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Fundamentals 2 > B-Cells and Complement > Flashcards

B-Cells and Complement Flashcards

1
Q

What type of immune response is used in vaccines?

A

T-dependent B cells responses

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2
Q

T-dependent B cell responses

A

form memory B cells

this response takes 10-14 days to manifest

can use Ig class switching and affinity maturation

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3
Q

T-independent B cell responses

A

respond to polysaccharide or LPS signals

mostly IgM response

fast (3-5 days)

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4
Q

What type of antibody activates the complement cascade?

A

IgM

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5
Q

T-dependent B cell response steps

A

Signal 1- B-cell binds antigen through it’s cell surface BCR. Crosslinking the BCR transmits activation signal to the nucleus

Signal 2- T helper cells and cytokines release signal to activate B cell

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6
Q

Where does T-dependent B-cell maturation occur?

A

Secondary lymphoid tissues

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7
Q

Examples of secondary lymphoid tissues

A

spleen

lymph nodes

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8
Q

CD40 and CD40L

A

costimulatory molecules that strengthen adaptive immunity response

between B-cells (CD40) and T-cells (CD40L)

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9
Q

Signal 1

A

B-cell binding to polysaccharide antigen

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10
Q

Signal 2

A

B-cell binding to other things like T-cell or cytokine

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11
Q

What is the end product of T-independent B cell response?

A

plasma cells

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12
Q

Plasma cells

A

acutely secrete antibodies

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13
Q

Memory B-cells

A

can be reactivated to become plasma cells to secrete antibodies

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14
Q

CD40

A

on B cells

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15
Q

CD40 L

A

on T cells

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16
Q

Is 2 signal system also found in T-independent B cell responses?

A

yes

Signal 1 - polysaccharide
Signal 2- TLR, complement receptors, cytokines

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17
Q

Affinity maturation

A

process by which antibodies gain increased affinity for the target antigen

result of somatic hypermutation of Ig genes in B cell regions

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18
Q

What is the primary mechanism of Ig diversification?

A

VDJ rearrangement

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19
Q

VDJ rearrangement

A

antibody gene segment rearrangement

occurs before antigen exposure

occurs in bone marrow

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20
Q

Where does affinity maturation occur?

A

Secondary lymphoid tissue

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21
Q

When does affinity maturation / isotype switching occur?

A

After antigen exposure

B-cells migrate to germinal centers of spleen and lymph node and undergo somatic hypermutation

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22
Q

Somatic hypermutation

A

uses enzyme activation induced deaminase to generate mutations in the antibody’s variable region

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23
Q

What is the result of somatic hypermutation?

A

some mutations improve Ab-antigen affinity

higher affinity B-cells will survive more

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24
Q

Affinity

A

strength of binding

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25
Q

Avidity

A

of binding sites available

(similar to valence)

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26
Q

What 2 isotopes do all new B cells produce?

A

IgM and IgD

27
Q

How do B-cells produce IgG, IgA and IgE?

A

hav to isotope switch

28
Q

Where is IgG?

A

mostly in the blood

29
Q

Where is IgA?

A

mucosal surfaces

also in secretory fluids

30
Q

IgM

A

can activate the complement cascade system

31
Q

How does the complement system kill pathogens?

A

inserts pore structures in the microbe that cause lysis and death

32
Q

IgG antibodies

A

uses phagocytosis to uptake pathogen

Fc region

(staph aureus uses Protein A to get around)

33
Q

IgE

A

provide immunity against parasites (helminths)

plays major role in allergies

34
Q

IgA

A

protect mucosal surfaces

35
Q

IgD

A

works in the gut

dampens the immune system

36
Q

Hyper IgM syndrome

A

helper T-cells cannot provide adequate assistance to B cells, therefore cannot make antibodies to T-dependent antigens

37
Q

what is inheritance pattern of Hyper IgM syndrome

A

X-linked recessive

38
Q

bonus: inheritance pattern of hemophilia

A

X-linked recessive

39
Q

Manifestations of Hyper IgM syndrome

A

suspectibility to pyogenic bacteria

40
Q

pyogenic bacteria examples(4)

A

H. influenzae

Strep pneumo

S. pyogenes

Staph aureus

41
Q

What do pyogenic bacteria normally require in order to kill them?

A

normally need to coat them in antibodies

(to make effective, long term antibodies you need T-cell dependent B-cell activation)

42
Q

How do you treat Hyper IgM syndrome?

A

IVIG therapy

43
Q

patients with deficiences in C5-C9 are suspectible to what?

A

Neisseria infection

44
Q

Graves disease

A

thyroid-specific autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone

not a systemic autoimmune disease

45
Q

ANA protein

A

high sensitivity

low specificity (15-20% of women have ANAs)

46
Q

Genetic polymorphisms and lupus

A

genetic polymorphisms can affect general pathways of immune regulation, including type I interferon production

47
Q

Type I IFN-alpha

A

normally produced by dendrictic cells

something viral can trigger IFN-alpha

then, if you have a genetic mutation IFN-alpha might really amp up ?

48
Q

What are 3 roles of complement system?

A

opsonin (tag pathogens)

anaphylatoxin

MAC (lyses microbes)

49
Q

What does complement deficiency lead to?

A

makes you suspectible to encapsulated bacteria infection

50
Q

Deficiencies of C1, C2 and C4 lead to …

A

infection by strep pneumo and H. influenza type B

these are all early complement components

51
Q

Deficiencies of late components (C5-C9) leads to?

A

increased Neisseia infections

52
Q

deficiency of C3 leads to

A

severe recurrent pyogenic infections in early life mostly by streptococcus

53
Q

What is most common deficiency of complement?

A

C2 deficiency

54
Q

Hereditary angioedema

A

C1-INH deficiency (regulatory complement protein)

classic pathway is chronically activated

increased bradykinin leads to swelling and smooth muscle contraction

55
Q

Factor H and DAF

A

examples of inhibitors that protect you from overactivation of complement system

56
Q

What are the 3 pathways of complement activation?

A

Alternative

Classical

Lectin

57
Q

Hyper IgM syndrome results in what antibody not being produced ….

A

IgG

(no CD40L for T-cell dependent B-cell activation)

58
Q

Why does Hyper IgM make you more suspectible to pyogeneic infection?

A

normally IgG will tag something for phagocytosis (opsonization) and this cannot occur

59
Q

Where does IgM class switching occur?

A

in germinal centers

60
Q

What antibodies do mature, naive B-cells express?

A

IgM and IgD

61
Q

What is the beginning of B-cell activation?

A

antigen presented to B-cell through MHC-II

62
Q

What causes hereditary angioendema?

A

C1 esterase deficiency

63
Q

How does C1 esterase def. cause angioendema?

A

C1 esterase normally breaks down bradykinin

having less C1 esterase means you will have more bradykinin which causes edema

64
Q

What is the inheritance pattern of C1 esterase def?

A

autosomal dominant

Fundamentals 2 (30 decks)

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