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In vivo depletion of NKR-P1 positive cells in the recipient prior to small bowel transplantation enhances graft-versus-host disease (GvHD) in the rat

Conference paper

Abstract

Recent evidence for major histocompatibility complex (MHC) class I antigen-directed recognition mechanisms of natural killer cells (NKs) have revived interests in investigating non-adaptive immune responses in the framework of solid organ transplantation. A semiallogeneic rat model of heterotopic small bowel transplantation (HSBTx) from male DA parental to male F1 hybrid rats (DA x LEW) was established to investigate the role of host NKs to attenuate graftversus-host (GvH)-mediated immunosuppression and tissue injury. By use of anti-NKR-P1 monoclonal antibody (mAb) 3.2.3, host NKs were depleted effectively in vivo after triple intraperitoneal injection prior to HSBTx. In contrast to non-depleted animals, an initial lack of NK activity in F1 hosts significantly decreased the mean survival (P < 0.01) and substantially enhanced graftversus-host disease (GvHD)-related damage to lymphoid and non-lymphoid target organs. These findings emphasize the important immunoregulatory role of host NKs during the early onset of GvHD.

Key words

Graft-versus-host disease (GvHD) Allogeneic lymphocyte cytotoxicity Natural killer cells Small bowel transplantation Major histocompatibility complex (MHC) 

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Copyright information

© Springer-Verlag Berlin Heidelberg 1996

Authors and Affiliations

  1. 1.Department of General and Thoracic SurgeryUniversity of KielKielGermany
  2. 2.Pittsburgh Cancer InstituteUniversity of PittsburghPittsburghUSA
  3. 3.Institute of ImmunologyUniversity of KielKielGermany

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