TY - JOUR
T1 - Mechanisms and mediators of inflammation
T2 - Potential models for skin rejection and targeted therapy in vascularized composite allotransplantation
AU - Hautz, Theresa
AU - Wolfram, Dolores
AU - Grahammer, Johanna
AU - Starzl, Ravi
AU - Krapf, Christoph
AU - Pratschke, Johann
AU - Lee, W. P.Andrew
AU - Brandacher, Gerald
AU - Schneeberger, Stefan
PY - 2012
Y1 - 2012
N2 - Vascularized composite allotransplantation (VCA) is an effective treatment option for patients suffering from limb loss or severe disfigurement. However, postoperative courses of VCA recipients have been complicated by skin rejection, and long-term immunosuppression remains a necessity for allograft survival. To widen the scope of this quality-of-life improving procedure minimization of immunosuppression in order to limit risks and side effects is needed. In some aspects, the molecular mechanisms and dynamics of skin allograft rejection seem similar to inflammatory skin conditions. T cells are key players in skin rejection and are recruited to the skin via activation of adhesion molecules, cytokines, and chemokines. Blocking these molecules has not only shown success in the treatment of inflammatory dermatoses, but also prolonged graft survival in various models of solid organ transplantation. In addition to T cell recruitment, ectopic lymphoid structures within the allograft associated with chronic rejection in solid organ transplantation might contribute to the strong alloimmune response towards the skin. Selectively targeting the molecules involved offers exciting novel therapeutic options in the prevention and treatment of skin rejection after VCA.
AB - Vascularized composite allotransplantation (VCA) is an effective treatment option for patients suffering from limb loss or severe disfigurement. However, postoperative courses of VCA recipients have been complicated by skin rejection, and long-term immunosuppression remains a necessity for allograft survival. To widen the scope of this quality-of-life improving procedure minimization of immunosuppression in order to limit risks and side effects is needed. In some aspects, the molecular mechanisms and dynamics of skin allograft rejection seem similar to inflammatory skin conditions. T cells are key players in skin rejection and are recruited to the skin via activation of adhesion molecules, cytokines, and chemokines. Blocking these molecules has not only shown success in the treatment of inflammatory dermatoses, but also prolonged graft survival in various models of solid organ transplantation. In addition to T cell recruitment, ectopic lymphoid structures within the allograft associated with chronic rejection in solid organ transplantation might contribute to the strong alloimmune response towards the skin. Selectively targeting the molecules involved offers exciting novel therapeutic options in the prevention and treatment of skin rejection after VCA.
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U2 - 10.1155/2012/757310
DO - 10.1155/2012/757310
M3 - Review article
C2 - 23049603
AN - SCOPUS:84867389239
SN - 1740-2522
VL - 2012
JO - Clinical and Developmental Immunology
JF - Clinical and Developmental Immunology
M1 - 757310
ER -