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- Graft-vs-Host Reaction
- OSF - 9
- Pages 130 & 131
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- Initiation of Host-vs-Graft Reactions:
- Initiation of Graft-vs-Host Reactions:
- ein allografts (grafts between same species) that differ from a
recipient at the class I and class II MHC loci (resulting in dissimilar
antigenic molecules), both the CD8+ and CD4+ cells of the host become
activated and the resulting immune response is against the grafted
tissue of donor
- ein allografts (grafts between same species) that differ from a
recipient at the class I and class II MHC loci (resulting in dissimilar
antigenic molecules), both the CD8+ and CD4+ donor cells become
activated and the resulting immune response is against the tissues of
the host (recipient)
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- Conditions that may cause a Graft-vs-Host Reaction:
- ethere are differences in tissue histocomaptibility between donor and
host
- ethe host is immunocompromised
- ethe graft cells are immunocompetent and are able to trigger an immune
reaction against host tissue
- eprocedures or products that may cause GVD when immunocompetent
lymphocytes are present include:
- ˇintrauterine transfusions
- ˇblood transfusions - whole, packed, or frozen
- ˇplatelet transfusions
- ˇplasma transfusions - fresh or frozen
- ˇtransplantation of fetal thymus
- ˇtransplantation of fetal liver
- ˇtransplantation of bone marrow
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- Graft-vs-Host Reaction (GVD) and Graft-vs-Host Disease (GVHD):
- ewhen the Graft-vs-Host reaction injures the host tissues such that loss
of function occurs in the affected area, it is then called Graft-vs-Host
Disease (GVHD).
- Classification of Graft-vs-Host Disease (GVHD):
- ebased on the histiologic pattern observed at site of tissue injury
- ˇacute GVHD:
- wepithelial cells necrosis in:
- -skin, liver, and GI tract
- wrash, jaundice, diarrhea, and pulmonary infiltrates
- wdeath may result from increased susceptibility to infections
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- Classification of Graft-vs-Host Disease (GVHD): continued
- ˇchronic GVHD:
- wpresence of fibrosis and atrophy of one of the target sites:
- -skin, liver, and GI tract
- wdysfunction of target site may lead to death
- woccurs in patients that have severe immunodeficiency
- woccurs in immunodeficient patients that have received transfusions
containing immunocompetent lymphocytes within 5 - 30 days
- wsecondary infections are frequently seen in patients with GVHD
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- Mechanism:
- enot well understood
- eNatural killer cells (NK) act as effector cells
- ebelief is that IL-2 activates NK cells to become lymphokine-activated
killer cells (LAK)
- eNK cells are seen attached to dying epithelial cells
- eLAK cells are not MHC-restricted and are able to lyse host cells
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- Treatment:
- etreated using immunosuppressive therapy in patients with GVH
- eimmunosuppressive therapy of little help in patients with GVHD
- ecyclosporine may help in patients with GVHD
- Prevention:
- ePatients who are immunocomromised should:
- ˇbe typed for HLA antigens
- ˇtested for compatibility with blood products
- ˇreceive blood products that have been irradiated to destroy viable
lymphocytes
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Notes
