I2: Transplantation

Front 1

grafts exchanges between _____ are accepted

Back 1

genetically identical individuals

Front 2

graft exchanges between ____ are rejected

Back 2

genetically dissimilar individuals are rejected

Front 3

example of HLA rejection haplotypes

Back 3

HLA-A1,A2 and HLA-A1,A1

Front 4

multiple MHC disparities lead to

Back 4

more vigorous rejection than do single locus disparities

Front 5

MHC class I + class II disparities lead to

Back 5

synergy- CD4+ helps the response/rejection of CD8+

Front 6

repeated exposure to allo-MHC leads to

Back 6

accelerated rejection

Front 7

Cytotoxic T lymphocytes are generally __ cells

Back 7

CD8+

Front 8

CTLs recognize

Back 8

MHC class I

Front 9

CTL kills cells by

Back 9

perforin/granzyme, Fas-mediated apoptosis, and TNF-alpha

Front 10

CD8+ pre-CTL growth and differentiation is promoted by

Back 10

CD4+ Th1 cells by IL-2

Front 11

Th cells are generally____cells that recognize_____

Back 11

CD4+ cells that recognize MHC class II

Front 12

cytokines produced by Th cells

Back 12

IL-2
IFN-gamma
IL-4
Chemokines

Front 13

large numbers of CD4+ T cells recognize

Back 13

allogeneic MHC directly as a cross-reaction

Front 14

Self APC consists of

Back 14

foreign peptide + self-MHC II

Front 15

Nonself APC consists of

Back 15

allogeneic MHC-II

Front 16

what cells use ADCC

Back 16

Macrophages, NK, Neutrophils

Front 17

Macrophages recognize target cells by

Back 17

antibody-dependent cellular cytotoxicity

Front 18

frustrated phagocytosis uses

Back 18

NO, superoxide and hydroltytic enzyme-mediated damage

Front 19

macrophages release ___ and are activated by___

Back 19

TNF-alpha
IFN-gamma

Front 20

NK cells recognize targets by

Back 20

ADCC and NK receptors (activating receptors)

Front 21

Nk cells kill by

Back 21

Fas-dependent and perforin/granzyme-dependent mechanisms

Front 22

NK cells produce

Back 22

IFN-gamma

Front 23

hyperacute rejection requires

Back 23

pre-formed anti-HLA or anti-ABO Ab in recipient

Front 24

hypercute rejection occurs within

Back 24

minutes

Front 25

mediators of hyperacute rejections

Back 25

IgG antibodies, complement, neutrophils, platelets (type II like hypersensitivity)

Front 26

acute rejections occurs within

Back 26

weeks to months

Front 27

the acute rejection is initiated by

Back 27

CD4+ and CD8+ T cells, NK cells and macrophages

Front 28

acute rejection is enhanced by

Back 28

IgG antibody

Front 29

symptoms of acute rejection

Back 29

fever, mononuclear cel infiltrate, organ tenderness, decline in organ function

Front 30

chronic solid organ rejection occurs in

Back 30

months to years

Front 31

chronic organ rejection has

Back 31

similar cellular and molecular mechanisms as in acute rejection

Front 32

chronic organ rejection leads to

Back 32

fibrosis and ischemic injury

Front 33

tissue typing determines

Back 33

recipient and donor HLA class I and Ii antigens

Front 34

ABO typing

Back 34

ABO is expressed on endothelial cells

Front 35

Major cross-match

Back 35

detects pre-formed recipient and anti-donor antibodies

Front 36

mixed lymphocyte reaction detects

Back 36

class II disparity and potential for Th and Tc cell activation

Front 37

xenotransplantation

Back 37

transplanting organs between 2 different species

Front 38

primary first-line rejection in xenotransplantation

Back 38

natural AB
IgM classical component pathway activation

Front 39

When is HSCT a viable treatment option

Back 39

congenital deficiencies of hematopoietic system
after chemo
primary immune deficiencies
selective autoimmune disorders

Front 40

stem cells come from

Back 40

bone marrow
peripheral
cord

Front 41

adverse effects of HSCT

Back 41

graft failure, delayed engraftment, ifections, GVHD, Tumor relapse

Front 42

Positive effects of HSCT

Back 42

erythroid, myeloid, lymphoid recovery
immune reconstitution

Front 43

three ways the immune system is reconstituted with HSCT

Back 43

cells that develop from engrafted stem cells
some transfer of mature donor lymphocytes
some residual host memory cells

Front 44

In GVHD

Back 44

donor T cells attack host MHC class I,II by secreting inflammatory cytokines, macrophages, CTL, and NK cells

Front 45

signs and symptoms of GVHD

Back 45

skin: rash, blistering, desquamation
GI: pain, diarrhea, vomiting
lliver: bile duc damage, elevated billirubin, jaundice, pain

Front 46

what increases the risk of GVHD

Back 46

HLA disparity
gender of donor/host
# donor T cells transferred
nature/duration of post-transplant immunosuppression