Exam 4 Immuno Flashcards

1
Q

mAb synthesis

A

B cell + V(D)L KO’d multiple myeloma cell

Nuclei fuse - mAb production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mice Can Heal Humans

A

Murine - 1x, HAMA
Chimeric - multi x, HACA (mouse VH/VL human Fc domain)
Humanized - good, HAHA (mouse CDRs)
Fully Human

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Natural Killers cells

A

Large, granular lymphocytes
Innate, recognize DAMPs
Kill by ADCC or NK receptor killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Antibody dependent cell-mediated cytotoxicity

A

IgG bind target cell

NK binds Fc and induces apoptosis in target cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tumor specific mAb mechanisms

A

Activate complement
Induce ADCC
Tag with radioisotope (imaging or killing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

BiSpecific T Cell Engager

A
Binds tumor (ex CD19 in Bcell lymphoma) and Tcell CD3
Ex: Blinatumomab (Philly negative ALL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Drug used in Solid Organ Transplant

A
Azathioprine/Mycophenolate
Glucocorticoids
Cyclosporin
Tacrolimus
Sirolimus (Rapamycin)
ATGAM
mAbs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Isohemagglutinins

A
IgM response to blood types (carbohydrate epitopes)
Naturally occurring (or at least close)
"Immunized" by 3-6 months
IgG is rare, but automatically high risk pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Rh Factor

A

Not naturally occurring, need to be exposed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hemolytic Disease of the Newborn

Erythroblastosis Fetalis

A

Rh+ fetus
Last trimester/at birth = exposure
Mom exposed -> will attack subsequent fetal RBCs
Fetus born excess bili (jaundice)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

RhoGAM

A

prevention

give to avoid mom become “immunized”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Heterophile Antibody

A

Cross reactive antibodies
Ex: Mono test using horse ab
Ex: Trep palli and beef heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HIV-1 virus binding

A

GP120 high affinity for CD4 (all T helper, also APC and DC)
Conformation change - CCR5 binds
GP120 moved by CCR5, GP41 fuses with membrane
GP41 is on virus and has large hydrophobic sections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HIV-1 virus in cell

A

Virus brings reverse transcriptase with integrase function
Activation site similar to IL-2 promotor (cross talk)
RT has high error rate - many viral variations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk groups

A

Long term survivors - CCR5 mutation, decreased express

Elite controllers - infected but effective T killers, HLA-B57

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diagnosis of HIV

A

Virus peaks at 6 weeks

Antibodies peak at 9 weeks

17
Q

HIV Tests

A
Quick fast (ELISA w/ antigen): high false positive
Check with Western for binding of GP120, GP41
Self test: check IgG in cravicular fluid: high false negative
18
Q

Evidence for Cancer Immunosurveillance

A

Immunodeficient (esp Tcell) = higher tumor rates
Activated Tcell against tumor = good prognostic sign
Spontaneous regression of tumors
Paraneoplastic syndromes = autoimmune mech

19
Q

Immunoediting categories

A
  1. Elimination
  2. Equilibrium
  3. Escape (upregulation of CTLA-4, PD-1)
20
Q

2 Types of Tumor antigens

A

Tumor associated antigens (abnormal or excessive expression)

Tumor rejection antigens (recognized by immune)

21
Q

2 Types of tumor mutations

Prognosis for mutation #

A

Driver: oncogenes/TSgene mutations
Passenger: more common, don’t affect growth
More mutations = more immuno targets = better prog

22
Q

T Cell and APC interaction mech

A
  1. Stimulation: CD28 (Tcell) to CD80/86 on APC
  2. Inhibition: CTLA-4 to CD80/86 (early brake)
  3. More inhibition: PD-1 to PD-L1 (late brake)
23
Q

Tumor resistance via CD80/86 and PD-L1

A

CD80/86 and PD-L1 not expressed on tumor, but on nearby immune cells
If invading cells: good prognosis, protecting self
If within tumor: bad prognosis, can’t attack tumor

24
Q

Immune mechs to kill tumor

A
  1. CTL - target high MHC cells
  2. NK - target low MHC cells
  3. Th1 - Activate M1 (tumor often creates M2 response)
  4. Antibody and complement
25
Q

5 Methods of Immunotherapy

A
  1. Specific immunization (patient DC + TAA protein)
  2. Innocent bystander killing (BCG vaccine)
  3. mAb anti-tumor
  4. Autologus cell therapy
  5. Chimeric antigen receptors
26
Q

Chimeric antigen receptors

A

CTL good killers, but need MHC with protein expression
Mix CTL with tumor target (mAb specificity)
BUT overagressive, hard to stop/control
New: Split CAR joined by small molecule