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Transplant Immunology Flashcards

Quiz 6 (48 cards)

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1
Q

Transplant Immunology Overview

A

-History: Medewar and acquired immunological tolerance
-Modern transplant: Immunological considerations clinical management

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2
Q

Describe the experiment for acquired tolerance of foreign cells (part 1)

A

-Adult mouse (strain A) + Skin graft from strain B mouse (not identical mice)
-about 11 days, there is rejection
-about 60 days: 2nd transplant (strain B)
-<6 days: rejection (accelerated rejection due to memory cells

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3
Q

Describe the experiment for acquired tolerance of foreign cells (part 2)

A

-FETAL mouse (strain A, 15-16 days gestation (immune system barely even there)) + injection of cell mix (strain B)
-8 wks: skin grat from stain B mouse
-TOLERANCE (showed that tolerance is achievable)

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4
Q

What is an autograft

A

transplant between 2 sites on same person/ animal

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5
Q

What is syngeneic graft

A

transplant between genetically identical animals or people (if have identical twin: not as good as autograft tho)

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6
Q

What is allograft

A

-most common source of organcs
-transplant between unrelated individuals of the same species

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7
Q

What is Xenograft

A

-new big field rn
-transplant between different species
-ie pig skin/ kidney

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8
Q

would transplant of a skin graft from a third, unrelated donor onto the same recipient lead to acute rejections or accelerated rejections?

A

most likely acute

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9
Q

What is transplant rejection caused by

A

-caused by a strong T cell response to ALLOANTIGENS

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10
Q

what are alloantigens

A

-antigens that differ between members of the same species (think allograft)
-main alloantigens are non-self MHC
-frequency of T cells specific for non-self MHS is relatively high

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11
Q

What is the answer to transplant rejection?

A

MHC matching between donor/ recipient (best is identical twins but always have minor HCs too)

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12
Q

What are minor histocompatibility antigens?

A

-any antigens generated from polymorphic self proteins
-could be literally any protein
-never perfect match unless identical twins and even then some variation maybe

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13
Q

What is direct allorecognition

A

APCs from the donor organ (with allogeneic MHC) travel to recipient lymph nodes and activate alloreactive T cells

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14
Q

Explain the scheme of allorecognition

A

-kidney graft w/ dendritic cells (donor DCs)
-donor DCs migrate to lymph node and spleen via blood, where they activate effector T cells
-Effector T cells migrate to graft via blood
-Graft is destroyed by effector T cells

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15
Q

What is indirect allorecognition

A

-uptake of allogeneic proteins by recipient APCs -> presentation to recipient T cells
-generally associated more with chronic rejection
-recipient’s DC take up and present graft’s antigen and activate immune system against graft

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16
Q

What is hyperacute rejection

A

-mediated by pre-existing antibodies (that happen to be against graft)
-can be to blood group antigens (ABO)
-antibody binding induces complement activation clotting cascade (inflammation -> cut off blood supply to graft and starce it of blood to kill it)
-rejection within minutes of transplant
-problem for xenografts (b/c foreign species)

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17
Q

ONLY for HSC (Hematopoietic stem cell transplants) : Graft vs Host disease

A

(the graft attacks the host -> want stem cells but sometimes some mature ones come along and attack host

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18
Q

How can you think about pregnancy as an allograft

A

-infant contains maternal MHC and self-antigens
-but also contains paternal MHC and self-antigens (recognized as foreign)
-Mechanisms at the placental barrier prevent this

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19
Q

What is an organ transplant

A

-kidney, liver, heart, lungs, pancreas intestines
-rejection is a big issue
-immunosuppressive drugs for the remainder of patients’ life

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20
Q

What is a tissue transplant

Study These Flashcards
A

-bones, tendons, ligaments, skin, heart valves, blood vessels, corneas
-rejection less of an issue for due to lack of internal vascular system

21
Q

brief overview of post-transplant immunosuppression

Study These Flashcards
A

-T cell focused
-side effects: hypertension, infection, hyperlipidemia post-transplant malignancy

22
Q

What is immunological chimerism similar to

Study These Flashcards
A

-Medewar’s mouse experiment… but humans

23
Q

What is Chimerism

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A

-Mech of action
-Donor-derived DCs set up shop in the recipient thymus
-negative selection of donor-reactive T cells
-Induced central tolerance for the donor cells not to be attacked
-also likely a role of Tregs and peripheral tolerance

24
Q

Why are donors a limiting factor

Study These Flashcards
A
  1. not enough donor organs
  2. not matched enough
25
How does Xenotransplantation work
-transplant across species: mainly pigs -> humans -Use CRISPR-CAS9 to alter pigs: knockdown 3 pig genes that would trigger the human immune system and add 6 human genes to promote tolerance of the organ
26
What is Human Pig Chimeras
-inject human stem cells into pig embryos -human cells seem to slow the growth/development of pic embryos
27
What are immunosuppressants
-any molecule that inhibits the immune response -can be any part of the immune system -main ones today: NSAIDs, corticosteroids, JAK inhibitors, mAn
28
What are NSAIDs
-Non-Steroidal Anti-Inflammatory Drugs -pretty much every OTC painkiller
29
What are Prostaglandins
-lipid derived hormones (derived from phospholipids -dependent on the COX enzymes -PGE2 is pro-inflammatory
30
What leads to inflammation through NFkB
-PGE2 binds GPCR -increases NFkB (proinflammatory)
31
What is the effect of PGE2 on T cells
key takeaway: turn up effector T cell response, turn down Tregs
32
What blocks the PGE2-induced NFkB inflammation?
-NSAIDS -reduces pain, swelling, redness, and fever
33
What protects the gut epithelial lining from NSAIDS
-COX-1
34
What are Corticosteroids
-exteremly important anti-inflammatory
35
What is prednisone
synthetic cortisol: corticosteroids
36
Explain corticosteroid signaling
-can cross membrane b/c hydrophobic -binds receptor that is also transcription factor (so direct, not rlly a signalling pathway) -can activate -can repress (change histone acetylation)
37
Why don't we use corticosteroids for autoimmune treatment
-long term use has severe side effects
38
What are JAK inhibitors
-JAK receptors are key for cytokine signaling -including pro-inflammatory cytokines -Block JAK= lower inflammation used for: autoimmune and some cancers
39
What are JAK3 specific to
lymphocytes
40
What are Tofacitinib
-original brand name: Xeljanz -Rheumatoid arthritis and ulcerative colitis -while there are some mild side effects, two potentially lethal ones are 1. opportunistic infections 2. cancer
41
How can monoclonal Abs used for immunotherapy
-generate mAb against immune cell surface proteins -those immune cells will get killed
42
What are five mechanisms that tumors use to avoid immune detections
-low immunogenicity -tumor treated as self antigen -antigenic modulation -tumor-induced immune suppression -tumor-induced privileges site
43
How to do M2 tumor-associated macrophages
-TAMs -M2 is about wound healing (anti-inflammatory) -cancer tricks them? protects cancer from immune system -also recruits Tregs
44
How do you treat M2 tumor-associated macrophages
-turn up immune system -inhibit an inhibitor of the immune system -CTLA-4 and PD1 inhibitor of the inhibitor CTLA-4
45
CTLA-4 prevents what
overactivation -bind B.7 to prevent T cell activation
46
What is PD1
-Programed cell Death protein 1 -protein found on T cells -binds PD-L (PD1 ligand) -found on many cell types -prevent autoimmunity
47
What is Chimeric Antigen Receptor (CAR) T cells
-take a part of a mAb that binds antigen speficic/ enriched on cancer -Fuse to the internal part of a TCR -Transform into patient cytotoxic T cell -if designed correctly, binding of antigen leads to TCR-like signaling -and this leads to cell killing
48
What are the three major downsides of CAR T cells
1. First, T cell exhaustion 2. super expensive 3. cytokine release syndrome

Immunology (14 decks)

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