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In situ effector mechanisms in rat kidney allograft rejection. I. Characterization of the host cellular infiltrate in rejecting allograft parenchyma.
Authors:Eeva von Willebrand  Anu Soots  P. Häyry
Affiliation:Transplantation Laboratory, Fourth Department of Surgery, University of Helsinki, SF 00290 Helsinki 29, Finland
Abstract:The infiltrating inflammatory cells were recovered with collagenase and DNase from rejecting rat kidney allografts and autografts in conditions where the enzyme treatment did not affect the expression of subclass-specific surface markers. As the differential distribution of the inflammatory cells in the dispersate was similar to the distribution of inflammatory cells in tissue imprints, and as any major blood contamination was excluded, we consider the results representative of the composition of the in situ infiltrate. At the peak of rejection on Day 6 after the transplantation, approximately 30% monocytes, 17% macrophages, 31% lymphocytes, 6% (T) lymphoblasts, and 10% (B) plasmablasts and plasma cells were present in the graft. The blast cell response, pathognomonic to immune activation, was less prominent in the recipient spleen, blood, and lymph nodes. Twenty-three percent of the infiltrating lymphocytes expressed the (T-cell-specific) Pta.A.1 surface antigen(s) and 14% were surface Ig positive. The remaining lymphocytes were double-negative “null cells.” In preparative cell electrophoresis most of the allograft-infiltrating lymphocytes carried the low electrophoretic mobility, characteristic to resting B cells. Approximately 70% of allograft-infiltrating macrophages and 50% of infiltrating monocytes but only 30% of the monocytes present in the recipient spleen expressed the Fc receptor to IgG, suggesting an activation (or increase in avidity) of this receptor during the influx of mononuclear cells into the site of inflammation and during maturation of monocytes into tissue macrophages. There was a strong in situ proliferative activity, far stronger than in the central lymphatic system of the recipient rat. After 1 hr in vivo pulse labeling with [3H]thymidine 24% of the infiltrating inflammatory cells carried the label. Most of the labeled cells were blasts or lymphocytes, but a small albeit distinct number of labeled monocytes were also present in situ. In contrast to the recipient spleen, where most of the labeled lymphoid cells had a high electrophoretic mobility of resting T cells, in the infiltrate most of the labeled lymphoid cells had a slow mobility of resting B cells.
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