ABSTRACT
Rat allogeneic heart or kidney grafts are rejected within 6 to 8 days, whereas lymphoid cells from the same donor transplanted intravenously across the MHC barrier are eliminated, in most part, within 6 h. We have found that donor specific transfusions (DST) significantly prolonged the survival time of organ allograft but accelerated destruction of i.v. transplanted lymphocytes. Partial elimination of transplanted lymphocytes was observed after third-party blood transfusion. Blocking of the MHC class I and II determinants on transplanted lymphocytes with monoclonal antibodies OX18 and OX6 did not have effect on the lymphocyte elimination kinetics. The effect of hyperacute elimination of allogeneic lymphocytes by DST-treated rats could be adoptively transferred with their sera, although the cytotoxic antibody titer against donor MHC antigens was in these sera low or hardly detectable. DST-recipient sera contained donor-specific IgG and IgM alloantibodies. It seems that these "enhancing" antibodies could block the MHC products on organ graft endothelial cells, thereby preventing attack of circulating donor-specific cytotoxic lymphocytes. At the same time they may opsonize the transplanted lymphocytes, thereby facilitating their recognition and removal in the lymphoid organs of graft recipient.
Subject(s)
Graft Rejection/immunology , Heart Transplantation/immunology , Lymphocyte Transfusion , Animals , Antibodies, Monoclonal/pharmacology , Antibody Specificity , Blood Donors , Cell Movement , Chromium Radioisotopes , Graft Survival/immunology , Immunoglobulin G/blood , Immunoglobulin M/blood , Isoantibodies/blood , Lymphocytes/cytology , Lymphocytes/drug effects , Organ Specificity , Rats , Rats, Inbred BN , Rats, Inbred Lew , Tissue Donors , Transplantation Immunology , Transplantation, HomologousABSTRACT
A case of an extensive arterial anomaly in the vertebral canal (Th5-S5) in a boy aged 3 years is described. Sudden onset of the disease with massive subarachnoid haemorrhage, loss of consciousness and signs of raised intracranial pressure suggested rather a lesion in the cranial cavity. The final diagnosis was made after myelography and spinal arteriography. In view of the extent of the lesion its radical removal was not possible. Embolization was done twice of the greatest vessels feeding the anomaly followed by decompression laminectomy. The patient is without neurological defects and pains. The case is reported in view of its rarity and atypical character of the lesion as well as its extent.
