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Abstract
The immune suppression that frequently accompanies severe injury undoubtedly contributes
to subsequent infectious complications. Various lymphocyte subpopulations may be identified
by surface antigen expression, and alterations in antigen expression by lymphocytes
may reflect host immune competence. Using monoclonal antibodies (Moabs) and dual-color
flow cytometry, we studied lymphocyte phenotypic expression in mice after either controlled
burn injury or hind-limb amputation, with use of peripheral blood, lymph node, and
spleen for cell preparation. Moabs were utilized specific for T cells (Lyt-1), helper/inducer
cells (L3T4), suppressor/cytotoxic cells (Lyt-2), B cells (IgG), and activated T cells
(Ia or IL-2 receptor). The assay techniques called for small amounts of tissue and
avoided gradient procedures that might result in selective loss of some lymphocyte
populations. The most consistent changes observed were depressions in percentages
of L3T4+ and Lyt-2+ cells in spleens of burned mice, accompanied by depression in Ia+ (possibly activated or proliferating) subsets of L3T4+ and Lyt-2+ cells, and the appearance of increased percentages of non-B, non-T lymphocytes. Changes
in lymph node cells were minimal. The major alteration seen in peripheral blood was
substantial depression of Ia+ subsets, although burned mice had increased circulating Lyt-2+ cells on several late postburn days. Burned mice, unlike limb-trauma mice, had marked
splenic hypertrophy with more than a 300% increase in spleen weight after the 30-day
postburn period. Eschar excision/implantation experiments indicated that splenic hypertrophy
and splenocyte phenotypic changes are related to the presence of burned tissue, which
suggests that burned tissue may partially mediate immune changes that accompany severe
burn injury.
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Article info
Publication history
Accepted:
November 22,
1988
Footnotes
☆Supported in part by National Institutes of Health grant GM-35259 and Office of Naval Research contract N-00014-56-C.
Identification
Copyright
© 1989 Published by Elsevier Inc.
