Immuno 14 Humoral Immunity And B Cells

Front 1

how is the hypervariable region of memory IgG different than the hypervariable region of secreted IgM of the same AG

Back 1

IgG has a better affinity for the AG

**same AG sepcificity but better binding affinity
**affinity matuation only occurs with TD b cell activation

Front 2

what region of the Ab is the idiotype

Back 2

where the AG binds

**antiidiotype AB binds here, blocks AG from binding. Can crosslink with Fcgamma to decrease AB production

Front 3

AB present in what 3 areas is mediated by hi\umoral immunity

Back 3

AB in the LYMPH, plasma, or tissue fluid

**Humoral immunity is hte BEST ay to fight EXTRAcellular bugs

Front 4

how do most vaccines work

Back 4

stim AB production, humoral response

Front 5

what are 5 effects that AB can have to kill bugs

Back 5

1, neutralize: bing bug to bug cant bind host cells

2. Opsinization/FcR mediated phago

3. Cb3 coated phago

4. Inlfammation

5. bacterial lysis (MAC complex)

**Cb3 phago, imflammation, and bacterial lysis are ALL through AB activation of complement

Front 6

what AB fx to stim compliment so that we can
1. Cb3 opsinization
2. inflammation
3. bacterial lyiss

Back 6

IgM IgG

Front 7

what are the 3 stages of B cell development

Back 7

1. Maturation: bone marrow
2. Activation: 2 lymph tissue
3. Differentiation: plasma or memory cells, class switching, afinity maturation

Front 8

in wht stage of develoopment to B cell class switch nad affinity maturation

Back 8

differentiation

Front 9

what part of B cell devleopmnet occurs in 2 lmph tissue

Back 9

Activation

Front 10

what stage of development created mature immunocompetent B cella

Back 10

maturation

**negative selsection in BM

Front 11

wht part of B cell development requires imunoglobin gene rearrangements

Back 11

maturation

**VDJ recombination to create the variable regiosn

Front 12

in a CD 19 B cell what is gpong on in the nucleus

Back 12

PRO B heave chain VDJ recombination so that it can be displayed in the pre lymphocyte stage

Front 13

in a PRO B cell what is on the surface, what is going on in the nucleus

Back 13

Recombined heave with surrogate light

**light chin rearrangement is occuring, the kappa chain goes first

Front 14

when do we start doing selection on B cells

Back 14

well we need them to already have their specificity of BOTH the heave and light so we select a the immature stage

Front 15

what does the B cell look like when it starts negative selsection, what Ig

Back 15

it has a developed variable region in the heavy and light chain (immature B) adn has IgM

Front 16

both mature and immature b have the fully developed heavy and light chain, how can we tell them apart

Back 16

all mature are NON reactive to self and can have IgM or IgD

immature however may be self reactive (at the immature stage they undergo negative selection) and they will ONLY have IgM

Front 17

XLA is due to what

Back 17

no tryosine kinase to go from pro to pre

Front 18

what is it when you cant have B cells mature past having CD19, ie they can never get the recombined heavy chain displayed

Back 18

cant go from pre to pro

XLA, missing tyrosine kinase

X linked agammaglobunemia

Front 19

what is the name of a B cell deficienct

Back 19

XLA

**NO B cells, lots of infections

Front 20

B cell activation occurs in what 3 places and what does it require

Back 20

secondary lymph tissue:
MALT
Spleen
LN

reqired AG

Front 21

so AG is required for activation, what if there is no AG

Back 21

then the B cell dies, we have constititive hematospoiese to keep up but most will die like this

Front 22

what does AG driven clonal selection of niaeve B cells lead to

Back 22

generation of plasma cells nad memory cells

Front 23

what type of AG can be used to activate b cells in T cell independent activation

Back 23

NON protein: polysaccharide, lipid, nucleic acid

**T cells can ONLY recognize peptide

Front 24

in T independent B cell activation what is croslinked

Back 24

either BCR BCR

OR

BCR CD2 (the compliment receptor for Cd3)

Front 25

what type of B activation gives lots of priliforation, what doesnt it do

Back 25

T independent for proliforation bit it does do lots of class switching or affinity maturation or memory generation

Front 26

if we have TONS of IgM what type of B activation was done

Back 26

TI

T independent: lots of proliforation with limited class switching and limited memory generation

Front 27

what kind of AG is recognized to T dependent (TD) activation of B cells

Back 27

protein or a thing BOUND to protein

**t recognize protein only. if we have an LPS AG it activated B via TI

Front 28

what is the interaction btwn Th and B for TD B cells activation

Back 28

TCR binds MHC II on the B
CD40 on B binds CD40L on T

Front 29

what cell has cd40, what has cd40l. when are these things used

Back 29

CD40: B
CD40L: Th

**used for TD B cell activation

Front 30

TD B cells actvation allows what

Back 30

class switching
affinity maturation
memory

Front 31

where does most T independent B cell activation occur? what AG? what effector B?

Back 31

Mucosa and marginal zone B cells in spleen (away from T cells)

it recognizes polysaccharides, lipids, nucleic acids and other non protein AG. it then makes lots of IgM (plasma effector. no class switch, no memory, no affinity)

Front 32

where does T dependent b cell activation take place? AG? Effector B?

Back 32

where there are also T cells, Follicular B cells, spleen, LN other lymph tissue with T also

Peptide AG

affinity matured, class switched, memory B cells (IgG, IgA IgE)

Front 33

what is the first signal in TD B activation? what does it lead to? compare to T cell activation

Back 33

BCR is crosslikned by peptide AG

leads to increased TF of: Myc NFAT NFkB and AP1 (recall in T cell activation all of these same ones except MYC were activated. T cells also required 2 signals to get to this pt)

Front 34

what TF are made in TD B cell activation after the first step. compare this with the TF made in T cell activation

Back 34

AP1
NFAT
NFkB
MYC

**for T cells all but Myc are made. recall T cell requires 2 signals before it got to this point

Front 35

so in TD b cell activation we have AG mediated crosslinkinf of BCR which leads to formation of Mcy, NFAT, NFkB, and AP1. what does this lead to

Back 35

1. Myc: mitosis/increased survival

2. increased expression of B7 (CD80/CD86) (recall B7 on B interacts with CD28 on T)

3. Increased IL2R IL4R

4. Migration out of lymph tissue and into T rich areas

Front 36

what causes the B cells to leave where they are and go to areas with lots of T cells in TD B cell activation

Back 36

B cel migration out of the follicle so they can receive the second signal

Front 37

does the first signal in TD B cell interaction require T cell

Back 37

nope, but the second signal does. so B cells are stim to migrate to areas of high T cell density by the 1 signal so they can receive the 2 signal that does require Th

Front 38

crosslinking of the BCR by AG (epitope) is what step in B activation? waht is the result

Back 38

1st step

Myc: mitosis/survival
NFAT
AP1
NFkB

**this first step causes LOTS of things: increased mitosis/survival, B cell expresses B7 (B7 will bind to CD28 on the T cell. this is the 2 signal for T cell activation), Increased cytokine secretion of T cells, AG processing and presentation in MHC II for APC. move to interact with T cell

**prepare for interaction with T cells

Front 39

when can B cells act as APC

Back 39

well after they receive their first signal for activation (BCR crosslink by AG) the B cell prepares to interact with T cell. One way it does htis is by AG processing and presentation in MCH II for APC to T cells

Front 40

what is a cool thing about B cell activation

Back 40

in the 2 step of B cell activation we have:
1. MCH II on B presenting to T cell (this is the 1 step for T cell activation)

2. B7 and Cd28 interaction (this is the 2 signal in T cell activation)

**when B cells interact with T cells for B cell activation they are activating the T cell in the process. Recripricol activation

**thses interactions allow the B to have CD40 and the T to have CD40L and the T secreted cytokines

Front 41

what is the 2 signal of B cell activation

Back 41

CD40L on T
T secretion of T cells

**1st signal was crosslink
**2nd is CD40L and cytokines from T interact with C to activate the B--> proliforation/differentiation

Front 42

plasma cells as effector B cells do what?

Back 42

SHort Lived: secrete IgM

LONG lived: relocate to BM, gut to make low levels of IgG and IgA (class switching has occured, further differnetiation thatn shortlived plasma_

Front 43

what can effector B cells do depending on what type of infection is present?

Back 43

can class switch to be a better IR,

CD40 CD40L and cytokines MUST be present for class switching (TD b activation)

**all isotypes will have the same AG specificity

Front 44

where do B cells go for affinity maturation? what do they become. who mediates it?

Back 44

germinal centers and then become memory, mediated by CD154 (same as CD40: CD40L)

Front 45

So... MHCII:TCR is the forst signal in ___ cell activation. CD 28:B& is the 2 signal in ______ cell activation. What other signal is required to activate a B cell

Back 45

T
T
CD40 (B) CD40L (T) and cytokine production

Front 46

what does CD154 do

Back 46

mediates affinity maturation in the geminal center for memory generation

Front 47

when we have BCR cosslinking what can happem

Back 47

IgM production

Front 48

when B cell is activated by TH1 what cytokine is made and what does it cause

Back 48

IFNg
IgG, opsinization

more cell mediated resopnses, but make IgG to aid phago by cell mediated

**humoral helps CMI

Front 49

when B cell is activated by TH2 what cytokine is made and what does it cause

Back 49

Il4
IgE

worms, mast cell degranulation

Front 50

what T cells make
IgG
IgE
IgA

Back 50

Th1L IFNg, opsinization

Th2: IL4. parasites, worms, eisonophiles, mast cells. Type 1 hypersensitivity

Mucosal Tissue TGFb, IL5. We want IgA in the mucosa.

Front 51

what is missing in hyper IgM

Back 51

no Cd40L on T cells. This means that B cells cant be activated via TD activation adn no class switching can occur
**CD40:CD40L as well as cytokines form T cells are required to get class switching

Front 52

if IFNg is around what class of Ig do we get? IL4? TGFb/IL5

Back 52

IFNg: IgG, phago

IL4: IgE, parasites worms, eosinophiles, mast cells

TGFb/IL5: IgA, important at mucosa

Front 53

if you dont have CD40L what happens

Back 53

no class switching,

Hyper IgM

Front 54

how do we class switch?

Back 54

the recombined VDJ will recombine with other constant regions.

ie IFNg will cause switch region to incorporate IgG with the same VDJ region (same AG specificity)

Front 55

is affinity hypermutation somatic hypermutation? what does it allow

Back 55

yep

**allows AB to bind AG better


**CD154 is the same as the CD40:CD40L interaction
**there is lots of RANDOM mutatinos in the variable region to make a better AG

Front 56

so we know that activated B cells rapidly proliforate what part of B cell development takes advantage of this

Back 56

affinity maturation, create point mutations int he hypervariable region to make a better AB

**they then are selsected by follicular dendritic cells

Front 57

what do folicular dendritic cells do

Back 57

they make sure that the B cells that will become memory are good at recognizing Ag after it has indergone affinity maturation

Front 58

what happens in the geminal centers in TD AB response

Back 58

1. B cells activate and migrate to germinal center

2. B cels proliforate

3. Somatic Hypermutation

4. B cells recognize AG on follicular dendritic cell adn survive

5. B that dont bind die

6. Generation of memory and AB secreting cells

Front 59

what happens to B cells after they do affinity maturation

Back 59

they are in the geminal centers nad pass by follicular cells, if they bind they live if they dony bind they die

**the follicular cells have AG on them

Front 60

CD154 on wht cell

Back 60

Th

**this is teh CD40L that interacts with the CD40 on the B cell

Front 61

we get memory cells when

Back 61

after class switching and affinity maturation

Front 62

what population of cells is ready to respond to an AG FAST once it is seen? have we seen this AG before?

Back 62

memory

yes

Front 63

what classes of AB are memory

Back 63

IgG IgA IgE

Front 64

what is the affinity of memory cells

Back 64

HIGH

Front 65

is the maximal B cell response closer to 7 days or 3 days for a primary IR, 2

Back 65

primary 7 days
secondary 3 days

Front 66

does TGFb that induces IgA from Th? what is from Th

Back 66

nope, TGFb is the most influential and comes from mucosa tissue

Th can secrete IL5 to make IgA but its not as tromng of a signal as TGFb

Front 67

how is the humoral IR turned off

Back 67

antiidiotype binding

Front 68

what happens whenthe b cells are secreting TONS of IgG adn the signal needs to be shut down

Back 68

IgG bind to AG adn forms AB:AG complex that binds to the Fcg and BCR on the B cell that is secreting that IgG AB

**the abundance of IgG will begin to corsslink the Fcg, this is the stop signal

Front 69

what is the stop signal for AB secretion

Back 69

when IgG binds Fcg receptors

**cross link BCR with Fcg via
1. AB feedback
2. Antiidiotypes

Front 70

are IgM and IgD part of the memory? where are they seen

Back 70

nope, they are on mature B cells

Front 71

what are the 2 stop signals (BCR is crosslinked by Fcg)

Back 71

1. AB feedback, IgG

2. Antiidiotypes: AB against variable region of AB. (AB AB) this is the idiotype. AntiAB binds AB and then the complex is phago and turns off B cells


excess production of IgG, or an IgG against the idiotype of the active BCR

Front 72

ppl with b cell problems are susceptible to what kind of infections? when do they start?

Back 72

pyogenic (pus, PMN
6-12 months, this is when the IgA from mom milk and IgG are gone

Front 73

ear infections, strep, diarrhea, pnemonia are commin in what kind of deficiency

Back 73

B cell

**encapsulated bacteria wont go away be we are missing the AB and compliment that will opsinize them for phago

Front 74

if you have XLA what will lmph tissue look like

Back 74

tonsils and adnoids are barely detectable, we dont have the B cells to take up space

Front 75

are boys or girls affected more with the B cell deficiency XLA

Back 75

boys

Front 76

what would CBC look like with XLA
Serum Ig
B cell numbers (Cd19 cells)
T cells
PMN
Macro

Back 76

low
low
normal
normal
normal

Front 77

bugs such as encapsulated bacterial (strep, staph) are cleared by _______ so when _________ is absent we see lots of infection

Back 77

opsinization by AB/complimant

**B cells

Front 78

how can we treat XLA

Back 78

no B cells bc we have a problem with tryosine kinase gettingus from pro to pre

**treat with IV Ig

Front 79

what is hyper IgM?

Back 79

no CD40:Cd40L (CD154) so no class switching, thus we get LOTS of IgM

Front 80

in Hyper IgM is IgA present

Back 80

nope, will have lots of oral sores bc notheing there for protection

Front 81

what does CBC look like for Hyper IgM
T cells
B cels numbers
Serum AB
Macro
PMN

Back 81

normal
normal
IgM high, others are low
normal
often neutropenia

Front 82

how can yo udistinguish XLA and Hyper IgM in CBC

Back 82

B cell numbers are low in XLA and normal in HyperIgM

Front 83

what is teh Dx for panic

Back 83

breif periods of fear/doom

1. must have 4 of the following
SOB, sweat, palpatations, tremor, tingle, feel like choking, chills, chest pain, abd pain, derealization, loss of control, fear of death
AND

2. 1 attack forrlowed by a m onth of concern about additional sttacks, worry about implications of attack, significant change in behavior as a result

argophobia can also be present, doent need to be

Front 84

can you have a panic episode w/o having a panic disorder

Back 84

sure thing

**disorder when you ahve concern of another attack, implications of attack and change in behaviour for a month following an attack

Front 85

what is OCD

Back 85

obsessions: thoughts, recognized and tried to supress

OR

Compulasion: behaviour driven by obsession in order to decrease stress

WAXES and WANES

Front 86

so females are usually more affected by anxiety disorders, what is one in which males and females are equal

Back 86

OCD

waxes and wanes

Front 87

will coke cause anxiety (drug)

Back 87

yep
PCP
Caffeine
Tobacco

Front 88

how deos asthma, MI and hyperthyroidism relate with anxity

Back 88

medical conditions that can have anxiety sx as part of presentation

Front 89

what is the dx for PTSD

Back 89

1. occurs after trauma (life threatening)
2. nightmares or flashbacks
3. Avoidance (3):
4. Hyperarousal
5. ONE MONTH
6. causs distress

Front 90

what are some of the types of avoidance seen in PTSD, how many are required fo dx

Back 90

3

detachment/numbing
anhedonia (no pleasure)
amnesia
restricted affext
active avoidance

Front 91

what are the 3 types of PTSD

Back 91

Acute: less than 3 mo
Chronic: more than 3 mo
Delayed onset: sx 6 mo after stress

Front 92

do males or females have PTSD more

Back 92

females

Front 93

whats the dif btwn PTSD and acute stress disorder

Back 93

occur in a shorter time span and for a shorter duration

Front 94

what is it...

PTSD
Acute stress disorder
social phobia
Specific Phobia
Adjustment disorder

Back 94

PTSD: after trauma, at least one month of inpairment

Acute Stress: PTSD but sx occur sooner nad last shorter

Social Phobia: at least 6 mo

Specific Phobia; immediate fear, recognized by pt

Adjustment: sx within 3 mo of stressor, when stressor removed sx releived within 6 mo

Front 95

how long is it for social phobia dx

Back 95

6 mo

Front 96

what are some features of social phobia

Back 96

hypersensitive to rejection
hard to be assertive
low self esteem
bad social skills

Front 97

does a person with a specific phobia relaize their fears are unreasonable

Back 97

yep

fear of dogs, boats, heights, spiders

Front 98

what is adjustment disorder

Back 98

stress wiwthin 3 mo of stressor, sx better in 6 mo