UCI SOM Gutman

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APC

antigen processing cells (all are phagocytic)

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Lymphoid tissues

lymph nodes, spleen, peyers patches et al, thymus, bone marrow, travel via the blood and lymph

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Iatrogenic

illness brought on by healer

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Innate immunity

no adaptive specificity, no memory, mucous membrane, phagocytes, complement, anti-bacterial peptides

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Adaptive immunity

specificity, memory, B and T cells

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Humoral immunity protects from what

protection from extracellular parasites (antibody mediated); test is if you can transfer immunity by injecting serum into a host

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Cell-mediated immunity protects from what

protection from intracellular parasites

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Active immunity

host creates own antibodies

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Passive immunity

antibodies are injected into host (not created by host)

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Challenge

the act of giving the host an antigen to see if it’s immune

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Afferent limb

where antigen uptake and processing takes place

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Central limb

where proliferation and differentiation takes place (formed in formal lymphoid tissues)

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Efferent limb

where target killing, tolerence, etc. occur

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Epitope

(=antigenic determinant) minimum target structure to which Ab binds

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Immunogen

elicits immune response

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Hapten

small molecule that, when combined to a larger molecule, will elicit an immune response

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Adjuvant

any material that increases the immunogenicity of some antigen (the water/oil antigen thingy)

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Physical manifestations of an antibody

precipitation for soluble Ag, agglutination for particulate Ag, and binding

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Biological effects of antibodies

protection, immobilization, cytolysis, opsonization

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Equivalence

point of most precipitate on the precipitin curve

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Prozone effect

antibody excess on precipitin curve resulting in less precipitation

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Ouchterlony

place antigen and antibody away from eachother in agarose gel and see where they precipitate (reversible)

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Radial immunodiffusion

place antigen in antibody and measure the diameter of the circle of precipitate to see how much lysis occured

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SRBC

sheep red blood cells

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Reverse agglutination

latex coated with antibody; antigen is added (way to check which antigen it is) and agglutination is checked

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Serological

typed by antibodies

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Passive hemagglutination

place antigen and antibody in many test tubes and see which ones clump on bottom (no agglutination b/c the antigens can roll over eachother to get to the bottom of the test tube) or which ones agglutinate and therefore have a broad smear across the bottom

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ELISA

Enzym-Linked ImmunoSorbent Assay; Ag is bound to plate, antibody is labeled with a visible dye

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Electrophoresis of normal serum (proteins from + to -)

albumin (most negative; closest to +), alpha 1, alpha2, beta, gamma (short, broad peak near zero)

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Bruton’s disease

x-linked; impaired maturation and development of antibodies (B-cell defect)

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RIA

RadioImmunoAssay (used radioactive isotopes); same as ELISA except ELISA is safer and currently used

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Equilibrium dialysis

used to analyze the binding of Ab to Ag and to determine valency and strength of binding

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Papain

cleaves IgG into 2Fab and Fc

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Pepsin

cleaves IgG into F(ab)2 and Fc (degraded)

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What does ab stand for in Fab

antigen binding

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What does c stand for in Fc

crystallizing

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What determines the class and subclass of an antibody

heavy chain

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Light chain types

kappa and lambda

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# of IgG subclasses, # binding sites, H-chain classes, and biological properties

4; 2; gamma 1, 2, 3, 4; c-fixing, placental x-fer

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# of IgM subclasses, # binding sites, H-chain classes, and biological properties

0; 10; mu; c-fixing, B-cell surface Ig

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# of IgA subclasses, # binding sites, H-chain classes, and biological properties

2; 2,4,6; alpha 1, 2; secretory Ig

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# of IgD subclasses, # binding sites, H-chain classes, and biological properties

0; 2; delta; b-cell surface Ig

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# of IgE subclasses, # binding sites, H-chain classes, and biological properties

0; 2; epsilon; reaginic Ig

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Order of concentration in Igs in serum

G>M>A>D>E; found in mg/ml

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Size of IgG

150 KDa

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Monoclonal proteins

myeloma proteins and Bence-Jones Proteins (L-chains)

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Monoclonal gammopathies

occurs when a certain immunoglobulin becomes homogenous

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CDR

complementarity determining region (hypervariable region of variable region of Igs)

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Affinity maturation

progression in the affinity of an Ig for its antigen over time

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complement

group of serum proteins activated by ag=ab complexes resulting in lysis or other stuff

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which complement proteins have cytolysis ability

C5b6789

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which complement proteins have anaphylotoxin activity

C3a, C5a

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which complement proteins have chemotaxis activity

C5a, C5b67

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Which complement proteins have opsonization activity

C3b

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Which complement proteins have tissue damage ability

C5b6789, PMN's

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MAC

membrane attack complex; all 3 complement pathways can produce MAC

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how is the classical pathway activated

heat

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complement pathway steps 1-5

1)S+A->SA 2)C1q, C1r, C1s->C1qrs 3)SA+C1qrs->SAC1qrs 3)C1qrs+C4->C1qrs/4b+C4a 4)C1qrs/4b+C2->C1qrs/4b2b+C2a 5)C4b2b+C3->C4b2b3b+C3a

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complement pathway steps 6-9

6)C4b2b3b+C5->C4b2b3b5b+C5a 7)C4b2b3b5b+C6+C7->C4b2b3b5b67 8)C5b67+C8->C5b678 9)C5b678+C9->C5b6789

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convertase

can cleave a complement protein

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alternate pathway

1)B+C3b->BbC3b+Ba 2)BbC3b+P->PBbC3b 3)PBbC3b+C3->PBb(C3b)2+C3a which can fix C5, C6 etc.

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what triggers the alternate pathway

microorganisms, parasites, aggregated immunoglobulin

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MBLECTIN pathway

1)MBLECTIN+mannan->MBLECTIN/mannan/MASP-1/MASP-2 which is a C4 convertase

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advantages/disadvantages of alternate and MBLECTIN pathways

don't need Ab to work; not very good specificity and no memory

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final effects of complement

lysis, opsoniziation and inflammation

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Immune complex disease

Ag-Ab complexes binding the bloodstream to blood vessels and kidney glomeruli

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one-shot serum sickness

immune complex disease that goes away quickly because the antigen is a one-shot activity; if the antigen is normal tissue, autoimmunity ensues

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how many kappa genes

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how many lambda genes

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how many heavy chain genes

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allelic variants of immunoglobulin genes

Km, G1m, G2m, G3m, G4m, Em, A2m

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how many isotypes of ig's are there; how many does each person have

14 different isotypes present in all humans

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allotype definition and how are they inherited

allelic variants within constant regions; inherited in mendelian co-dominant fashion

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idiotype

unique combination of Vh and Vl

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clonal selection/expansion

the proliferation of antibody cell specific to a certain antigen

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affinity maturation

as a response progresses, the antibodies with higher affinity will be selected

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combinatorial joining

joining a random V-region with one of the 5 J-segments in Kappa or several D-segments in heavy chain

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combinatorial association

random association of H- and L-chains

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germ-line theory

for every kappa-chain V-region, there exists one unique germ-line gene

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somatic theory

only one germ-line gene exists and somatic mutation accounts for all kappa-chain v-regions

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on what chromosome are the kappa genes

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on what chromosome are the lambda genes

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on what chromosome are the heavy chain genes

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j-segments

piece on a kappa chain between the V and C regions

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what two immunoglobulins can be produced simultaneously and continuously by B-cells

IgM and IgD

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what determines whether an Ig is execreted versus in a membrane-bound form

alternate mRNA splicing

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TCR

T-cell receptor

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3 differences in structure/expression of TCR's compared with Ig

1)TCR has a single combining site 2)somatic mutation does not occur in TCRs 3)TCR's only exist as membrane-bound molecules

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RAG-1 and RAG-2

two recombinase enzymes necessary for TCR and IgR V(D)J recombination; knock-out of RAG proteins leads to inability to produce mature T and B cells

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kappa gene structure

V(n), J, C

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lambda gene structure

V(n), J, C1, J, C2, J, C3, J, C7

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heavy chain gene structure

V(n), D, J, Cmu, Cdelta, C gamma till ends with Calpha2

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CMI

cell-mediated immunity

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what produces most immunoglobulins

plasma cells

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ratio of H and L-chains in normal plasma levels as opposed to myeloma cells

similar ratio in normal cells; way more L-chains in myeloma cells (these become bence-jones proteins)

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where does carbohydrate add onto (not the Asn, but what part of Ig) the Ig in normal cells

only H-chain (myeloma cells put them on Vh and Vl)

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when and to whom is the J-chain added

just prior to being secreted; on IgM and IgA

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IgA secretion 4 steps

1)(IgA)2 or 3 is secreted into extracellular space 2)epithelial cells have S-piece precursor that binds IgA 3)IgA with Sp is transported to the other side of epithelial cell, Sp is cleaved into 2 pieces 4)IgA with one part of Sp is secreted into lumen

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how many idiotypes does one AFC produce

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allelic exclusion

for every immunoglobulin gene in a B-cell or plasma cell, only one allele is expressed

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heavy chain class switching; can you go backwards?

M to D to G to A to G to E to A; you cannot go back

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how are membrane IgM's and free IgM's different

C-terminal sequence; no J-chain on membrane IgM's and they are therefore monomeric

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what does a virgin B-cell only produce

membrane-bound IgM

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difference among virgin B-cells, memory B-cells, and plasma cells

virgin B-cells produce only membrane-bound Ig's; virgins turn into memory B-cells after first antigen and produce membrane bound and secretory Ig's; these become plasma cells after second antigen stimulation and only secrete Ig's

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why start with IgM

its avidity compensates for lack of affinity but it is very expensive to make; as person develops, she can make IgG's with higher affinity and with less cost

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erythroblastosis fetalis

results from infants blood reaching the mother's bloodstream during birth, creating antibodies and those antibodies attacking the next child

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isoagglutinins

natural antibodies against whichever of the A and B antigens is not present in that persons RBCs

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crossmatching

mixing donor RBCs with acceptor RBCs to make sure it will work

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stem carbohydrate structure, B structure, A structure

RBC—O-GLU(-Nac)-GAL-FUC; B has a GAL on the stem's GAL; A has a NAc on B's extra GAL

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what class of Ig's are made against foreign blood groups

IgM

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% of population that is Rh-

15%

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% of population that is A, B, AB, O

40%, 10%, 5%, 45%

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what kind of natural antibodies do we have against Rh

NONE

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HDN

hemolytic disease of the newborn (same as erythroblastosis fetalis)

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exchange transfusion

total replacement of infant's blood to remove the anti-Rh antibodies and provide undamaged RBCs

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RhoGam

anti-Rh antibody injected into the mother so that she doesn't develop them so as to stop erythroblastosis fetalis

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MHC

major histocompatibility complex; HLA in human, H-2 in mouse

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HLA

human leukocyte antigen system is the name of the MHC in humans

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first set rejection

primary immune response to a graft (the first rejection)

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isograft/syngeneic graft

graft from a genetically identical individuals

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allograft

transplant from one individual to another with a different genotype

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second set rejection

second rejection to the same graft but is much quicker

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is graft rejection a cell mediated or humoral mediated immunity

cell mediated

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what can transfer only humoral or only cellular immunity

serum can only transfer humoral, but nothing can transfer just cellular

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immunological enhancement

when circulating antibodies protect a graft from rejection

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what are the antigens triggering graft rejection

cell surface glycoproteins=histocompatibility complex

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HLA class I and class II genes

I-A,B,C (these are SD); II-D (DP, DQ, DR) (these are LD)

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H-2 class I and class II genes

I-D,L,K II- I-A, I-E

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Ir genes

immune response genes which encode class II antigens (specifically in mice)

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serologically determined (type I in HLA)

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lymphocyte determined (mixed lymphocyte reaction) (type II in HLA)

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which cells express class I antigens

all nucleated cells

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which HLA class is the major target for graft rejection

class I

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do all cells express class II

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class III genes

C2, C4, and B (S in mouse) code for complement components

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what do class II molecules do

required for the process of antigen presentation to helper T-cells

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graft-versus-host reaction

the graft attacks the host

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3 conditions of graft vs. host rxn to occur

1)graft must contain immunocompetent cells 2)graft must be capable of recognizing foreign antigens on host tissue 3)recipient must be incapable of rejecting the grafted tissue

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