Humoral Immunity Flashcards

1
Q

what receptors are expressed on naive B cells

A

IgD and IgM

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2
Q

what proteins help transmit signals from the BCR complex

A

Igalpha and Igbeta

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3
Q

CD21

A

b-cell marker what receives co stimulatory signals from complement

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4
Q

where are B and T cells distributed in the lymph node?

A

b- follicles, t- paracortical regions

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5
Q

What happens when a t-dependent antigen gets presented to a b cell

A

proliferation and upregulatoin of CD80. it down regulates CXCR5 and upregulates CCR7, which moves it to the paracortical region. it takes in the Ag and processes it into a MHC class 2 complex for presentation to a CD4 T cell.

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6
Q

what is the importance of CD40L

A

this is expressed on t cells and activates b cells during t-dependent humoral responses. It strengthens the b cells response to the antigen and sends it back to the germinal center, where it will proliferate and differentiate into plasma and memory b cells

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7
Q

what is the difference between a plasma cell and a memory b cell?

A

plasma cells are shortlived and generate antibodies. memory cells live in the bone marrow and are ready to proliferate into plasma cells in the case of a second exposure

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8
Q

what is the difference between a primary and secondary response?

A

primary responses take about a week. Serum IgM appears first, followed by G and A.

secondary responses are much faster b/c of existing memory cells from a first exposure. the primary ab class will be IgG and it will have a higher affinity for the Ag than previously

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9
Q

serum memory/clonal selection

A

older, lower affinity plasma and memory cells are replaced by newer, higher affinity cells in the bone marrow

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10
Q

describe class switching

A

upon CD40 ligation, Abs can switch isotypes in the germinal center. this occurs b/c the VDJ sequence gets translocated downstream of the IgM C region. where the VDJ region moves to is regulated by the cytokines present. when it is done moving, the intervening DNA is cut out, leaving a new mRNA transcript but the same specificity

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11
Q

TGF-B is associated with class switching to which type?

A

IgA

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12
Q

affinity maturation

A

occurs in germinal centers where B cells proliferate and somatic mutations are occuring. slight mutations change the affinity for the Ag, and it gets bound increasingly as proliferation continues. thus, only high affinity mutations will be able to out compete a limited supply of Ag, and competitors will die off, leaving only highly specific Abs.

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13
Q

describe t-indpendent activation

A

non-peptide Ags. usually bind with tighter affinity to epitodes and activate multiple BCRs b/c of repeating epitopes, so the b-cell can still mount a response

usually see a IgM response peaking earlier than T-D responses, however no class switching is seen w/o t help. affinity maturation and memory b cell formation isnt seen

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14
Q

describe the status of the immune system in newborns

A

they have more mature T or B cells than adults, but their immune systems are very immature and cannot yet mount responses. reasons for this include:

sequential expression of genes for Ag specific receptors
immaturity of B and helpter T cells
APC immaturation

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15
Q

describe passive immunity in the newborn

A

newborn cells have IgM only, so they receive IgG across the placenta from mom, and slowly start making their own after birth

IgA only begins getting made after 1-2 months, and IgA from breast feeding is used until that point

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16
Q

immune-exclusion in newbrons

A

IgA coats the whole GI tract and prevents the access of pathogens

17
Q

neutralization/adherence/colonization

A

“neutralization” can be done by the Ab on its own if it binds irreversibly to a pathogen and disrupts its function. this would prevent adherence or colonization of the pathogen. IgA is very good at this.

18
Q

FcR

A

Fc receptors. used for activating effector cells. some examples include

phagocytes: macrophages and NK cells phagocytose opsinized pathogens
mast cells/basophils: respond to IgE Fc receptors

19
Q

ADCC

A

antibody dependent cellular cytotoxicity- lysis of the target cell d/t FcR interactions via TNFa or perforins

20
Q

discuss the role of Abs and complement in phagocytosis

A

an opsinized pathogen greatly enhances the effectiveness of phagocytosis by

  1. increasing interaction time
  2. increasing the activation of the phagocyte
  3. recuiting more phagocytes
21
Q

immune adherence

A

when both complement and Abs are bound to a pathogen

22
Q

respiratory burst

A

the increased metabolic demand in phagocytosis d/t the use of ROS and nitrogen intermediates to kill

23
Q

phagolysosome

A

after injestion by a phagocyte, and resulting invagination vescile is a phagosome, which then fuses with degranulation granules to form a phagolysosome

24
Q

complement system- a subunit vs b

A

b stays covalently bound

25
Q

C3 and C5 convertases

A

3- c4bc2b- attracts c3

5- c4bc2bc3b- attracts c5

26
Q

membrane attack complex

A

c5-c9- c5-8 induce c9 to enter the membrane and polymerize into a circular pore, causing cell death

27
Q

difference between lectin and classical pathways

A

classical is initiated by c1, whereas mannose-binding lectin (MBL) initiates the lectin pathway b/c they are structurally similar

28
Q

how does the classical complement pathway begin?

A

with the binding of IgM or two close IgG receptors. C1 binds their FcRs

29
Q

describe the alternate pathway of complement

A

there is a normal, spontaneous breakdown of C3 to C3b, and how it reacts to its neighboring cells determines the outcome.

if it is near activators, c3b will bind well with Factor B (cleaved by Factor D) and form the c3bBb enzyme complex that converts more C3 to C3b and it enters the complement cascade

if it is near deactivators, it binds very well with Factor H, will be inactivated by Factor I.

30
Q

anaphylatoxins

A

the released subunits C3a and especially C5a attract neutrophils, promote adhesion, respiratory burst and degranulation

31
Q

hereditory angioedema

A

patients lack inhibition on C1

32
Q

where does most complement regulation occur

A

c3 and c4-