Iho Immune Sys 2

Front 1

Failure of ThCells to activate Bcells via CD40L:CD40 binding (respectively) causes this disease:_______________

Back 1

Hyper IgM Syndrome

Front 2

Cell surface molecule that recognizes foreign antigen and is part of the INNATE Imm System

Back 2

TLRs

e.g. TLR4 binds to LPS; TLR2 binds to G+

Front 3

What is the main difference btw TD antigen and TI antigen in activating Bcells?

Back 3

•TD antigen- B2cell
–Signal1: Ag:Ab membrane bind
–Signal2: direct B2cell:Th2cell interaction; CD40L:CD40L

•TI antigen: B1cell
–TLR4 (LPS binds)
–Bcell's specific Ig receptor

Front 4

Is it logical to expect TI antigens to activate immature Bcells? Why or why not?

Back 4

Yes, bc direct TLR4 binding on T0Cells doesn't req. membrane bound ABs present for activation

Front 5

What immune cell binding is analogous to the CD40:CD40L binding of TD antigens?

Back 5

B7:CD28 in Tcells

Front 6

What two traits are conferred to IgG3 by its long linear tail?
1.
2.

Back 6

1. Better at COMPLEMENT/Fc binding
2. Higher turnover rate (d.t. serum proteases)

Front 7

What kinda epitopes to ABs like more, linear or conformational?

Back 7

CONFORMATIONAL
Can you describe the difference btw linear & conformational?

Front 8

T/F a given MATURE (but not active) Bcell can produce both IgD and IgM

Back 8

TRUE

Why? It occurs at the level of mRNA

Front 9

Different mRNA Poly-A sites yield different IgX's.

–If the second Poly-A stop is read, ___ is made.
–If the fourth Poly-A stop is read, ___ is made.

Back 9

2nd stop = IgM
4th stop = IgD

Front 10

Pre-RNA transcripts have TWO Poly-A sites within the Cµ gene segment, if __ , __ _____ are spliced out, then _________ IgM is made

Back 10

splice M1, M2 exons out?

Then you're cookin' with SECRETED IgM!!!!!

Front 11

Name the cytokine needed for IgA:

Back 11

TGF-ß

Front 12

Name the cytokine(s) needed for IgE:

Back 12

***IL-4***, IL-5 (IL-4 also can give IgG1)

Front 13

Name the cytokine needed for IgG3 & IgG2a :

Back 13

IFN-g

Front 14

What the hell does Miller Genuine Draft have to do with adaptive immunity?

Back 14

MGD are the only possible memory B-cell types.

There are NO IgE/IgA memory cells!!!

Front 15

The Poly-A site for this form IgM has cistine in to help form S-S bonds.

Back 15

secretory IgM!

S-S hydrophilic!

Front 16

T/F IFN-g can kill tumor cells directly in high enough concentrations

Back 16

TRUE

Front 17

Low levels of GM-CSF creates T__cells while high levels of GM-CSF creates T__cells

Back 17

Low GM-CSF= Th1
High GM-CSF= Th2

Front 18

Other than virus infections, how can Th1 cells see the exact Ag's they need on MHC II to stimulate CTLs?

Back 18

Th1 cells can see "self" Ag's if a cross presentation rxn occurs (though most often Th1 cells see viral stuff)

Front 19

What are the two major obstacles to activating CTLs? (hint: think MHC)

Back 19

1. Specific Ag peptide must be eaten/presented by Mø etc.

AND

2. Th1 cell must have already previously seen that specific Ag on an MHC II (it won't be able to activate CTL if it hasn't)

Front 20

The JAK/STAT pathway revs up in cells in the presence of this cytokine: ___

Back 20

IFN (class II cytokines)

Front 21

How do cytokine receptors work?

(Hint: think alpha, beta, gamma)

Back 21

Three subunits that synergistically bind cytokine.
Low- alpha only
Med- alpha + gamma (signal transducer)
High- alpha + gamma + beta

Front 22

What are the consequences of signaling via a common cytokine subunit?

Back 22

REDUNDANCY

e.g. IL-3 & IL-5 induce Eos prolif. and basophil degranulation

Front 23

Name 2 dx's treated with IFN-a, IFN-b, IFN-g:
1.
2.
3.

Back 23

1. IFN-a= HepatitisB/C, CML, other tumors

2. IFN-b= MS

3. IFN-g Chronic Granulomatous Disease

Front 24

Name the only cytokine to use 7tm G-ptn receptor: ___

(Hint: chemokine)

Back 24

IL-8 is the only chemokine to use 7tm G-ptn

Front 25

How do T-reg cells do God's work?

Give to specific mechanisms:

Back 25

T-reg's make IL-10 and TGF-ß

IL-10: stops Mø's from makin IL-12, prevents Th1 cells

TGF-ß: Blocks Th2 cells

Front 26

Name two MAJOR outcomes of Th1/APC binding:

1.
2.

Back 26

1. Th1 cell activated to make IL-2, IFN-g etc.

2. APC is licensed to present to CTL-Ps (activate naive CTLs to killer CTLs)

Front 27

CD3 ____-_____ ICAMs do the signal transduction for TCR killin'!

Back 27

CD3-zetz-chain-ICAMs transduce signals for TCRs (MHC I for CTLs)

Front 28

CTLs are up close and personal killers, what adhesion molecule(s) do they use to attack?

Back 28

CD2 & LFA-1 are used to come in close for the kill.

Front 29

Major difference btw NK cell and CTL ability?

Back 29

1. CTLs have memory (NKs don't)
2. NK cells show indiscriminate killing! (when MHC I is insufficiently presented)



NK cells skip sniper school! (no thymus, no TCR/MHC restriction)

Front 30

These cells are activated by CD1d:Ag presentation:

Back 30

1. g/dT-cells

2. NKT cells

Front 31

What do B1cells, g/dT-cells, & NKT cells all have in common?

1.
2.
3.

Back 31

1. NO MEMORY
2. RECOGNIZES CARBS
3. Limited repertoire

Front 32

Which adaptive immune response is best for intracellular parasites? Why?

Back 32

Th1 cells are best: granulomata form, dx is STOPPED

Th2 response: ABs form, but can't really work well. Usually dx can progress, become systemic (e.g. TB, Leprosy)

Front 33

What's the difference btw "INSIDE OUT" and "OUTSIDE IN" transplant rejection?

Back 33

INSIDE OUT=B-cell mediated: ABs form against donor Ag's; leads to vasculitis w/fibrinoid necrosis

OUTSIDE IN=T-cell mediated:
CD4+'s recognize donor Ag's on HLA II, bring out the stormtroopers; CD8+'s bind (CD28:B7) and KILL

Front 34

Hyper-acute rejection begins with ______(a set-up) and ends with ________*.

Back 34

Starts with ABs (humoral rejection) and ends with COMPLEMENT FIXATION (*an Arthus like rxn follows)

Front 35

The damage done in all types of kidney rejection is due mainly to _________.

Back 35

ISCHEMIA

(coagulative necrosis- vasculitis/fibrinoid necrosis)

Front 36

Name two unsurprising gross features of Chronic kidney rejection.

Back 36

1.) Tubular ATROPHY

2.) Interstitial FIBROSIS

Front 37

What's the 1º difference btw hyper-acute and acute rejection?

Back 37

Acute can take wks, months, or yrs and is a priori



Hyperacute involves prior set-up (blood transfusion, pregnancy, prior transplant)

Front 38

BOARD TIP:

RBCs in urine (give 3 causes)

Back 38

1. Vasculitis
2. Infarction
3. Trauma

Front 39

BOARD TIP:

PMNs in urine = ?

Back 39

Infection!

Front 40

BOARD TIP:

Eos in urine = ?

Back 40

Allergic Interstitial Nephritis!

Front 41

BOARD TIP:

Lymphocytes in urine (of kidney transplant) = ?

Back 41

Transplant rejection!

Front 42

Give two urine clues for acute GLN:

Back 42

1.) Dysmorphic RBCs
2.) RED CELL CASTS (RBCs embedded in ptn matrix)

Front 43

What is more important than donor matching for heart and liver transplant patients?

Back 43

Space is more important (You can do a liver transplant in Cloquet)

Front 44

Give four shitty consequences of immunosupression:

Back 44

1.) Opportunistic Infections (viral/veggie)

2.) EBV-induced Lymphoma

3.) Kaposi Sarcoma

4.) HPV-induced Carcinoma

Front 45

What are two ways we ameliorate the effects of immunosuppressive drugs?

Back 45

1.) Interrupt CD28:B7 binding by blocking donor B7

2.) Give recipient some of the donor's dendritic cells. Induces tolerance to donor antigens, results in CHIMERISM

Front 46

How does one get blue arteries?

(Hint: The same way they get purple peepee!)

Back 46

P. aeruginosa
Klebsiella pneum.
E. coli

metabolites

Front 47

If bone marrow transplant pts have their immune system fried prior to surgery, what's the risk?

Back 47

Drama begins when donor T-cells recognize host HLA Ag's