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immuno: transplants and tumors Flashcards

1
Q

graft between identical twins (syngeneic, histocompatible)

graft rejection?

A

isograft

no graft rejection anticipated

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2
Q

allograft

A

btw same species
histoincompatible
rejection expected

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3
Q

alloreactive responses

A

IR against alloantigens (Ags that differ btw members of the same spp)

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4
Q

alloantibodies

A

Ab against alloantigens

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5
Q

graft btw diff species

A

xenograft

graft will be rejected

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6
Q

this transplant has a high success rate and no tissue typing due to immune privilege

A

corneal

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7
Q

allogenic BM/HSC transplant

A

bone marrow
peripheral blood
umbilical cord blood or placental blood

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8
Q

blood can be enriched for HSC pops by

A

hemapharesis or tx donor with CSFs (colony stim. factors)

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9
Q

CSFs (such as GM-CSF, IL-3) can enrich donor blood for

A

CD34+ HSC

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10
Q

the BM recipient is tx with

A

anti-mitotic drugs and irradiation (BM ablation) prior to donation

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11
Q

autologous HSC from BM

A

collect CD34+ HSC from BM–>cryopreserved–>ablative tx–>HSC thawed and infused

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12
Q

IR causes graft rejection: supporting evidence

A

2nd-set rejection happens faster
histo: lympho and mono infiltrate
athymic pts do not reject (need T cells)
slow rejection via IS dampening (lymphos, CMI)

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13
Q

hyperacute rejection

A

few hrs
preformed Abs to MHC, BG ags–>
activation of complement–>recruit. phagos, platelet activation–>thrombosis–>hemorrhage–>necrosis in transplant
fever, leukocytosis, loss of transplant function
CMI not involved

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14
Q

hyperacute rejection may be result of

A

ABO blood group incompatibility
Previous incompatible transplantations
Previous blood transfusions from a related donor
Pregnancy

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15
Q

acute rejection

A

begins few days-14 days complete
not prev. sensitized mostly, some 2nd set
infiltration lymphos, monos–>CTLs phagocytize and present transp. Ag to help T cell
reaction against MHC and mhc Ags

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16
Q

acute rejection may be prevented by

A

immsuppr tx: Abs against T lymphos: cortsters, other drugs

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17
Q

chronic rejection is a Type ???

A

Type 3 hypersensitivity

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18
Q

acute rejection is a Type ???

A

Type 4 hypersensitivity: CMI (Abs also)

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19
Q

chronic rejection

A 
mos-yrs
slowly lose function
activation of CD4+ cells-->macro, CTL activation, Abs agains alloAgs (HLA class I), classical comp. pathway activation, ADCC
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20
Q

chronic rejection depends on…

A

imm. mechanisms that are active and cause histo changes

lymphoid prolif–>formation of follicles over time–>fibrotic changes (scarring)

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21
Q

immsuppr tx for chronic rejection

A

useless, damage already took place

Rituximab may slow down chronic rejection until other organ can be found

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22
Q

graft vs host reactions (GVH)

A

transplanted lymphocytes mount Type IV hypersn rxn against recipients tissues
(lymphos competent and host imm compromised)
occurs in BM transplant of with lymphos that “piggy back”

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23
Q

GVH s/s

A

rash, hepato-spenomegaly, lymphadenopathy, diarrhea, anemia, weight loss, wasting

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24
Q

leukemia pts that receive HSC transplant may have..

A

graft vs leukemia effect

donor T cells recognize minor histocompatibility/tumor sp. Ags–>donor cells attack/kill leukemia cells

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25
Q

major histocompatibility complex (MHC)

A

main influence on graft acceptance/rejection

-transplantation Ags

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26
Q

MHC is on…

gene products…

A 
short arm of chromosome 6
HLA, closely linked genes: 
MHC class I: A, B, C 
MHC class II: DP, DQ, DR
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27
Q 
HLA class I expressed on...
vs HLA class II...
A

all nuc. cells

subset of hematopoeitic cells (dendritic) and thymocytes (but can be induced, as via IFN-y)

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28
Q

combo of the 6 MHC alleles makes up a

total number of HLA alleles expressed

A

haplotype
1 inherited from each parent- 2 total–>genotype
12 (6 loci x 2 haplotypes)

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29
Q

genetic polymorphism

A

multiple stable allelic forms of one gene in a population

-basis of forensics, paternity testing, DNA ancestry, tissue matching

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30
Q

??? initiate graft rejection without the requisite for processed peptide

A

HLA class II molecules

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31
Q

key initiating even in acute allograft rejection

A

direct activation of rec. CD4+ T cells by non self HLA class II on grafted tissue, or carried into recipient by “passenger leukocytes” in transplant

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32
Q

direct recognition

A

recog. of non self HLA (w/out processing foreign peptide)–>stimulus to recipient’s T cells
(unlike conventional IR)
up to 5% clones may respond (vs. 0.01-0.0001% if need TCR to bind self HLA class II and foreign peptide)

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33
Q

indirect recognition

A

recipient’s APC process donor Ag and present to T cells

chronic rejection

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34
Q 
HLA class II: most potent transplantation Ag
good paring btw donor and rec at ??? locus is assoc. with longest graft survival
A

HLA-DR

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35
Q

mechanisms activation

A 
activation CD4+ T cells via recog of foreign HLA class II (+/- peptides) 
rec. CD8+ T cells directly activated by non self HLA class I but need CD4+T cell via *IL-2* production for full activation
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36
Q

important cytokines in graft rejection are mostly…

immune response is Type….

A

Th1

Type 1 IR

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37
Q 
??? induces accumulation and activation of macros and inc. HLA class II expression 
macros may become cytolytic for transpl. cells
A

INF-y

38
Q

??? increases HLA class I expression–>cytolysis of transplanted cells

A

INF-y, INF-a/B, TNF-a/B

39
Q

??? is cytotoxic to graft cells

A

TNF-B

40
Q

HLA matching of primary importance for..

A

kidney and BM allografts

less so for heart, liver

41
Q

reason for rejection in HLA match

A

minor histocompatibility Ags

-not as rapid

42
Q

while testing compatibility, ALWAYS do this first

A

Blood type

otherwise hyperacute rejection

43
Q

genotype of HLA via

A

PCR and sequence analysis

sn, rapid, accurate

44
Q

HLA sequence based typing

A

automated DNA seq. and computer analysis for HLA typing
sp. HLA genes:
exon 2 in Class II genes
exon 2, 3 in Class I genes

45
Q

mixed lymphocyte reaction (MLR)

A

both donor and recipient cells combined, see if react
2-way: mixed in presence of H3-thymidine
if lymphos respond, cells will prolif and incorp. radioactive thymidine, + response
1-way: 1 is fixed, can’t prolif
either way, if +–>don’t do transplant

46
Q

corticosteroids

A

inhibit gene expression (encoding cytokines/rec) in mult. cell types, down reg adhesion rec, inhibit phago and HLA mol. expression
often + antimetabolites

47
Q

antimetabolites

A

(mitotic inhib, cytotoxic drugs) inhib lymph prolif, purine antags (azathioprine, mercaptopurine), DNA alkylating agents (chlorambucil, cyclophosphamide), methotraxate (folic acid antag that blocks purine biosyn)
(originally dev. to tx ca)

48
Q

blocking agents

A

MoAbs against CD3 (block activation of both T cell types)
and against IL-2R (CD-25, IL-2 rec)
also against B7, CD28 (co-stim. molecules)

49
Q

cyclosporine

A

fungal metabolite, anti-rejection
interferes w. gene transcription in T cells
(IL-2, IL-4, IFN-y, IL-2r)
effective prior transplantation, not during episode

50
Q

FK 506 (Tacrolimus) and rapamycin

A

newer fungal metabolites, sim activity, diff structure to cylcosporine

51
Q

total lymphoid irradiation

A

destroys many cell types, but also more radiation-sn T cells

52
Q

goals of rejection prevention research

A

find agent that induces graft tolerance yet does not induce global immune suppression

53
Q

main theory of ca immune: mutations in genes for neoplastic cells also lead to…

A

changes in expressed proteins

-should result in recog. of that protein as non self by immune system

54
Q

evidence for IR to tumors

A

imm. suppr individuals have higher incidence tumor occurence/recurrence
newly transpl. tumors are rejected at high rate/more rapidly in animals prev. exposed to similar tumors (anamnestic IR, like 2nd set rejection)
imm. surveillance theory
lympho/mono infiltrates in solid tumors

55
Q

immune surveillance theory: mech for allograft rejection evolved to protect against..

A

neoplasms, NK cells important

56
Q

innate immunity

A

NK cells (via killer inhib. receptors) recog. lack of self HLA on tumor cells
large granular lymphos, capable of lysing virus-inf. cells/tumor cells w.out HLA + Ag recog.
no memory, occurs w.out precedent cell prolif

57
Q

adaptive immunity

A

humoral immune response to tumors

cell mediated responses

58
Q

tumor cells may be lysed by

A

IgG and IgM Ab and complement
-esp. singe tumor sells and metastases
less effective if tumor is large or encapsulated

59
Q

tumor cells may be destroyed by ??? if opsonized by ???

A

phagos

IgG

60
Q

Abs may neutralize spread of tumor cells by

A

sterically interfering with tumor cells’ ability to adhere to surrounding tissue and/or metastasize

61
Q

ADCC

A

tumor Ags induce Abs(IgG) that bind tumor cell
K cell ( has Fc rec) attaches to tumor cell through Ab “bridge”
subst. released from K cells when close contact tumor cell–>apoptosis tumor cell (killing mech)

62
Q

K cell can be..

A

NK*, CTL, eosin, macro, neutro, etc

63
Q

CD8+ CTLs recognize tumor Ags thru

A 
HLA class I molecules, then destroy tumor cell
*single most important defense*
64
Q

CTL is dependent on..

A

Th1 cytokines like IL-2

65
Q

activated macros destroy tumor cells by rel.

A

lysosomal enzymes and TNF-a onto tumor cell surface

66
Q

lymphokine-activated NK cells (LAK)

A

heterogenous, mostly NKs, lymphoid cells
from peripheral blood of ca pts (IL-2 presence) allows IR to escalate in vitro, transfused back w. IL-2
-not v. successful, toxic and $$

67
Q

tumor-infiltrating lymphos (TIL)

A

NK, some T cells removed from tumors, Cx in presence of IL-2, transferred back with IL-2, low success

68
Q

CD4+ T helper cells: do what??

A

produce cytokines that activate macros, induce CD8+ CTL activity, upreg HLA class I (on tumor cells), and HLA class II (APCs)

69
Q

most imp. cytokine produced by CD4+ is ??? which acts by ???

A 
IFN-y: attracts/activates macros to area of Ag and prev. emigration away 
upregulates HLA class I and II expression
70
Q

production of ??? is key to activation of

A

CTL and NK cells

71
Q

why IR not always effective at eliminating tumors: imm.priv. site

A

eye, brain, gonads, out layers of skin

“can hide”

72
Q

why IR not always effective at eliminating tumors: anergy of infiltrating T cells due to …

A

lack of co-stim. molecules on tumor cells OR production of factors by tumor cell that inhibit T cell function
PGs and IL-10 (Th1 inhib. cytokine)

73
Q

why IR not always effective at eliminating tumors: global imm. suppr

A

TGF-B: can inhib. Th1 response, dec. NK cell cytolytic activity, inhib. Ag uptake and presentation, dampen CD4+ and CD8+ function

74
Q

why IR not always effective at eliminating tumors: dec. imm. recog due to ??

A

dampened HLA molecule expression on tumor cells

75
Q

why IR not always effective at eliminating tumors: Ag modulation (“escape”)

A

tumors can alter Ag make-up regularly

-one that is least antigenic may survive IR

76
Q

why IR not always effective at eliminating tumors: blocking factors

A

prevent recog of tumor cells as foreign, i.e. coating in polysacchs

  • sec. Ags may “bind-up” Abs in circulation, prev. them from reaching Ags on tumor cell
  • also “blocking Ab” may coat tumor cells preventing recog by CTL
77
Q

why IR not always effective at eliminating tumors: size of tumor mass

A

ability of IS to destroy, remove tumor is INVERSELY proportional to size (harder to remove if larger)
-inaccessibility of imm. comps to interior

78
Q

tumor immunotherapy

A

MoAbs sp. for surface molecules for initiating tumor cell killing via ADCC, opsonization and phagocytosis

79
Q

Rituximab

A

anti-CD20

targets B cells in B cell lymphoma

80
Q

Her2/neu protein

A

targets tumor cells in breast/ovarian ca

81
Q

Certruximab

A

anti-EGFR

target ca cells in colorectal, head, neck ca

82
Q

Tositumomab

A

anti-CD20 conj. to iodine 131 (toxic molecule)

tx non-Hodgkin’s lymphoma

83
Q

tumor immunotherapy: vaccination

A

HPV to prev. cervical ca (6, 11, 16, 18)

84
Q

GVH reaction sustained and increased severity via

A

MHC II induced expression: inc. number of cells expressing MHC II as well as inc. expression

85
Q

T cell deficiency, B cell proliferation (more Lambda than Kappa), think…

A

leukemia, B cell lymphoma

86
Q

B cell lymphoma common in HIV+..

A

dec. CD4+ T cells (leaders), loss of control

87
Q

tx B cell lymphoma with..

A

Ritixumab (anti. CD20)

compl. activation, MAC activation–>tumor cell lysis

88
Q 
cerv/axillary LAD
hyperCa, high LDH, inc. WBC counts, inc. atypical cells
B cells, neutros, eosins WNL
almost all CD4+ T cells, lack of CD8+ 
think...
A

T cell tumor
HTLV (if anti-HTLV IgG+)
if clonal, came from initiated cell
virus may “confound” antiviral Ag so can’t fight off tumor

89
Q

tumor produced factors that can influence anti-tumor response

A

PGs
IL-10
TGF-B
(dec. T cell response)

90
Q

Hep C

inc. liver enzymes, inc. a-FP–>

A

hepatocellular carcinoma

look for transplant: HLA genotyping (PCR) and seq., MLR (have time)

91
Q

4 hrs

elev. liver enzymes, spiked fever, low complement

A 
hyperacute rejection
*did not do ABO*
happens fast due to preformed AB
complement being "used up"
*no tx can save graft*

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