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T Kuramochi

Publications and source records attributed to T Kuramochi.

At least 55 records · Page 3Linked to original sources
PubMed1989

Cross-reactivity between human and canine helper and suppressor T cell antigens using monoclonal antibodies RPA-T4 and HuLy-m8.

The murine monoclonal antibodies RPA-T4 and HuLy-m8, specific for a framework determinant of human helper/inducer and suppressor/cytotoxic T cell antigens, cross-reacted with canine cell membrane molecules recognizing a biomolecular complex (50,000 to 55,000 daltons) similar to that described in humans. We investigated the distribution of these helper and suppressor T cell-like antigens on canine peripheral blood lymphocytes. With complement-mediated lymphocytotoxicity, 34% and 35% of the canine lymphocytes expressed the helper T cell-like antigens and the suppressor-like T cell antigens, respectively. When the lymphocytes were treated with RPA-T4 and HuLy-m8, the respective helper and suppressor function was significantly inhibited.

Animals↗
PubMed1989

Expression of interleukin-2 receptor (IL-2R) in feline peripheral blood lymphocytes.

A monoclonal anti-interleukin-2 receptor (IL-2R) antibody has been identified as a putative antibody against the human IL-2R. In the present study, anti-Tac antibody CD-25 was used to determine cell expressing IL-2 receptor in feline peripheral blood lymphocytes by means of direct immunofluorescence tests and complement-mediated lymphocytotoxicity tests. With complement-mediated lymphocytotoxicity, approximately 18% of feline peripheral blood lymphocytes expressed the receptors. By the direct immunofluorescence test, we found approximately 22% of IL-2R positive cells in lymphocytes of feline peripheral-blood.

Animals↗
PubMed1987

Cross-reactivity between human and feline Ia antigens, using a monoclonal antibody HLA-D.m1.

A murine monoclonal antibody HLA-D.m1 produced against human Ia antigens which react with 10% to 30% of human peripheral-blood mononuclear cells was found to react with greater than 90% of feline mononuclear cells. The antigen was not expressed on granulocytes. By direct immunofluorescence, 7% to 41% of feline lymphocytes expressed surface immunoglobulins. In mixed-lymphocyte reaction, the addition of antibody HLA-D.m1 to cultures abolished proliferation. These studies indicate that most feline peripheral-blood mononuclear cells express Ia-like antigens.

Animals↗
PubMed1987

Characterization of feline T and B cells.

Feline peripheral-blood lymphocyte populations (n = 22) were examined for the following markers: rosette formation with guinea pig erythrocytes (GPE-T cells), rosette formation with human RBC (HRBC-T cells), rosette formation with sheep RBC, mixed rosette formation with GPE-T cells and HRBC-T cells (total T cells), erythrocyte antibody-complement rosettes, and surface immunoglobulin. An average of 28% +/- 7% (range, 16% to 39%) of the feline lymphocytes formed rosettes with GPE-T cells, and 27% +/- 7% (range, 11% to 36%), with HRBC-T cells. An average of 57% +/- 9% (range, 33% to 75%) of the lymphocytes formed mixed rosettes. The erythrocyte antibody-complement rosette-forming cells and surface immunoglobulin-bearing cells were found in peripheral blood lymphocytes (10% +/- 6% and 24% +/- 8%, respectively). The murine monoclonal antibodies OKT 11 and HuLy-m1, specific for a framework determinant of human E-rosette receptor antigens, cross-reacted with feline cell membrane molecules recognizing a bimolecular complex (45,000 to 50,000 daltons) similar to that described in persons. We investigated the distribution of these E-rosette receptor-like antigens on feline lymphocytes. By complement-mediated lymphocytotoxicity, about 30% of the feline lymphocytes expressed the antigens. When lymphocytes were treated with HuLy-m1 antibody, spontaneous rosette formation with HRBC-T cells was significantly inhibited.

Animals↗
PubMed1983

Autologous rosette forming cells in patients with renal diseases.

We studied the distribution of autologous rosette forming cells (ARFC) in the peripheral blood of 30 healthy adult donors, 30 patients with IgA nephropathy, 20 patients with primary glomerular diseases, eight patients with systemic diseases and 25 patients with other renal diseases. The mean percentages of ARFC were markedly reduced in the IgA nephropathy patients compared with the healthy adult donors. The values for ARFC were even more significantly reduced in IgA nephropathy patients compared with patients with primary glomerular diseases, systemic diseases and other renal diseases. This means that the immunoregulatory abberation in IgA nephropathy primarily involves T cells.

Adult↗
PubMed1979

Proton transfer kinetics in the lowest excited state of 1,N6-ethenoadenosine as revealed by fluorescence lifetime measurements.

Fluorescence lifetimes have been examined of 1, N6-ethenoadenosine (epsilon Ado), 1-methyl-ethenoadenosine (m1 epsilon Ado+), 9-methyl-ethenoadenosine (m9 epsilon Ado+), N1-deazaethenoadenosine (N1-deaza-epsilon Ado, and 9-methyl-N1-deazaethenoadenosine (m9N1-deaza epsilon Ado) at various pH's in the 7.5 approximately 1.5 region and at 20 degrees C. From an analysis we have reached the following conclusions. (1) The observed fluorescence of epsilon Ado is caused by the unprotonated, neutral, excited species epsilon Ado not not only at pH 7 but also at pH 2. (2) pKa of the excited epsilon Ado is lower than that of the ground state epsilon Ado. (3) The rate constant of protonation in the excited state is about 10(10) sec-1 M-1.

Adenosine↗
PubMed1976

Nonessential role of neutrophils as mediators of hyperacute cardiac allograft rejection in the rat.

The presence of neutrophils within the graft has been widely emphasized as a characteristic feature of hyperacute rejection, and analogies have been drawn to the Arthus reaction, in which neutrophils are essential mediators of tissue damage. To evaluate the role of neutrophils as mediators of graft destruction in hyperacute rejection, we studied a series of 16 heterotopic ACT strain rat cardiac allografts in skin-presenitized Lewis strain recipients, all of which recieved prior treatment with cyclophosphamide and methotrexate or heterologous rabbit antirat polymorphonuclear globulin. Fourteen recipients showed significant depression in levels of circulating neutrophils prior to transplant, and neutrophils were not detected in 13 allogrates at the time of functional rejection. There was no abrogation of hyperacute rejection in this series and the characteristic pattern of vacular and myocardial damage was not altered by the absence of neutrophils from the graft. Although the possibility that neutrophil-derived agents may contribute to late graft destruction cannot be excluded, this study has shown that neutrophils are neither essential nor specific participants in hyperacute allograft rejection in this model.

Animals↗
PubMed1975

A controlled sequential morphologic study of hyperacute cardiac allograft rejection in the rat.

A series of heterotopic cardiac allografts from ACI strain rat donors to ACI skin-presensitized Lewis strain recipients was examined by light and electron microscopy at intervals from 1 minute to 24 hours for a sequential morphologic study of hyperacute rejection. Syngeneic Lewis hearts grafts in ACI skin-presensitized Lewis recipients provided controls. Extensive platelet aggregation throughout the vasculature of the allografts in the presence of a largely intact endothelium was the initial morphologic event, which was present by 1 minute posttransplant and absent in all syngeneic controls. This was followed by widespread endothelial damage. Endothelial damage preceded neutrophil margination and emigration in the graft. Neutrophil degranulation or evidence of phagocytosis was not observed within the 1st hour. At 6 and 24 hours, degranulated forms were common and apparent extrusion of granule contents with progressive ischemic injury. Segmental occlusion of the vasculature by platelet plugs and progressive disruption and loss of capillaries combined with an increase in permeability may result in myocardial ischemia. Neutrophil-derived agents do not appear to be of major significance in hyperacute rejection during the early posttransplant phase, but may play a role in mediating myocardial injury if the allograft survives for alonger period. However, on morphologic grounds, it is suggested that microcirculatory hypoperfusion with resultant ischemia is a major determinant of myocardial damage and graft function. No significant change was noted over the observation period in peripheral neutrophil or platelet counts when compared to syngeneic controls, and a slight reudction in specific cytotoxic antibody titer in the allografts was immediate but very transient.

Animals↗
PubMed1974

Organ specificity in hyperacute rejection of canine heart and kidney allografts.

To clarify the organ specific nature of hyperacute rejection, 14 puppies were presensitized by multiple skin grafts and spleen cell injections prior to receiving either a heart or kidney allograft from the respective donors. Of this group, 7 received orthotopic heart allografts and 7 received kidney allografts. All heart allografts were rejected between 3 and 28 hours, and all kidneys between 0 and 24 hours as judged by cessation of urine flow from the ureterostomies. In contrast, all 11 animals in a recent series of heart allografts in non-sensitized puppies survived the operation, and rejected between 7 and 17 days. There was a significant correlation in both groups between preoperative cytotoxic antibody titer in the recipient serum and graft survival time. The preoperative titers were all above 1:1,024 but were greatly reduced within 2 hours after transplantation. At the time of rejection, antibody could be eluted from the rejected organs. In contrast to the kidneys, in which 2 of 7 grafts ceased to function immediately after revascularization, all hearts resumed beating and functioned well for at least several hours. At autopsy, the myocardium was pale and edematous and histologically polymorphonuclear leukocytes were prevalent in and around the small vessels and among myofibers. Both IgG and IgM antibody was detected in sarcolemma of the myocardium and to a lesser extent in the intima and adventitia of the small vessels by the fluorescent antibody technique. Biopsies of the rejected kidneys showed polymorphonuclear leukocyte infiltration, typical of hyperacute rejection. Marked fluorescence of IgG and IgM in the glomeruli and peritubular capillaries was observed. This study indicates that both organs rejected hyperacutely in our experimental model and participation of the preformed antibody in effecting this change was strongly suggested.

Animals↗