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HDM Midterm > 2 Hour Surprise Complement Lecture > Flashcards

2 Hour Surprise Complement Lecture Flashcards

1
Q

Immunization

A

Ag stimulus that stimulus specific adaptive immune response that can be recalled during subsequent infections
Passive - Ab/antiserum only
Active - intro Ag that induces adaptive immune response

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2
Q

Herd immunity

A

Immunity acquired when a critical number of individuals in a population are vaccinated

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3
Q

Considerations for immunization schedule

A

Timing of exposure
Immunological maturity of child
Passively transferred Ab that may interfere with immune response of vaccine
Interference

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4
Q

Passively transferred maternal IgG is completely degraded

A

At 9 months of age

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5
Q

Criteria for effective vaccine (only indicated item)

A

Must induce protective T cells
Some pathogens, particularly intracellular, are more effectively dealt with by cell-mediated responses
Also need T cells to activate B cells for Ab production

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6
Q

Inactivated vaccines contain

A

Killed/ inactivated viruses
Subunits or components
Toxoid
Conjugated Ag

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7
Q

Adjuvants

A

Increase vaccine efficacy
Bacterial components or media that prolongs exposure or induces mild inflammation to attract phagocytes (increases chance that Ag will be picked up and presented)

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8
Q

Conjugate vaccines

A

Capsular polysaccharides from pathogenic bacteria elicit a t independent response
Must conjugate the vaccines by linking to a polysaccharide to Ag or toxoid to form an immunogen (t-dependent Ag)

HiB vaccine

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9
Q

Immunological tolerance

A

Unresponsiveness of adaptive immune system to Ag as a result of inactivation or death of Ag-specific lymphocytes, induced by exposure to the Ag

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10
Q

Factors that promote immune tolerance

A 
Soluble, aggregate free, simple small molecules
Improper processing 
Oral/IV presentation 
Age (too young or too old) 
Dose (too large or small)
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11
Q

Characteristics that promote adaptive immune response

A 
Large, aggregated complex molecules 
Proper processing 
Subcutaneous or IM exposure 
Intermediate dose 
not young af or old af
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12
Q

Functions of complement

A 
Triggering, amplification of inflammation 
Attraction of phagocytes by chemotaxis 
Clearance of immune complexes 
Cellular activation 
Direct microbial killing
Development of humoral response
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13
Q

Classical pathway is activated by

A

Ab-Ag complex stimulates C1 binding

Either IgG or IgM (must bind multiple globular domains of C1q in order to activate)

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14
Q

Alternative pathway activated by

A

Spontaneous lysis of C3

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15
Q

Lectin pathway initiated by

A

MBL binding lectin and recruiting MASP1 + MASP2

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16
Q

C1qrs can be inhibited by

A

C1 inhibitor

Binds C1r and C1s to prevent cleave of C4 and C2

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17
Q

C3 convertase classical pathway consists of

A

C4b2a

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18
Q

C5 convertase classical pathway consists of

A

C4b2a3b

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19
Q

Inserts into membrane and forms small pore

A

C4b67

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20
Q

Recruits 10-16 copies of C9

A

C8

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21
Q

Host cells protect themselves from spontaneous lysis of C3 by expressing high levels of what on their cell surface

A

Sialic acid

22
Q

Factor D

A

Cleaves factor B –> Bb and Ba

23
Q

Binds C3bBb and C3bBb3b and prevents increases half-life

A

Properdin

24
Q

Alternative C3 convertase

A

C3bBb

25
Q

Alternative C5 convertase

A

C3bBb3b

26
Q

Binds N-acetylglucosamine on bacterial cell wall to induce autocleavage of MASP1 and MASP2

A

Ficolin

27
Q

Deficiency resulting in: High degree of SLE from failure to clear circulatory immune complexes - deposits on endothelial cells and activates alternative complement, local inflammation

A

C2 deficiency

28
Q

Deficiencies in Factor H and Factor I mimic

A

C3 deficiencies - unregulated C3b generation exhausts C3 from serum

29
Q

Deficiency results in increased susceptibility to Neisseria gonorrhoeae and N. meningitidis

A

MAC deficiencies (C5-C9)

30
Q

Factor I

A

Cleaves C3b and C4b
Cofactors: Factor H, MCP, C4BP, CR1
SERINE PROTEASE

31
Q

Factor H

A

Binds C3b and displaces Bb

Also serves as a cofactor for Factor I cleavage of C3b

32
Q

C4BP

A

C4 binding protein - binds C3b and displaces C2

Cofactor for Factor I cleavage of C4b

33
Q

DAF functions in a similar capacity as what two RCAs?

A 
Factor H (alternative pathway) 
C4BP (classical pathway)
34
Q

MCP

A

Also known as CD46

Cofactor for Factor I cleavage of C3b and C4b

35
Q

DAF

A

Displaces C2b from C4b (classical)
Displaces Bb from C3b (alternative)
Aka inactivates the C3 convertases

36
Q

CD59

A

Blocks C9 binding and prevents formation of MAC

37
Q

Vibronectin

A

S protein - prevents C5b67 from penetrating (heh) membrane

38
Q

Hereditary Angioneurotic Edema

A

C1 inhibitor deficiency
Swelling attacks from physical trauma/emotional stress
Affects extremities, face, GI tract
Treat with androgens (increase transcription of C1 inhibitors)

39
Q

Paroxysmal nocturnal hemoglobinuria

A

Deficient DAF
Hemolytic disorder with spontaneous episodes of RBC lysis, leukocytes, platelets sensitive to complement
Treat with EPO

40
Q

Type III Hypersensitivity

A

Little Ab and excess Ag will lead to small immune complexes that are not cleared from circulation because they do not fix complement –> local inflammation –> basophils degranulation, platelet aggregation –> increase vascular permeability –> complex deposition –> attract neutrophils who further mess it up
==> increased Bp and vascular turbulence

41
Q

Biological functions of complement

A 
Opsonization (C3b, and a little C4b) 
Waste management (C3b binds CR1 of RBCs to transport Immune complexes to spleen/liver) 
Cell lysis (mac)
Inflammatory mediators (anaphylatoxins C3a, C5a, C5b67)
42
Q

Prokinin

A

Also known as C2b - cleaved by plasmin to yield kinin –> edema

43
Q

Epstein Barr virus abuses complement to gain entry into cells by

A

Using CR2 as a receptor for attachment

44
Q

Measles utilizes the complement system to infect cells by

A

Using MCP (CD46) as a receptor

45
Q

West Nile hijacks complement machinery by

A

Coating viral particles in C3b to gain entry into cells by CR3

46
Q

Neisseria meningitidis escapes complement degradation by

A

Expressing protein on its cell surface that block the formation of convertases

47
Q

CH50 assay tests for

A

Test ability of patients blood to perform Complement mediated hemolysis

48
Q

Classical deficiency

A

Increases risk of developing immune complex diseases like SLE

49
Q

MBL deficiency

A

Increases risk of infection by yeast sacchromyces cerevisiae and encapsulated bacteria

50
Q

Alternative pathway deficiency

A

Decreases opsonization activity and increases risk of infection by encapsulated bacteria

51
Q

C3 deficiency

A 
Leads to 
Defective opsonization 
Defective leukocyte chemotaxis 
Decreased bactericidal killing activity (no MAC)
Also indicated in immune complex disease
52
Q

MAC deficiency

A

Increased risk of infection to N. meningitidis

HDM Midterm (10 decks)

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