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T Kakiuchi

Publications and source records attributed to T Kakiuchi.

123 records · Page 7Linked to original sources
PubMed1981

Immune complexes in Takayasu's arteritis.

We examined sera and Fc receptor-bearing lymphocytes from peripheral blood of patients with Takayasu's arteritis for the purpose of investigating the presence of immune complexes (IC). IC in sera were assayed by solid-phase conglutinin-binding test. Seven of 29 patients exceeded the normal range of circulating IC. IC combined with Fc receptors were estimated by enumerating EA-RFC. EA-RFC of lymphocytes from patients with Takayasu's arteritis were 13.0% and those of normal controls were 29.1%. Low EA-RFC in the patient group increased significantly when lymphocytes were incubated with EA after rising lymphocytes with medium at 37 degrees C. On the contrary, EA-RFC from healthy subjects did not increase after rinsing cells. These findings indicate that IC combined with Fc receptors and hindered EA rosette formation and that rinsing cells with medium at 37 degrees C removed IC from Fc receptors. Comparable results were obtained by a membrane immunofluorescence method using FITC-conjugated anti-human immunoglobulin. In order to confirm that EA rosette formation was really blocked by IC, lymphocytes from a healthy donor were incubated with heat-aggregated human IgG. Incubating cells with IgG aggregates caused reduction of EA-RFC and these lymphocytes restored their ability to form rosettes with EA by rinsing cells with medium at 37 degrees C. In conclusion, we could confirm the presence of IC both in sera and on lymphocyte Fc receptors in some cases of Takayasu's arteritis.

Adult↗
PubMed1981

Responses of B cells with or without C3 receptors to polyclonal B cell activators.

Responses of B cells with or without receptors for C3 (CR) to polyclonal B cell activators (PBA) were studied. Mouse spleen cells were incubated with sheep red blood cells (SRBC) coated with antibody and complement to form rosettes, and they were separated by Ficoll-Hypaque density sedimentation into populations depleted of and enriched with lymphocytes bearing CR (CRL). These 2 populations were cultured with lipopolysaccharide (LPS), purified protein derivative of tuberculin (PPD), or dextran sulfate (DxS) and assayed for anti-TNP PFC. The CRL-depleted population responded well to LPS, poorly to PPD, and it showed practically no response to DxS, whereas the CRL-enriched population seemed to respond poorly to LPS but well to both PPD and DxS. The low responsiveness of the cRL-depleted population to PPD and DxS could not be explained by a shift of time-kinetics, by the dose-response profile of the responding cells, or by the depletion of adherent cells. Suppressor T cells did not take part in the reduced responses, since the treatment of the population with anti-Thy 1.2 plus complement could not restore the responses. These results indicate that B cells with CR [CR(+) B cells] respond well both to PPD and DxS, whereas the cells without CR [CR(-) B cells] respond poorly to PPD and DxS. It was difficult to evaluate the low responsiveness of CR(+) B cells to LPS because of the high background PFC of the cRL-enriched population.

Animals↗
PubMed1980

Specificity of an anti-murine B cell serum.

An antiserum (ABS) specific for murine B cells was prepared in rabbits by immunization with lymph node cells from nude mice as reported previously (1). To make the antiserum specific for antibody-forming cell precursors (AFCP) extensive absorption was required with mouse serum, erythrocytes and thymus cells. Even after ABS was no longer cytotoxic for thymus cells, further absorption with thymus cells was necessary to make it ineffective for plaque-forming cells (PFC). The correlation between cells bearing C3- or Fc-receptors and the cells bearing antigen(s) to which ABS reacts was studied. In the residual spleen cells treated with ABS and complement, there were some EAg and EAmCm rosette-forming cells. There were also some spleen cells reacting with ABS even after depletion of C3- and/or Fc-receptor-bearing cells. These results show that the antigen(s) to which ABS reacts could be a marker on B cells different from C3- or Fc-receptors. Spleen cells reacting with ABS were compared with cells bearing C3- or Fc-receptors various days after birth. The cells sensitive to ABS increased in spleens earlier after birth than those with C3- or Fc-receptors.

Absorption↗
PubMed1980

Antigen specific receptors on murine B cell lineage. 1. On antibody forming cells in various stages of immune response.

In this study it was examined whether or not antigen specific receptors are on direct and indirect plaque-forming cells (PFC). Spleen cells from mice primed both with horse red blood cells (HRBC) and sheep red blood cells (SRBC) were incubated with HRBC to make rosettes and fractionated on Ficoll-Hypaque density gradient. Both direct and indirect HRBC-PFC were depleted from the interface fraction. The depletion was antigen specific and inhibited by the preincubation of spleen cells with antiserum against kappa- or mu-chain for direct PFC and with antiserum against kappa- or gamma 1-chain for indirect PFC. The depletion was not due to the rosette formation mediated by Fc-receptors which might be on antibody forming cells, because PFC were not eliminated by the density gradient sedimentation after incubation of spleen cells with SRBC coated with anti-SRBC IgG antibody in our experimental conditions. Our results show that the antigen specific immunoglobulin receptors are on the cells producing IgG antibody after primary or secondary immunization as well as on the IgM antibody-forming cells even in late stage of immune response.

Animals↗
PubMed1980

Antigen specific receptors on murine B cell lineage. 2. Different effect of rosette-forming cell depletion on IgM and IgG antibody forming cell precursors in primary and secondary response.

Spleen cells from unprimed mice or those primed with horse red blood cells (HRBC) were depleted of rosette-forming cells (RFC) with HRBC by the Ficoll-Hypaque density sedimentation, and the cells were examined in the adoptive transfer system whether they could raise IgM or IgG antibody-forming cells (AFC) after an immunization with HRBC. When spleen cells were pooled from unprimed mice, the response to HRBC of those depleted of RFC with HRBC (HRBC-RFC) was decreased to about a half in both IgM and IgG AFC. On the other hand, when spleen cells were from mice primed with HRBC, the response to HRBC of those depleted of HRBC-RFC was decreased dramatically to 1/20 of that of original cells in IgG AFC, but it was decreased to about a half in IgM AFC. In the time course of the response to HRBC of RFC-depleted spleen cells from mice primed with HRBC, an early IgG response was abolished but the late one was as high as that of untreated spleen cells. These results suggest that the depletion of RFC is most effective on the depletion of direct precursors of the secondary IgG AFC.

Animals↗
PubMed1980

Effect of lipopolysaccharide (LPS) on the thymocyte response to PHA: strain difference.

Thymocytes responded well to PHA in terms of [3H]-TdR incorporation if they were precultured in the presence of LPS, whereas fresh thymocytes or thymocytes pre-cultured in the absence of LPS responded poorly to PHA. The PHA response of thymocytes pre-cultured with LPS for several hours was similar to that of fresh spleen cells in the kinetics and dose-response profiles. The effect of LPS was found on thymocytes from BALB/c.Cr, AKR/Jms, and DDD/1 mice, but was not observed on those from C3H/HeJms and C57Bl/6J mice, indicating that there is a strain difference in the PHA responsiveness of LPS-pre-cultured thymocytes. In contrast to thymocytes, the response of spleen cells to PHA was enhanced in both C57Bl/6J and BALB/c.Cr mice by pre-culture with LPS.

Animals↗
PubMed1976

Preparation and effects of an anti-B cell serum.

An heterologous antiserum specific for bone marrow-derived cells (B cells) was prepared by immunizing rabbits with lymph node cells from nude mice. After absorption with mouse red blood and thymus cells, the antiserum killed a population of cells from various lymphoid organs and the cytotoxic effects were inversely related to those of anti-theta antibody. When bone marrow or spleen cells were treated with the antiserum and guinea pig complement before transfer into irradiated mice, the number of plaque-forming cells was greatly reduced in the spleen of the recipient. Pretreatment of thymus cells with the antiserum in a similar way resulted in no inhibition of hemolytic plaque. When spleen cells from mice previously immunized with sheep red blood cells were treated with the antiserum and complement, the formation of hemolytic plaque was not affected. These findings indicated that the antiserum was specific for B cells and that the number of antigenic determinants on B cells to which the antiserum reacted decreases during differentiation into antibody-forming cells.

Absorption↗
PubMedDate not supplied

A case of non-Hodgkin's lymphoma following long-term corticosteroid therapy for Addison's disease.

A 76-year-old Japanese woman had suffered from fatigue, weight loss, and cutaneous hyperpigmentation at the age of 38 years and was diagnosed as having tuberculous Addison's disease. Since then, corticosteroids had been administered effectively as hormonal replacement. At the age of 75 years, the patient presented with a progressive, painless swelling in the left eyelid due to an ill-defined tumor of rubbery consistency in the superotemporal aspect of the orbit. Computed tomography, magnetic resonance imaging, and scintigraphy revealed a wide distribution of tumors, but not in the adrenal gland, which led to the suspicion of systemic malignant lymphoma. Histopathologic examination of the excised orbital tumor was compatible with non-Hodgkin's lymphoma of the B-cell type. We believe this is the first report of Addison's disease presenting with non-Hodgkin's lymphoma. This disease process was characterized by the development of a lymphoid malignancy after long-term corticosteroid therapy to control the adrenal insufficiency, and by the widespread involvement of the lymph nodes and orbit but not the adrenal gland. Corticosteroid-induced abnormal immune state was considered to be the pathogenesis of this unusual complication.

Addison Disease↗