Polymerase chain reaction (PCR) technology was employed to examine peripheral blood and synovial T increased synovial expression of V/i14 was found, but only in the synovial fluid samples. Reduced expression of V#1, Vj64, V/i5.1, V/i10, V,816, and V/i19 was also observed in synovial T cells. These results indicate that biased V,8 gene utilization in different peripheral compartments of RA patients can be observed in unselected T cell populations, and are consistent with the conclusion that populations of T cells expressing these V/i gene products may be involved in the pathogenesis of the disease. (J. Clin. Invest. 1993. 92:2688-2701

No abstract

Graft rejection after marrow transplantation is generally thought to be mediated by alloreactive immune effector cells of host origin. Transfused blood products also contain immune cells capable of alloreactivity against both donor graft and host. To reduce the risk of transfusion-associated graft-versus-host disease (GVHD) and graft rejection, standard procedure is to irradiate all blood products with at least 1,500 rad before transfusion. We report a patient with chronic myelogenous leukemia who developed graft rejection and GVHD after receiving a T-cell-depleted transplant from a serologically HLA-A, B, DR/DQ matched and mixed lymphocyte culture (MLC) nonreactive unrelated donor. Cytogenetic analysis of marrow cells collected at the time of graft rejection revealed a PH1-negative female karyotype that was not consistent with donor cells. Use of specific minisatellite DNA probes (YNH 24, H-RAS, and 3′ HVR) revealed the exclusive presence of third- party (neither donor nor recipient) restriction-fragment-length polymorphisms (RFLP) in both peripheral blood and marrow. Repeat RFLP analysis 3 days later showed persistence of this unique third-party banding pattern. DNA-based HLA-typing, using polymerase chain reaction (PCR) and oligonucleotide probe hybridization, also showed these cells to be derived from an individual whose HLA-DR type was distinct from donor and recipient. Together, these findings suggested the presence of a proliferating population of transfused cells possessing alloreactivity against both donor graft and host, despite prior irradiation of all blood products with 2,000 rad. Limiting dilution analysis to assess the frequency of irradiated lymphocytes able to respond to mitogen revealed an approximate 5- to 6-log reduction at 1,500 to 2,000 rad as compared with unirradiated controls. These data indicate that a small percentage of lymphocytes can survive irradiation at these doses and suggest that existing blood-product irradiation guidelines may require reassessment, especially in T-cell-depleted transplant recipients.

Maternally transmitted antigen (Mta) is a murine cell-surface molecule defined by the reactivity of specific H-2 nonrestricted cytotoxic T lymphocytes (CTL-s). Maternal transmission appears to be under control of a stable genetic factor in the cytoplasm of the ovum. In view of the known maternal inheritance of mitochondria we have assessed their involvement in Mta expression using the mitochondria specific poison Rhodamine 6G (R6G). We report here that Mta expression in somatic cell hybrids requires functional mitochondria from the Mta+ parent cell line. Mta expression was dominant in hybrids from the fusion of Mta+ and Mta- cells. However, pretreatment of the Mta+ parent with R6G resulted in hybrids which were Mta-, or diminished in Mta expression. These data strongly implicate mitochondrial DNA (mtDNA) in the expression of a cell-surface molecule, and define a system for studying a previously unrecognized mitochondrial function. To our knowledge, this is the first evidence for mitochondrial control of the expression of a cell membrane molecule in eukaryotes.