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MIMM 214 > B Cells 8 > Flashcards

B Cells 8 Flashcards

1
Q

What are the 6 key functions of Ab?

A
  1. neutralization
  2. opsonization
  3. complement + MAC –> phagocytosis, lysis
  4. ADCC on NK cells –> apoptosis of infected cells
  5. ADCC on granulocytes –> Ab binds pathogen, then degranulation
  6. transport
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2
Q

what allows Igs to do their roles?

A

Fc receptors

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3
Q

what are Fc receptors?

A

transmembrane receptors that bind the Fc portion of Igs

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4
Q

what cells are Fc receptors found on? (7)

A
  1. macrophages
  2. granulocytes
  3. DCs
  4. mast cells
  5. B cells
  6. epithelial cells
  7. neutrophils
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5
Q

what is each FcR specific for?

A

specific for the constant Fc region of one class of Ig

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6
Q

what is important to trigger signaling?

A

crosslinking FcR

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7
Q

what is crosslinking?

A

more than 1 FcR binds an Ab that is bound to an Ag –> must occur to have signaling

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8
Q

what are the 4 roles of FcR?

A
  1. degranulation
  2. opsonization
  3. transport/maintenance of serum Ab levels
  4. ADCc
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9
Q

how do FcR bridge the gap btwn adaptive and innate?

A

allows non-specific immune cells to take advantage of antigen-specific antibodies

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10
Q

describe how opsonization works

A

aggregation of Ag binding will allow crosslinking of FcRs on phagocyte surface –> triggers intracellular signaling for phagocytosis

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11
Q

what Ab are involved in opsonization?

A

IgG

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12
Q

does free IgG trigger opsonization?

A

no!! it can bind FcR but without Ag there is no signaling

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13
Q

since opsonization requires aggregation of IgG, what does this mean about the number of epitopes required?

A

for opsonization, the phagocyte must have multiple epitopes on its surface to allow multiple IgG to bind and aggregate, thus allowing crosslinking

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14
Q

describe IgG subclasses

A

subclasses have distinct effector capabilities: some are good at complement fixation, some are good at ADCC by NK cells

but ALL bind to FcR and allow opsonization

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15
Q

describe ADCC on NK cells

A
  1. IgG binds antigen on surface of target cell
  2. NK cells have FcRs for IgG –> FcR recognizes IgG
  3. crosslinking –> signaling
  4. NK cell releases toxic granules –> apoptosis
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16
Q

describe ADCC vs innate activation of NK cells

A

ADCC requires IgG, innate requires absent MHC I as activating signal

both release the same toxic granules to kill

17
Q

when is ADCC required instead of innate activation of NK cells?

A

normally, our cells present self-protein to show they’re healthy BUT if a virus hijacks this machinery, viral proteins will be presented and act as epitopes, allowing ADCC and the cell can still be killed

18
Q

what is IgE involved in?

A

allergy, asthma, helminths, protozoa

19
Q

is IgE made in large or small quantities?

A

small quantities, but potent effects

20
Q

what is the role of IgE?

A

induce degranulation of eosinophils, basophils, mast cells to damage large pathogens

21
Q

describe eosinophil and mast cell activation

A
  1. TH2 cytokines activate eosinophils and mast cells
  2. IgE binds FcR on eosinophils and mast cells
  3. IgE can bind Ag and degranulate
22
Q

describe mast cells at baseline

A

they do have IgE bound to FcR at baseline but not crosslinked –> no signaling

23
Q

what types of things can be neutralized?

A
  1. toxins
  2. viruses –> internalized
  3. intracellular bacteria
24
Q

what Ig classes are involved in neutralization? what do they do?

A

IgG and IgA bind to toxins/pathogens to prevent them from binding their targets

25
Q

where is IgA found (4)?

A
  1. mucous in gut
  2. milk from mammary glands
  3. tears
  4. saliva
26
Q

describe neutralization of toxins

A

normally, toxin binds cellular receptors and is endocytosed where it has toxic effects

Ab binds toxin to BLOCK binding to cellular receptor

27
Q

describe neutralization of bacteria

A

Ab block colonization of bacteria

28
Q

describe neutralization of viruses

A

Ab binds virus, blocking binding to virus receptor and fusion

29
Q

what is the result of complement activation?

A

forms MAC, inflammation, and/or opsonization

30
Q

what complement pathway is involved in complement activation by Ab? how does it work

A

classical

C1q can bind Ab on pathogen surface, triggering signaling cascade to make C3 convertase and cleave C3 –> C3a + C3b

31
Q

how can Ab link adaptive to innate?

A

thru classical pathway of complement

32
Q

which 2 types of Ig can trigger complement cascade? which is most effective?

A

IgM and IgG

IgM most effective for complement

33
Q

why is IgM most effective for complement? (5)

A
  1. first Ab produced
  2. lower affinity –> no SHM
  3. pentavalent –> 10 binding sites! makes up for lower affinity
  4. good place for C1q to bind
  5. forms dense Ab-pathogen complexes that are efficiently engulfed
34
Q

why are FcRs important for transport?

A

allow targeting of diff Ig classes to diff parts of the body

35
Q

where are IgA, IgE, and IgG each located?

A

IgA –> found in mucosal tissue, breast milk (passive immunity)
IgE –> near epithelial surfaces
IgG –> widely distributed everywhere in serum, in fetus

36
Q

what Ab do newborns have in circulation?

A

IgG

37
Q

how do FcRs allow Ig transport across barriers

A

ex. Ab bind epithelial surface, endocytosed, then released on the opposite side

38
Q

where is IgD found?

A

a minor (0.2%) component of blood but is present in higher levels in secretions of upper respiratory tract

39
Q

what is the function of IgD?

A

bind basophils and mast cells so they release AntiMicrobial Peptides (AMPs), cytokines, and chemokines

(not well understood)

MIMM 214 (33 decks)

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