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IHO > Week 4 Diebel > Flashcards

Week 4 Diebel Flashcards

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1
Q

L - selectin and CCR7

A

hone and bind in lymph node. High in NAIVE T CELL and low in EFFECTOR CTL

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2
Q

IL-2R (CD25)

A

Binds IL-2. Low in naive t cell and HIGH in effector CTL

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3
Q

CD44 and LFA-1

A

home and bind in inflammation

low levels in naive CTL and HIGH in effector CTL

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4
Q

Naive t cell surface

A

does NOT produce IL2 or cd25

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5
Q

cd3, cd8 and cd25

A

ACTIVATED effector CTL

if cd25 -, than it is naive CTL

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6
Q

CD40L

A

present on th1

sends IFN gamma TOWARDS APC to release IL12

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7
Q

IL12

A

cytokine to induce CD8 to effector

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8
Q

CD25 naive vs effector

A

naive: only alpha chain. Low affinity for IL2
effector: alpha, beta and gamma chain. HIGH affinity for IL2

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9
Q

TCR-cd3 complex

A

found on CTL and binds mhc1 on target cells

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10
Q

LFA1

A

found on CTL and binds ICAM on TARGETS CELLS AT SITE OF INFLAMMATION. Converts to high affinity for short period of time to hold cell and than leaves 5-10 minutes later

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11
Q

Perforin

A

released by CTL to form pore in target cell (similar to C9)

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12
Q

Granzymes

A

released by CTL which enter cell and activate apoptosis

WORKS ON BID AND/OR CASPASE PATHWAY TO APOPTOSIS INFECTED CELL

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13
Q

Fas ligant

A

Is on the CTL
Activates Fas receptor in target cel and triggers apoptosis by cleavage of caspases
Activates CASPASE 8, goes to bid, release ctyo C from nito, activate caspare 9
KNOW WORKS ON BID OR CASPASE PATHWAY TO LEAD TO CELL DEATH

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14
Q

TNF killing?

A

CTL can release TNF to kill infected cells

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15
Q

CD2

A

Found on CTL

Binds to LFA3 on target cell

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16
Q

NK Stimulators

A

ifn a, ifn b, ifn gamma, TNF alpha, IL15

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17
Q

CD56 low

A

90% of blood NK cells. Unique to NK.

Most effective killers

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18
Q

CD56 high

A

10% of blood NK cells. Unique to NK.
Release cytokines. Major is IFN gamma
No granules

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19
Q

NK triggering?

A

looking for LACK OF MHC and STRESS RESPONSE

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20
Q

NK release of IFN gamma when lack MHC

A 
tilt to th1
inhibit th2
induce il12 from macrophages
make macrophages to become M1
Stimulate other NK cells in the environment
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21
Q

NK vs CTL differences

A

NK express CD16
no rearrangement or education
No co receptor binding needed for NK when binding MHC (to recognize)

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22
Q

NK vs CTL similarities

A

BOTH express FasL
Both release perforin and granzyme
Both express and release TNF

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23
Q

CD94 - NKG2A

NK receptor

A 
High affinity
BINDS HLA-E
Inhibitory signal
trumps any activation signal if bound
DONT KILL CELL
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24
Q

NKG2 family

NK receptor

A

BINDS TO MHC
Specifically, BINDS HLA-E with high affinity
Mostly activating

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25
Immunoglobin like receptors
KIR = killer cell immunoglobulin like receptors BIND to MHC 1 (binds classical ones) HLA-A,B,C Mostly inhibitory
26
Lectin like receptor structure
CD94 bound to NKG2A, NKG2C, etc heterodimer complex (nkg2d is homodimer) Most are activating, unless NKG2A which TRUMPS all and INHIBITS
27
HLA leave ER?
can only escape ER if it has peptide loaded
28
HLA-E and leader peptide
leave ER, and binds CD94/NKG2A (on NK) and says LEAVE CELL ALONE
29
NKG2D on NK cells
Binds MHC1 which are made when: Activator and recognizes stress ligands on target cells Made in oxidate stress, mass proliferation, viral infection. (ACTIVATING LIGANDS) Ligand is ULBP and MICA/B activating TO KILL THE CELL IF NKG2A is not bound
30
Stress activating signal + inhibitory signal bound to MHC1
No death
31
Activating stress signal and NO MHC1 present
Death
32
KIR
killer cell immunoglobin like receptor | MOSTLY INHIBITORY. DONT KILL CELL
33
Antibody dependant cell mediated cytotoxicity ADCC
``` all bind ot Fc receptor macro, neutro and eosin kill by cytolytic enzyme TNF release by NK mono and macro Perforin release by eosin and NK granzyme release by NK ```
34
Licensing system
APC licensed by TH1 or TH17 if want to go on to activate CD8 PAMP and TLR can license APC CTL-P activated by LICENSED APC 1. TCR and MHC1 on licensed APC 2. CD28: cd80/86 3. Il2 secreted by th1/17 to activate CTL
35
characterisitcs of DENDRITIC
1. endo or phagocytosis 2. activated by pattern recognition receptor 3. increases mhc2 once in lymph 4. normally have cd80/86 mhc2 and cd increase when become mature dendritic 5. activates naive, effector and memory
36
characteristics of MACRO
1. phagocytosis 2. activated by pattern recognition receptor, and by tcell. 3. must be activated to express cd80/86 and mhc2 4. activates effector and memory
37
characteristics of bcell
1. always presenting mhc2 2. need activation to express co stimulatory molecules cd80/86 3. present soluble antigens
38
tap1 / tap 2
transporter associated with antigen processing Transports peptides from CYTOSOLIC pathway to RER High affinity for 8-16 long amino acids
39
ERAAP
ER associated aminopeptidase | cleaves peptide to 9AA to fit best in MHC1
40
Calnexin
Holds MHC clas 1 alpha chain and ensures proper folding. Once b2 micro binds, calnexin releases the MHC1
41
Invariant chain(CD74)
bound to MHC2 when it leaves golgi. helps fold it and hlep transport to the cytoplasmic vesicles (MHC2 plus invariant is trimer).
42
CLIP
``` Small fragment of invariant chain left over after proteolytic cleavage takes place (class 2 assocaited invariant chain peptide) ```
43
HLA-DO
expressed only in b cells and thymus. block exchange of clip and peptide
44
HLA-DM
Promotes exchange between clip and peptide to allow expression on cell surface
45
CD8 decrease from low MHC1
4 years or later before problems, probably cd8 loss. Prone to URI from bacteria due to repeat viral infection. Would die if didnt have some help form CD4. CD4 levels fine if MHc2 works
46
CD4 loss
Seen very early, maybe even loss of life. Inviable
47
Normal ratio of cd4:cd8
2 to 1
48
Ratio of cd4:cd8 in MHC1 problem
Much higher CD4 count | Lymphocyte range should be normal
49
relation of low MHC1 and low CD8
as t cell mature in thymus, they have both cd4 and cd8. If only 1% of mhc1 present, most t cells are maturing will be cd4 because not enough mhc1 present to stimulate maturing of cd8
50
Cause of MHC1 defect
Lacking promoting enzyme to activate transciption, cant transport mhc1 to surface* Problem in TAP complex was problem in example
51
NK and low MHC1 relation
NK would be high due to low MHC1 and stress signal
52
MHC2 defiency cd4:cd8 ratio
1:3. CD8 levels will be normal but CD4 very low.
53
MHC2 defiency blood levels
HIGH neutrophils and LOW lymphocytes. | Hypogammaglobulinemia as well
54
MHC2 defiency presentation
Auto recessive trait | health problems VERY EARLY IN LIFE. Mild form of SCID. SCID would have low T cell as well
55
treatment for MHC2 defiency
hematopoietic stem cell transplantation
56
Cause of MHC2 defiency
Defects in transcription factors required for expression of MHC2
57
RAG1/ RAG2 and Tdt
Expressed in early Pro-bell (heavy chain) and light chain (small pre-bcell)
58
Late pro-bcell to memory cell expresses:
CD19, 20 and CD40
59
Expressed B cell development stem cell to early pro-bcell
CD34 and c-kit
60
Immunoglobubin expression
Pre-bcell to plasma
61
CD79A AND B expressed:
early pro-bcell to memory cell
62
Major cytokines for bcell development
IL7 help from common lymph to b cell lineage B-lymphocyte stimulator (using BR3 receptor) helps b cell survive IL4, IL3 and low molecular weight b cell growth factor help differentiate
63
B1 B cell
t-independant activation no memory CAN replenish. normal bcell cannot
64
TI-1 antigen
bacterial cell wall components LPS (many are PAMPS) activate B1 B cell
65
TI-2 antigen
large polysaccharides with repeating antigents (dextran, flagellin, polio) binds by crosslinking BCR -activate B1 B cell
66
b cell response to TI-1
TLR4 (polyclonal activation) or BCR (clonal activation) | PRODUCE IgM ONLY
67
B cell response to TI-2
``` IgM stimulation cd4 can help class switch ```
68
Tcell CD44
required to localize to thymus. not found later on in subscapsular cortex
69
c-kit tcell
always present but low in final steps. Required for REPLICATION
70
t cell CD25 (IL-2R)
required for IL-2 driven replication

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