       Document 0941
 DOCN  M9620941
 TI    Immune responses to major histocompatibility complex homozygous lymphoid
       cells in murine F1 hybrid recipients: implications for
       transfusion-associated graft-versus-host disease.
 DT    9602
 AU    Fast LD; Valeri CR; Crowley JP; Department of Medicine, Rhode Island
       Hospital, Providence 02903,; USA.
 SO    Blood. 1995 Oct 15;86(8):3090-6. Unique Identifier : AIDSLINE
       MED/96017243
 AB    Graft-versus-host disease (GVHD) is currently encountered after bone
       marrow transplantation and transfusion. GVHD associated with transfusion
       (TA-GVHD) in apparently immunocompetent recipients has been recently
       reported with increasing frequency. A consistent finding in many of
       these cases is that the recipient received blood from a donor homozygous
       for one of the recipient's HLA haplotypes. However, the observed
       frequency of TA-GVHD is much lower than the estimated probability of
       this donor/recipient combination. The potential role of recipient immune
       responses in controlling TA-GVHD was investigated using an analogous
       murine model in which GVHD is induced by the injection of parental
       lymphoid cells into unirradiated F1 hybrid recipients. The effect of
       various immune manipulations of the recipient of GVHD induction was
       assessed by determining the number of donor lymphoid cells required to
       induce GVHD responses. Whereas depletion of recipient CD4+ cells
       increased the number of donor cells needed to induce GVHD, depletion of
       recipient CD8+ and natural killer cells resulted in fewer donor cells
       being needed to induce a GVHD response. These studies suggest a central
       role for functioning recipient CD8 and natural killer cells in the
       down-regulation of TA-GVHD development in recipients.
 DE    Animal  Crosses, Genetic  CD4-Positive
       T-Lymphocytes/IMMUNOLOGY/*TRANSPLANTATION  CD8-Positive
       T-Lymphocytes/*IMMUNOLOGY  Graft vs Host Disease/*IMMUNOLOGY  H-2
       Antigens/*IMMUNOLOGY  Human  Infant  Isoantibodies/*BIOSYNTHESIS  Killer
       Cells, Natural/*IMMUNOLOGY  Lymphocyte Depletion  Mice  Mice, Inbred A
       Mice, Inbred CBA  Mice, Inbred C57BL  Spleen/CYTOLOGY  Support, Non-U.S.
       Gov't  Support, U.S. Gov't, Non-P.H.S.  Support, U.S. Gov't, P.H.S.
       JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

