Allografts processing

Also known as antibody-mediated rejection, humoral rejection is the process of creating graft-specific antibodies.1,4 This type of rejection occurs less frequently than cell-mediated acute rejection. Humoral rej ection is characterized by deposition of immunoglobulins and complement in allograft tissues. Treatment for this type of rejection is not well defined, yet several reports have shown that treatments such as plasmapheresis, immunoglobulin therapy, rituximab, and/or antithymocyte globulin maybe effective. 

Tolerance is the process that allows organ-specific antigens to be accepted as self.2,6 This would mean that the immune system would cease to respond to the allograft, and immunosuppressive medications would not be necessary. Immune tolerance has not been accomplished successfully in humans.2,6... 

Until recently, it has been difficult to dissect the relative role of each che-mokine in the inflammatory processes leading to allograft rejection, especially as many chemokines and chemokine receptors are seemingly redundant (2,8). Indeed, during allograft rejection, the expression of many chemokines and chemokine receptors can be detected in the allograft—only a few of which represent viable targets for therapeutic intervention (5,6). 

Although in the early 1990s several antibodies were developed that inhibited leukocyte-endothelial cell interaction to prevent e.g. allograft rejection or inflammatory processes [72], more effort is nowadays put into the development of small molecule antagonists and antisense oligonucleotides for this purpose [73,74], A selection of more recently reported clinical studies with antibodies is summarized in Table 1.2. 

After tissue transplantation, the severity and the period of rejection depend on the tissue type, and this process involves the specificity and memory components of the immune response. Avrion Mitchison in the 1950s observed that allograft immunity could be transferred by the components of the cellular immune response, and antibodies present in the serum that were part of the humoral response were not associated with this process. Future studies delineated the role of T lymphocytes in the allograft rejection process, and the role of both CD4+ and CD8+ cells was established. 

Smdies in the 1970s showed that cyclosporin inhibits humoral immunoreactions, and that it had a selective effect on T-cell dependent immunoreactions and that its effect was reversible. Cyclosporin is considered to interfere with the process for primary T-cell activation. In this way the formation of T-effector cells, cytotoxic T-lymphocytes or killer lymphocytes, which have the dominant function in cell mediated immune reactions like rejecting an allograft in transplantation surgery and delayed hypersensitivity reaction, is prevented. 

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