title: Activation antigen expression on peripheral blood neutrophils following rat small bowel transplantation. NKR-P1 is a novel antigen preferentially expressed during allograft rejection.
abstract: This study used flow cytometric analyses to monitor activation antigen expression (MHC class II; interleukin-2 receptor, p55IL-2R and 3.2.3/NKR-P1 antigen) on peripheral blood neutrophils following rat small bowel transplantation. The rat 3.2.3 antigen is a member of the NKR-P1 family of natural killer (NK) cell-associated molecules, which are expressed at high levels on NK cells and lymphokine-activated killer cells, and low levels on at least one T cell subset. Peripheral blood neutrophils in normal animals express very low or undetectable levels of NKR-P1. Detectable levels of NKR-P1 were induced as early as day 1 following small bowel transplantation in all allografted animals, whereas expression was only rarely detected in isografted animals. In addition, NKR-P1 density was significantly higher in allografted animals and was maintained as rejection developed. MHC class II and p55IL-2R expression was also induced following transplantation. The mechanisms of induction and functional relevance of NKR-P1 expression on neutrophils remain to be defined. However, the concomitant increased expression of MHC class II and p55IL-2R suggest NKR-P1 to be a neutrophil activation marker and implicate a potential role for NKR-P1+ neutrophils in small bowel allograft rejection. This hypothesis is further supported by the loss of detectable peripheral blood neutrophils only with developing rejection. Flow cytometric analysis of neutrophil activation antigen expression may be useful for monitoring human small bowel transplant recipients.
authors.forename: G A
authors.initials: GA
authors.lastname: Webster
authors.forename: M J
authors.initials: MJ
authors.lastname: Bowles
authors.forename: M S
authors.initials: MS
authors.lastname: Karim
authors.forename: R F
authors.initials: RF
authors.lastname: Wood
authors.forename: A G
authors.initials: AG
authors.lastname: Pockley
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000096:biosynthesis*; D006084:Graft Rejection / Q000276:immunology*; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis*; D007421:Intestine, Small / Q000637:transplantation*; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type; D008285:Major Histocompatibility Complex; D008297:Male; D055651:NK Cell Lectin-Like Receptor Subfamily B; D018375:Neutrophil Activation / Q000502:physiology; D009504:Neutrophils / Q000276:immunology*; D051381:Rats; D011919:Rats, Inbred Strains; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis*; D014184:Transplantation, Homologous; D015854:Up-Regulation / Q000276:immunology
chemical_list: D000954:Antigens, Surface; D000949:Histocompatibility Antigens Class II; C527203:KLRB1 protein, human; D037181:Lectins, C-Type; D055651:NK Cell Lectin-Like Receptor Subfamily B; D015375:Receptors, Interleukin-2