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Untitled - D Ank Unlimited

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graft arteriosclerosis 301 graft-vs.-host reaction (GVHR)<br />

White graft<br />

First set<br />

Second set<br />

graft arteriosclerosis<br />

Intimal smooth muscle cell proliferation that occludes graft<br />

arteries. It may occur 6 to 12 months following transplantation<br />

and leads to chronic rejection of vascularized organ<br />

grafts. It is probably attributable to a chronic immune<br />

response to alloantigens of the vessel wall. It is also termed<br />

accelerated arteriosclerosis.<br />

graft facilitation<br />

Prolonged graft survival attributable to conditioning of the<br />

recipient with IgG antibody, which is believed to act as a<br />

blocking factor. It also decreases cell-mediated immunity.<br />

This phenomenon is related to immunologic enhancement<br />

of tumors by antibody and has been referred to as immunological<br />

facilitation (facilitation immunologique).<br />

graft rejection<br />

The immunologic destruction of transplanted tissues or<br />

organs between two members or strains of a species differing<br />

at the major histocompatibility complex (MHC)<br />

for that species (i.e., HLA in humans and H-2 in mice).<br />

The rejection is based upon both cell-mediated and<br />

antibody-mediated immunity against cells of the graft by<br />

the histoincompatible recipient. First-set rejection usually<br />

occurs within 2 weeks after transplantation. The placement<br />

of a second graft with the same antigenic specificity as the<br />

first in the same host leads to rejection within 1 week and is<br />

termed second-set rejection. This demonstrates the presence<br />

of immunological memory learned from the first experience<br />

with the histocompatibility antigens of the graft. When the<br />

donor and recipient differ only at minor histocompatibility<br />

loci, rejection of the transplanted tissue may be delayed,<br />

depending upon the relative strength of the minor loci in<br />

which they differ. Grafts placed in a hyperimmune individual,<br />

such as those with preformed antibodies, may undergo<br />

hyperacute or accelerated rejection. Hyperacute rejection of<br />

a kidney allograft by preformed antibodies in the recipient<br />

is characterized by formation of fibrin plugs in the vasculature<br />

as a consequence of the antibodies reacting against<br />

endothelial cells lining vessels, complement fixation,<br />

polymorphonuclear neutrophil attraction, and denuding of<br />

the vessel wall, followed by platelet accumulation and fibrin<br />

0<br />

2<br />

5 days<br />

4<br />

6<br />

7 to 8 days<br />

8<br />

10<br />

Time of rejection (in days, after transplantation)<br />

First Set rejection (skin graft rejection)<br />

Types of skin graft rejection.<br />

12 at 14 days<br />

12<br />

plugging. As the blood supply to the organ is interrupted,<br />

the tissue undergoes infarction and must be removed.<br />

graft-vs.-host disease (GVHD)<br />

Disease produced by the reaction of immunocompetent<br />

T lymphocytes of the donor graft that are histoincompatible<br />

with the tissues of the recipient into which they have been<br />

transplanted. Attributable to MHC or MiHA mismatching.<br />

For the disease to occur, the recipient must be immunologically<br />

immature, immunosuppressed by irradiation or drug<br />

therapy, or tolerant to the administered cells. The grafted<br />

cells must be immunocompetent. Patients develop skin<br />

rash, fever, diarrhea, weight loss, hepatosplenomegaly,<br />

and aplasia of the bone marrow. The donor lymphocytes<br />

infiltrate the skin, gastrointestinal tract, and liver. The<br />

disease may be either acute or chronic. Murine GVHD is<br />

called runt disease, secondary disease, or wasting disease.<br />

Both allo- and autoimmunity associated with GVHD may<br />

follow bone marrow or hematopoietic stem cell transplantation.<br />

Of patients receiving HLA-identical bone marrow<br />

transplants, 20 to 50% still manifest GVHD, with associated<br />

weight loss, skin rash, fever, diarrhea, liver disease,<br />

and immunodeficiency. GVHD may be either acute, which<br />

is an alloimmune disease, or chronic, which consists of both<br />

allo- and autoimmune components. The conditions requisite<br />

for the GVH reaction include genetic differences between<br />

immunocompetent cells in the marrow graft and host tissues,<br />

immunoincompetence of the host, and alloimmune<br />

differences that promote proliferation of donor cells that<br />

react with host tissues. In addition to allogenic marrow and<br />

hematopoietic stem cell grafts, the transfusion of nonirradiated<br />

blood products to an immunosuppressed patient<br />

or intrauterine transfusion from mother to fetus may lead<br />

to GVHD. GVHD is most common in bone marrow and<br />

hematopoietic stem cell transplantation but rare in solid<br />

organ transplants.<br />

graft-vs.-host reaction (GVHR)<br />

The reaction of a graft containing immunocompetent T<br />

cells against alloantigens of the genetically dissimilar tissues<br />

of an immunosuppressed recipient. Criteria requisite<br />

for a GVHR include: (1) histoincompatibility between the<br />

14<br />

G

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