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Fig. 10.2 ABO antibody depletion in recipient's circulation using plasma exchange
sepsis, disseminated intravascular coagulopathy, splenomegaly, and/or hyper-
splenism or a combination of these. HLA antibodies, granulocyte- or platelet-
specific antibodies, as well as proinflammatory cytokines (e.g., TNF, interleukins)
are involved in the pathogenesis of the FNHTR. In TRALI acute HLA antibody and/
or cytokine-mediated non-cardiogenic pulmonary edema develops, as a result of
severe capillary leakage, in response to transfusion. The manifestation and evolu-
tion of GvHD depend on several factors such as the degree of HLA similarity
between donor and recipient, the level of immunosuppression of recipient, and the
quantity and viability of infused donor lymphocytes [ 6 ] . Conversely, donor-speci fi c
transfusions could result with positive effect on the overall outcome in patients
treated by renal transplant [ 25, 26 ] .
References
1. Snell GD, Dausset J, Nathenson S (1976) Histocompatibility. Academic, New York, pp
181-237
2. Bidwell JL, Navarrete C (eds) (2000) Histocompatibility testing. Imperial College Press,
London
3. Howell MW, Navarrete C (1996) The HLA system: an Update and relevance to patient-donor
matching strategies in clinical transplantation. Vox Sang 71:6-12
4. Tiercy JM (2002) Molecular basis of HLA polymorphism: implications in clinical transplanta-
tion. Transpl Immunol 9:173-180
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