Cell-Mediated Toxicity--Diebel Flashcards
This receptor interaction is important in the licensing of APC by CD4+ T-cells
CD40/CD40L interaction
This receptor interaction is important in activating a CTL-precursor into a CTL
CD28/B7 interaction with licensed DC
How does a CD4+ T-cell “license” a DC?
CD40/CD40L interaction signals DC to also present MHC-I
this is “licensing”–permitting it to present on both MHC
*normally we think DC activate CD4+, and that is true. but CD40/CD40L interaction is important for licensing while MHC/CD3 interaction is important in the opposite direction*
CD25
high affinity IL-2 receptor
*expressed only on CTLs, not CTL-precursors*
L-selectin and CCR7
expressed by naïve CTL
*they bind and have affinity in nodes, keeps them put*
CD44 and LFA-1
found only on CTL
*tropic for inflammed tissue*
How do CTLs kill bad cells?
perforin holes, granzyme cleaveage of caspaces
FAS-FASL interaction –> caspace cascade
What is the normal blood concentration of NK-cells?
5-10% of lymphocytes
What are the two subtypes of NK-cells?
CD56-low (90%)
*killer cells*
CD56-high (10%)
*cytokine releasing cells*
CD56
differentiates killer NK-cells (90%) from cytokine-releasing NK-cells (10%)
Killing mechanism of NK-cells
perforin + granzymes
FAS/FASL
*same as CTL*
CD16
expressed by NK-cells
NK marker
*16 year old drivers are natural killers*
Lectin-like receptors
- what do they bind
- activity
bind HLA-E and MHC-I-like molecules
-usually activating (except NKG2A–inhibitory)
Immunoglobulin-like Receptors
- what do they bind
- activity
- bind most MHC-I molecuels (HLA-A, -B, -C)
- most are inhibitory
NKG2A
NK-cell receptor
- what does it bind
- what does it do
- binds HLA-E
- supreme inhibitory signal (inhibits NK-cell even if other stimulatory signals are present)
