Recipient CD8+ cells are responsible for the rapid elimination of allogeneic donor lymphoid cells.

Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

Recipient CD8+ cells are responsible for the rapid elimination of allogeneic donor lymphoid cells.

J Immunol. 1996 Dec 1;157(11):4805-10. Unique Identifier : AIDSLINE MED/97098705
Fast LD; Department of Medicine, Rhode Island Hospital and Brown; University School of Medicine, Providence 02903, USA.

Abstract: Blood transfusion can result in a variety of immunologic responses, including alloimmunization, transfusion-associated graft-versus-host disease, and immunosuppression that results in increased postoperative infection rate, and can also result in increased survival of allografts. One of the many factors influencing the resulting immunologic responses from a blood transfusion is the persistence of the donor leukocytes. A recent study has shown that almost all (99.9%) allogeneic leukocytes are removed within 2 days following transfusion but did not characterize the mechanism responsible for the rapid removal of allogeneic donor cells. Using a murine model these studies show that it is recipient CD8+ T cells that are responsible for the rapid elimination of allogeneic lymphocytes in naive recipients. Effective elimination was dependent on the donor/recipient combination and required that the donor cells express at least one MHC class I disparity to be recognized by the recipient CD8+ cells and that the donor cells also be able to induce additional responses that were needed by the CD8+ cells to manifest full activity. The perforin pathway was the predominant pathway used by the recipient CD8+ cells to mediate this elimination.

Keywords: Animal *Blood Transfusion Cytotoxicity, Immunologic CD8-Positive T-Lymphocytes/*IMMUNOLOGY G(M1) Ganglioside/IMMUNOLOGY Histocompatibility Antigens Class I/METABOLISM Killer Cells, Natural/IMMUNOLOGY Lymphocytes/*IMMUNOLOGY Membrane Glycoproteins/GENETICS/IMMUNOLOGY Mice Mice, Inbred CBA Mice, Inbred C3H Mice, Inbred C57BL Mice, Inbred DBA Mice, Knockout Support, Non-U.S. Gov't Transplantation, Homologous JOURNAL ARTICLE
970228
M9721854

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