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pubmed-article:3065337pubmed:abstractTextImmunosuppression and its associated infectious complications have long been recognized as consequences of major thermal trauma, though the factors that mediate this suppression remain unclear. A murine split-thickness skin graft model was developed to investigate the role of a large surface area wound in the initiation of immunosuppression in the absence of burn injury. Significant T cell-mediated immunosuppression was demonstrated following wounding and immediate repair with either syngeneic or allogeneic split-thickness skin grafts. These results are consistent with previous experiments in a murine burn model treated by escharectomy and resurfacing with syngeneic composite full-thickness skin. Data also supports the concept that mediators of inflammation at the wound site play an important role in postburn immunosuppression. Furthermore, these results suggest that the use of skin allografts during the early postburn period does not adversely affect cell-mediated immunity in any way that could be abrogated by primary autografting.lld:pubmed
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pubmed-article:3065337pubmed:authorpubmed-author:BakerC CCClld:pubmed
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pubmed-article:3065337pubmed:authorpubmed-author:KupperT STSlld:pubmed
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pubmed-article:3065337pubmed:volume9lld:pubmed
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pubmed-article:3065337pubmed:pagination354-8lld:pubmed
pubmed-article:3065337pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:3065337pubmed:articleTitleImmunologic alterations following excisional wounding and immediate repair with syngeneic or allogeneic skin grafts.lld:pubmed
pubmed-article:3065337pubmed:affiliationYale University School of Medicine, New Haven, CT 06510.lld:pubmed
pubmed-article:3065337pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3065337pubmed:publicationTypeComparative Studylld:pubmed