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Block 6 Week 1 Colt > L5 B cells and Humoral Immunity - Hudig > Flashcards

L5 B cells and Humoral Immunity - Hudig Flashcards

1
Q

What are the effectors of Humoral immunity>?

A

abs

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2
Q

HOw is humoral immunity transferred?

A

Transferred via serum containing Abs or by Abs alone (alone: tetanus toxoid or rattlesnake venom)

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3
Q

How long do cross-species Abs last?

A

5-7 days

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4
Q

What is the only way to transfer cellular immunity?

A

by transferring whole cells

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5
Q

Why is it not feasible to transfer cellular immunity?

A

If not inbred, t cells are rejecte because MHCI and II Ags are mismatches and lead to killing of the transferred cells

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6
Q

T/F: specific Ab concentrations are constant for life

A

false, they drop

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7
Q

What is the function of an adjuvant?

A

activates macrophages to produce IL1 and tNF-a

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8
Q

What does the release of TNF-a and IL1 from adjuvant stim’d macrophages cause?

A

activates helper T and b cells; keeps immunogen localized

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9
Q

An IM vaccine produces what Ig?

A

IgG

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10
Q

An oral vaccine produces what kind of Ig?

A

IgA

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11
Q

Is IV a good route for vaccine delivery?

A

NO

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12
Q

what is the effect of repeated exposure or boosting of an Ag?

A

incerased quantity and affinity for IgG and IgA

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13
Q

What are the three cases in which high AFFINITY is important?

A
  1. Anti-botulin toxin–Ab competition with the cell receptor for the toxin
  2. Anti-Ebola virus–maximal efficacy
  3. Tetanus toxoid–multiple boots, small amounts must be effective because of rapid clearance of the toxin
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14
Q

What two Ig’s need high avidity?

A

IgM and IgA

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15
Q

Define affinity?

A

binding strength of a single Fab Ag binding site for a single antigenic epitope

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16
Q

define avidity?

A

Avidity: total combined binding strength of a complete Ig molecule for a complex Ag

Like velcro: each tooth is affinity and the whole strip is avidity

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17
Q

Why is high avidity important for IgA and IgM?

A

Bacteria and viruses have repeating epitopes in membranes, flagella, and capsules–its where they bind

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18
Q

Which Ig’s have multiple subtypes and what are they?

A

IgA1-2, IgG1-4

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19
Q

What kinds of secretions have IgA?

A

Breast milk, gut tears, saliva, vagina

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20
Q

Where do you find IgA?

A

GI and respiratory tracts

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21
Q

What is the fate of maternal IgA in breast milk?

A

Maternal IgA from milk remains in baby’s gut, does not significantly enter the baby’s blood circulation

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22
Q

What is the half life of IgA?

A

6 days

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23
Q

What is the function of IgA?

A

Neutralization of microbes and toxins at sties of adhesion to the gut wall

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24
Q

how many binding sites do the Ig’s have?

A 
A 4
D 2
E 2
G 2
M 10
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25
Q

Where do you find IgD?

A

VIRGIN b cells

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26
Q

does iGD have a J chain?

A

no

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27
Q

what modification does IgD have?

A

glycosylated

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28
Q

What is the first and second Abs Ig’s made in response to infection?

A
  1. IgM

2. IgG

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29
Q

What is the function of IgE

A

defense against helminths via mast cell degranulation

30
Q

does igE have a j chainh?

A

no

31
Q

what mod does IgE have?

A

glycosylation

32
Q

IgG has (high/low) affinity for Abs

A

high

33
Q

what is the half life of IgG1/2/4?

A

21-24 days

34
Q

what is the halflife of IgG3?

A

7-8 days

35
Q

what three Ig subclasses can fix C?

A

IgM, IgG1, IgG3

36
Q

Which Ig crosses the placenta?

A

IgG

37
Q

Describe the affinity and avidity of IgM

A

low affinity, high avidity

38
Q

what is the half life of igM?

A

5 days

39
Q

What Ig classes are found in secretions?

A

IgA and IgM

40
Q

What are the five means by which IgG antibodies can preotect humans against pathogens?

A
  1. Neutralization of microbes and toxins by IgG binding
  2. Blocks bacterial adhesion in the gut;
  3. Blocks viral adhesion
  4. Complement activation
  5. Ab-dependent cellular cytotoxicity effected by NK cells
41
Q

Describe the neutralization of microbes by igG binding?

A

Blocks binding of diphtheria and tetanus toxins–needs high affinity

42
Q

Give an example of bacterial adhesion in the gut being blocked by aBs?

A

Salmonella into macrophages, pilin protein in Neisseria

43
Q

What three big name viruses are blocked from adhering to the GI tract by abs?

A

poliovirus, rotavirus, enterovirus

44
Q

What is the result of Ab activated complement?

A

a. Opsonization and phagocytosis of microbes with Abs by macrophages and neutrophils

45
Q

what is the most common C protein used by Ab activated C?

A

C3

46
Q

C3b, iC3b, C3dg, C3d are (blank) bound via thioester linkage to tag yeast or bacteria

A

covalently

47
Q

Are bacteria and yeast likely to be LYSED by the C system?

A

NO

48
Q

what is good example of complement causing lysis?

A

i. Anti-A and anti-B blood group Abs are IgM; good at lysing RBCs

49
Q

what are the four criteria to activate ADCC? What cell is the effector?

A

1.Target cell must have membrane Ags
2.Must be IgG1 or IgG3
3.Need high avidity to the Fc receptor
4.CANNOT BE YEAST OR BACTERIA
effected by NK cells

50
Q

What cells are normally recognized by ADCC?

A

our cells with virions budding out

51
Q

what other two cell types do NK cells take care of?

A

tumor cells and virally infected cell in innate immunity

52
Q

How can you measure targeted cell death in the lab?

A

release of radioactive 51Cr; all cells take it up but only lysed cells will release it and you can measure the amount of radiation produced

53
Q

describe the process of transferring IgA into the gut lumen?

A

1.IgA moves across basement membranes, binds SECRETORY COMPONENT (poly-Ig receptor) bound to GI epithelial cell basal side
2. Endocytosis
3.Release of IgA dimer + secretory component into lumen
ONLY IN SECRETIONS is secretory component still bound

54
Q

what other IgM in secretions has secretory component?

A

IgM

55
Q

WHere do we find large numbers of mast cells?

A

lung, gut, and mucosa

56
Q

(monomeric/multivalent) Ags are needed to trigger mast cells and basophils

A

MULTIVALENT

57
Q

Multivalent Ag cross-links to bound Ig(blank)

A

IgE

58
Q

Can monomeric Ags trigger degranulation?

A

NO

59
Q

Are mast cells only loaded with a single type of IgE?

A

NO, they can respond to a variety of antigens

60
Q

What receptor does IgE bind to on mast cells?

A

FcE receptor

61
Q

what protein are people with penicillin allergies also allergic to?

A

egg proteins

62
Q

What is passive immunity?

A

○ Rapidly confers immunity even before the individual is able to mount an active response; does not induce long-lived resistance to pathogen.

63
Q

How the fuck does Rho-gam work?

A

Prevents RHDneg mom from reacting to RHDpos baby from mixing of blood at birth
Induced Ab feedback inhibition
1. IgG Ab to RHD ag given to mom
2. Ab binds to baby RhDpos RBCs 3. RBC-Ab complex binds to specific B cells IN MOM for RhD epitope
4. Binds Fc-IgG receptor
5. RhD specific B cell signaling is blocked; anti-RhD B cells in mom make no Ab

64
Q

What triggers fusion of the virus with the cell and entry of viral DNA?

A

acidificatiion of the endosome

65
Q

what protein do Abs bind to prevent bacterial adhesion?

A

adhesins, duh

66
Q

What happens to toxins once they are endocytosed?

A

they dissociated from the toxin:receptor complex to free the active toxin chain

67
Q

what are the two ways to diagnose IgE allergic responses?

A

intradermal skin prick or IgE serum tests (ImmunoCAP, Immunolite or HY Tec)

68
Q

What system is used intracellularly in mast cells to cause degranulation?

A

kinase-phosphorylation system

69
Q

What two Ig’s do virgin B cells show?

A

IgM and IgD

70
Q

HOw many igG’s do you need close together to fix C?

A

2`

Block 6 Week 1 Colt (11 decks)

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