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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
Avidity
of binding sites available (similar to valence)
26
What 2 isotopes do all new B cells produce?
IgM and IgD
27
How do B-cells produce IgG, IgA and IgE?
hav to isotope switch
28
Where is IgG?
mostly in the blood
29
Where is IgA?
mucosal surfaces also in secretory fluids
30
IgM
can activate the complement cascade system
31
How does the complement system kill pathogens?
inserts pore structures in the microbe that cause lysis and death
32
IgG antibodies
uses phagocytosis to uptake pathogen Fc region (staph aureus uses Protein A to get around)
33
IgE
provide immunity against parasites (helminths) plays major role in allergies
34
IgA
protect mucosal surfaces
35
IgD
works in the gut dampens the immune system
36
Hyper IgM syndrome
helper T-cells cannot provide adequate assistance to B cells, therefore cannot make antibodies to T-dependent antigens
37
what is inheritance pattern of Hyper IgM syndrome
X-linked recessive
38
bonus: inheritance pattern of hemophilia
X-linked recessive
39
Manifestations of Hyper IgM syndrome
suspectibility to pyogenic bacteria
40
pyogenic bacteria examples(4)
H. influenzae Strep pneumo S. pyogenes Staph aureus
41
What do pyogenic bacteria normally require in order to kill them?
normally need to coat them in antibodies (to make effective, long term antibodies you need T-cell dependent B-cell activation)
42
How do you treat Hyper IgM syndrome?
IVIG therapy
43
patients with deficiences in C5-C9 are suspectible to what?
Neisseria infection
44
Graves disease
thyroid-specific autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone *not a systemic autoimmune disease*
45
ANA protein
high sensitivity low specificity (15-20% of women have ANAs)
46
Genetic polymorphisms and lupus
genetic polymorphisms can affect general pathways of immune regulation, including type I interferon production
47
Type I IFN-alpha
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
What are 3 roles of complement system?
opsonin (tag pathogens) anaphylatoxin MAC (lyses microbes)
49
What does complement deficiency lead to?
makes you suspectible to encapsulated bacteria infection
50
Deficiencies of C1, C2 and C4 lead to ...
infection by strep pneumo and H. influenza type B *these are all early complement components*
51
Deficiencies of late components (C5-C9) leads to?
increased Neisseia infections
52
deficiency of C3 leads to
severe recurrent pyogenic infections in early life mostly by streptococcus
53
What is most common deficiency of complement?
C2 deficiency
54
Hereditary angioedema
C1-INH deficiency (regulatory complement protein) classic pathway is chronically activated increased bradykinin leads to swelling and smooth muscle contraction
55
Factor H and DAF
examples of inhibitors that protect you from overactivation of complement system
56
What are the 3 pathways of complement activation?
Alternative Classical Lectin
57
Hyper IgM syndrome results in what antibody not being produced ....
IgG (no CD40L for T-cell dependent B-cell activation)
58
Why does Hyper IgM make you more suspectible to pyogeneic infection?
normally IgG will tag something for phagocytosis (opsonization) and this cannot occur
59
Where does IgM class switching occur?
in germinal centers
60
What antibodies do mature, naive B-cells express?
IgM and IgD
61
What is the beginning of B-cell activation?
antigen presented to B-cell through MHC-II
62
What causes hereditary angioendema?
C1 esterase deficiency
63
How does C1 esterase def. cause angioendema?
C1 esterase normally breaks down bradykinin having less C1 esterase means you will have more bradykinin which causes edema
64
What is the inheritance pattern of C1 esterase def?
autosomal dominant

Fundamentals 2 (30 decks)

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