Cytotoxicity

Question 1

CD8 Location Molecules (2)

Answer 1

Reduced CD62L so you don’t go into LNs

VLA-4 can bind VCAM on vasoendothelium to transport to infected tissues

Question 2

CD8 Target Cell Binding

Answer 2

CD2 and LFA-1 interact w/ target cell, when TCR binds it causes an LFA-1 conformational change that forms a REALLY tight bind so you don’t get cytoxins everywhere

Question 3

Two Ways CD4 Th1s Increase CD8 Activation

Answer 3

Increase costim B7 molecule expression on APC

Provide IL-2

Question 4

2 Notable Differences b/w Apoptosis and Necrosis

Answer 4

Cleaved DNA/Implosion vs. No DNA cleave/cellular contents everywhere

Question 5

Activation of Apoptotic DNA Cleavage

Answer 5

Granzyme B activates caspase cascade Caspase 3 which releases I-CAD, the inhibitor of CAD (Capase Activatable DNase)

Question 6

3 Targets of Caspase 3

Answer 6

Lamin prots for cell integrity
DNA repair enzymes (PARP)
I-CAD

Question 7

Mt Involvement in Apoptosis

Answer 7

Granzymes targets BID, and truncated BID (tBID) disrupts mt outer membrane releasing cytochrome c which binds Apaf 1 and the complex activates caspase 9.

Question 8

Pro Life and Pro Death Genes

Answer 8

Bcls are pro life by forming stabilizing pores

Anything else with B or Puma is prodeath by inhibiting Bcl

Question 9

Death Ligand-Death R Pathway of Apoptosis

Answer 9

Fas and FasL (both trimers) are mainly expressed on activated T cells. They bind, the intracytoplasmic death domain (DD) of Fas recruits FADD which activates the caspase. Important for controlling immune response and preventing lymphoproliferative disorders