The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses

Barbara Wasowska, David N. Howell, William M. Baldwin, Fred Sanfilippo

Research output: Contribution to journalArticle

Abstract

Donor-specific blood transfusion (DSBT) given 1-2 weeks prior to transplantation prolongs the survival of fully allogeneic ACI (RT1") renal allografts in PVG (RT1C) recipients from 6-8 days to >100 days. We have previously demonstrated that ACI kidneys transplanted to autologous blood transfusion (ABT)- or DSBT-pre-treated PVG recipients stimulated an increase in CD8+(OX8+) cells in the peripheral blood by 6 days after transplantation. To determine whether this increase represents a general expansion of the entire CD8+ population or only a subpopulation of CD8+ cells, subset analysis was performed on peripheral blood lymphocytes depleted of cells reactive with monoclonal antibodies against rat a/9 T cell receptor (TCR), CD8, or NK cells (R7.3, 0X8, or 3.2.3, respectively). Phenotypic studies of PBL depleted of CD8+ cells demonstrated that all 3.2.3+ NK cells coexpressed CD8; depletion of 3.2.3* PBL revealed a secondsubpopulation of CD8+3.2.3~ cells comprised predominantly of a/8TCR+ T cells. In naive PVG rats the prevelence of these two CD8 subpopulations was approximately equal. Both ABT- and DSBT-pretreated renal allograft recipients demonstrated a significant and equivalent expansion of the CD8+ cell subpopulation that coexpresses the 3.2.3 NK marker. In contrast, the second subpopulation of CD8+3.2.3- cells did not change significantly after allografting. There were also no differences between DSBT and ABT pretreated rats in activity of PBL against the NK targets YAC-1 and Doxie at 6 days after renal transplantation, though the level of activity was modestly increased compared with naive controls. These findings indicate that renal transplantation in the rat is associated with a significant increase in PBL with the NK phenotype (CD8+3.2.3+) and a modest increase of NK activity, but that DSBT enhancement does not affect this NK cell response.

Original languageEnglish (US)
Pages (from-to)136-142
Number of pages7
JournalTransplantation
Volume54
Issue number1
StatePublished - 1992
Externally publishedYes

Fingerprint

Blood Transfusion
Natural Killer Cells
Allografts
Tissue Donors
Kidney
Autologous Blood Transfusions
Blood Donors
Kidney Transplantation
Transplantation
Homologous Transplantation
T-Cell Antigen Receptor
Monoclonal Antibodies
Lymphocytes
T-Lymphocytes
Phenotype
Population

ASJC Scopus subject areas

  • Transplantation
  • Immunology

Cite this

Wasowska, B., Howell, D. N., Baldwin, W. M., & Sanfilippo, F. (1992). The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses. Transplantation, 54(1), 136-142.

The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses. / Wasowska, Barbara; Howell, David N.; Baldwin, William M.; Sanfilippo, Fred.

In: Transplantation, Vol. 54, No. 1, 1992, p. 136-142.

Research output: Contribution to journalArticle

Wasowska, B, Howell, DN, Baldwin, WM & Sanfilippo, F 1992, 'The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses', Transplantation, vol. 54, no. 1, pp. 136-142.
Wasowska, Barbara ; Howell, David N. ; Baldwin, William M. ; Sanfilippo, Fred. / The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses. In: Transplantation. 1992 ; Vol. 54, No. 1. pp. 136-142.
@article{29528cfdbe684eb3a18832d24cb01009,
title = "The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses",
abstract = "Donor-specific blood transfusion (DSBT) given 1-2 weeks prior to transplantation prolongs the survival of fully allogeneic ACI (RT1{"}) renal allografts in PVG (RT1C) recipients from 6-8 days to >100 days. We have previously demonstrated that ACI kidneys transplanted to autologous blood transfusion (ABT)- or DSBT-pre-treated PVG recipients stimulated an increase in CD8+(OX8+) cells in the peripheral blood by 6 days after transplantation. To determine whether this increase represents a general expansion of the entire CD8+ population or only a subpopulation of CD8+ cells, subset analysis was performed on peripheral blood lymphocytes depleted of cells reactive with monoclonal antibodies against rat a/9 T cell receptor (TCR), CD8, or NK cells (R7.3, 0X8, or 3.2.3, respectively). Phenotypic studies of PBL depleted of CD8+ cells demonstrated that all 3.2.3+ NK cells coexpressed CD8; depletion of 3.2.3* PBL revealed a secondsubpopulation of CD8+3.2.3~ cells comprised predominantly of a/8TCR+ T cells. In naive PVG rats the prevelence of these two CD8 subpopulations was approximately equal. Both ABT- and DSBT-pretreated renal allograft recipients demonstrated a significant and equivalent expansion of the CD8+ cell subpopulation that coexpresses the 3.2.3 NK marker. In contrast, the second subpopulation of CD8+3.2.3- cells did not change significantly after allografting. There were also no differences between DSBT and ABT pretreated rats in activity of PBL against the NK targets YAC-1 and Doxie at 6 days after renal transplantation, though the level of activity was modestly increased compared with naive controls. These findings indicate that renal transplantation in the rat is associated with a significant increase in PBL with the NK phenotype (CD8+3.2.3+) and a modest increase of NK activity, but that DSBT enhancement does not affect this NK cell response.",
author = "Barbara Wasowska and Howell, {David N.} and Baldwin, {William M.} and Fred Sanfilippo",
year = "1992",
language = "English (US)",
volume = "54",
pages = "136--142",
journal = "Transplantation",
issn = "0041-1337",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - The effects of donor-specific blood transfusion enhancement of rat renal allografts on host NK cell responses

AU - Wasowska, Barbara

AU - Howell, David N.

AU - Baldwin, William M.

AU - Sanfilippo, Fred

PY - 1992

Y1 - 1992

N2 - Donor-specific blood transfusion (DSBT) given 1-2 weeks prior to transplantation prolongs the survival of fully allogeneic ACI (RT1") renal allografts in PVG (RT1C) recipients from 6-8 days to >100 days. We have previously demonstrated that ACI kidneys transplanted to autologous blood transfusion (ABT)- or DSBT-pre-treated PVG recipients stimulated an increase in CD8+(OX8+) cells in the peripheral blood by 6 days after transplantation. To determine whether this increase represents a general expansion of the entire CD8+ population or only a subpopulation of CD8+ cells, subset analysis was performed on peripheral blood lymphocytes depleted of cells reactive with monoclonal antibodies against rat a/9 T cell receptor (TCR), CD8, or NK cells (R7.3, 0X8, or 3.2.3, respectively). Phenotypic studies of PBL depleted of CD8+ cells demonstrated that all 3.2.3+ NK cells coexpressed CD8; depletion of 3.2.3* PBL revealed a secondsubpopulation of CD8+3.2.3~ cells comprised predominantly of a/8TCR+ T cells. In naive PVG rats the prevelence of these two CD8 subpopulations was approximately equal. Both ABT- and DSBT-pretreated renal allograft recipients demonstrated a significant and equivalent expansion of the CD8+ cell subpopulation that coexpresses the 3.2.3 NK marker. In contrast, the second subpopulation of CD8+3.2.3- cells did not change significantly after allografting. There were also no differences between DSBT and ABT pretreated rats in activity of PBL against the NK targets YAC-1 and Doxie at 6 days after renal transplantation, though the level of activity was modestly increased compared with naive controls. These findings indicate that renal transplantation in the rat is associated with a significant increase in PBL with the NK phenotype (CD8+3.2.3+) and a modest increase of NK activity, but that DSBT enhancement does not affect this NK cell response.

AB - Donor-specific blood transfusion (DSBT) given 1-2 weeks prior to transplantation prolongs the survival of fully allogeneic ACI (RT1") renal allografts in PVG (RT1C) recipients from 6-8 days to >100 days. We have previously demonstrated that ACI kidneys transplanted to autologous blood transfusion (ABT)- or DSBT-pre-treated PVG recipients stimulated an increase in CD8+(OX8+) cells in the peripheral blood by 6 days after transplantation. To determine whether this increase represents a general expansion of the entire CD8+ population or only a subpopulation of CD8+ cells, subset analysis was performed on peripheral blood lymphocytes depleted of cells reactive with monoclonal antibodies against rat a/9 T cell receptor (TCR), CD8, or NK cells (R7.3, 0X8, or 3.2.3, respectively). Phenotypic studies of PBL depleted of CD8+ cells demonstrated that all 3.2.3+ NK cells coexpressed CD8; depletion of 3.2.3* PBL revealed a secondsubpopulation of CD8+3.2.3~ cells comprised predominantly of a/8TCR+ T cells. In naive PVG rats the prevelence of these two CD8 subpopulations was approximately equal. Both ABT- and DSBT-pretreated renal allograft recipients demonstrated a significant and equivalent expansion of the CD8+ cell subpopulation that coexpresses the 3.2.3 NK marker. In contrast, the second subpopulation of CD8+3.2.3- cells did not change significantly after allografting. There were also no differences between DSBT and ABT pretreated rats in activity of PBL against the NK targets YAC-1 and Doxie at 6 days after renal transplantation, though the level of activity was modestly increased compared with naive controls. These findings indicate that renal transplantation in the rat is associated with a significant increase in PBL with the NK phenotype (CD8+3.2.3+) and a modest increase of NK activity, but that DSBT enhancement does not affect this NK cell response.

UR - http://www.scopus.com/inward/record.url?scp=0026633745&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026633745&partnerID=8YFLogxK

M3 - Article

VL - 54

SP - 136

EP - 142

JO - Transplantation

JF - Transplantation

SN - 0041-1337

IS - 1

ER -