• All three complement pathways
converge at the formation of the C5 convertase (C3b2a4b or C3bBbC3b)
• C5 initiates the generation of the Membrane Attack Complex (MAC)
• Membrane attack complex is the result of deposition of C5b, C6, C7, C8, and C9 in
target cell membranes
• This pore structure disrupts osmotic integrity, resulting in cell death
✔✔Innate defense against infection:
Lysis of bacterial and cell membranes? - ✔✔Responsible complement component:
, Membrane attack complex (C5b-C9)
✔✔Innate defense against infection:
Opsonization - ✔✔Responsible complement component:
Covalently bound C3b, C4b
✔✔Innate defense against infection:
Induction of inflammation and chemotaxis by anaphylatoxins - ✔✔Responsible
complement component:
C3a and C5a (anaphylatoxins) and their receptors on leukocytes
✔✔Interface between innate and adaptive immunity:
Augmentation of antibody responses - ✔✔Responsible complement component:
C3b and C4b and their proteolyzed fragments bound to immune complexes and
antigen; C3 receptors on immune cells
✔✔Interface between innate and adaptive immunity:
Enhancement of immunologic memory - ✔✔Responsible complement component:
C3b and C4b and their fragments bound to antigen and immune complexes; receptors
for complement components on follicular dendritic cells
✔✔Interface between innate and adaptive immunity:
Enhancement of antigen presentation - ✔✔Responsible complement component:
MBL, C1q, C3b, C4b, and C5a
✔✔Interface between innate and adaptive immunity:
Potential effects on T cells - ✔✔Responsible complement component:
C3, C3a, C3b, C5a
✔✔Complement in the contraction phase of the immune response:
Clearance of immune complexes from tissues - ✔✔Responsible complement
component:
C1, C2, C4; covalently bound fragments of C3 and C4
✔✔Complement in the contraction phase of the immune response:
Clearance of apoptotic cells - ✔✔Responsible complement component:
C1q; covalently bound fragments of C3 and C4. Loss of CD46 triggers immune
clearance
✔✔Complement in the contraction phase of the immune response:
Induction of regulatory T cells - ✔✔Responsible complement component:
CD46