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Biomedical subjects

K Kuribayashi

Publications and source records attributed to K Kuribayashi.

At least 127 records · Page 7Linked to original sources
PubMed1987

Induction of activated natural killer cells from murine spleen cells primed in vivo and subsequently challenged in vitro with the streptococcal preparation OK432.

The present study shows that natural killer cell-mediated cytotoxicity of BALB/c mouse spleen cells to syngeneic tumor cells was augmented by in vivo priming or in vitro stimulation with the streptococcal preparation OK432. The augmentation of spleen cell cytotoxicity to syngeneic tumor cells by in vivo priming alone with OK432 was lower than that obtained by in vitro stimulation alone with OK432. When the murine spleen cells primed in vivo with OK432 were rechallenged in vitro with OK432 at various intervals, the natural cytotoxicity was more strongly enhanced than that seen with in vitro stimulation alone. The cell surface phenotype of killer cells activated with OK432 was Thy 1+ and asialo GM1+, suggesting the activated natural killer cell. Next, mice were transplanted with syngeneic colon adenocarcinoma cells, and primed in vivo with OK432. These spleen cells were subsequently challenged in vitro with OK432. These spleen cells displayed a strong cytotoxic activity not only to the transplanted adenocarcinoma cells but also to other syngeneic tumor cells.

Adenocarcinoma↗
PubMed1987

Regulatory action of immune B cells on delayed-type hypersensitivity in mice.

Suppressor cells in delayed-type hypersensitivity (DTH) to soluble protein antigens were induced in vitro from BALB/c spleen cells. Transfer of these cells into syngeneic recipients resulted in suppression of the hosts' DTH responses in an antigen-specific manner. These suppressor cells were characterized as B cells by their adherence to nylon-wool columns, resistance to treatment of anti-Thy 1, -Ly 1, and -Ly 2 antibodies plus complement, adherence to anti-mouse immunoglobulin-coated dishes, and nonadherence to uncoated plastic dishes. In addition to being radiation sensitive, these suppressor B cells showed the capability of binding to the primed antigen. Thus, it was demonstrated that our in vitro-induced suppressor cells were antigen-specific B cells. When these suppressor B cells were transferred into the recipients, serum titers of specific antibodies were elevated and effector phase suppressor T cells were induced in the recipients. These results suggest that suppressor B cells exert their suppressor activity through the idiotype-anti-idiotype network.

Animals↗
PubMed1987

Selective deficiency in IL-2 production and refractoriness to extrinsic IL-2 in immunodeficiency with hyper-IgM.

Various lymphokines are inducible by the stimulation of T-cell mitogens, phytohemagglutinin, and concanavalin A. A 32-year-old female with an atypical type of immunodeficiency with hyper-IgM was evaluated for possible defects in the production of several immunoregulatory lymphokines. Although the mitogens appeared to bind effectively to the specific surface receptors of patient peripheral blood lymphocyte (PBL), the proliferative responses were significantly decreased. The culture supernatant of patient PBL stimulated by the mitogens contained only a trace amount of interleukin 2 (IL-2) activity. Addition of recombinant IL-2 to the cultures concomitantly with the mitogens could not restore the decreased responses of patient PBL. Tac antigen expression of patient PBL induced by the mitogens was moderately impaired. These data suggest that there is a defect in both IL-2-producing and IL-2-responding cells. In contrast, the culture supernatant of mitogen-stimulated patient PBL contained B-cell growth and differentiation factors as well as interferon-gamma activities equal to those of the control. These results suggest that there are independent regulatory pathways for the production of IL-2 and other T-cell-derived lymphokines.

Adult↗
PubMed1987

Hepatitis-associated aplastic anemia with systemic plasmacytosis.

An autopsy case of hepatitis associated aplastic anemia was presented. A 58-year-old Japanese female with non-A, non-B hepatitis was admitted on August 2, 1983. Moderate grade of fever and hemorrhagic diathesis appeared on September 16, when hepatitis was evaluated as being under resolving. The peripheral blood and bone marrow findings were consistent with aplastic anemia. Since infection was suggested by increased levels of serum gammaglobulin and CRP, treatment with antibiotics as well as prednisolone and blood transfusion was initiated. Since September 21, gradual tenderness and edema on the right lower abdominal wall appeared. She died on October 3. On postmortem examination, systemic plasmacytosis with lymphadenopathy and septic monilial infection was revealed. Numerous plasma cells were atypical, but were immunohistochemically proved to be polyclonal. The bone marrow showed a massive and diffuse plasma cell proliferation with extremely scarce myeloid cells and megakaryocytes. There was a large granulomatous lesion with monilial infection in the wall of the ileocecum. By these findings, systemic plasmacytosis was suspected to be due to chronic monilial infection. The pathogenesis of systemic plasmacytosis in aplastic anemias and in other diseases were discussed with relation to the present case.

Anemia, Aplastic↗
PubMed1987

Immunologic identification of lymphocyte subsets in experimental murine myocarditis with encephalomyocarditis virus. Different kinetics of lymphocyte subsets between the heart and the peripheral blood, and significance of Thy 1.2+ (pan T) and Lyt 1+, 23+ (immature T) subsets in the development of myocarditis.

To clarify the immune mechanism in myocarditis, immunofluorescence techniques with laser flow cytometry were used to examine serial changes in lymphocyte subsets in the heart, spleen, and peripheral blood of DBA/2 and BALB/c mice inoculated with encephalomyocarditis virus (Experiment I). B cells were identified by staining with fluorescein isothiocyanate-labelled rabbit anti-mouse immunoglobulin. T-cell subsets were identified with rat anti-Thy 1.2, and nonpolymorphic Lyt 1 and Lyt 2 monoclonal antibodies plus fluorescein isothiocyanate-labelled anti-mouse immunoglobulin. On days 7 and 14 postinfection, the percentage of Thy 1.2+ (pan T) cells in both strains had decreased in the peripheral blood; B cells showed no significant changes throughout the entire period. On the other hand, Thy 1.2+ (pan T) and Lyt 1+, 23+ (precursor and immature) T cells appeared to occupy the major portion of the myocardium on days 7 and 14 when congestive heart failure developed. To confirm this, serial immunohistologic studies (immunoperoxidase staining) of the hearts of DBA/2 and BALB/c mice with encephalomyocarditis virus-induced myocarditis were performed (Experiment II). In Experiment II, most of the stained cells in the hearts of both strains were Thy 1.2 positive and Lyt 1 and Lyt 2 positive on days 7 and 14. Thus, Experiments I and II demonstrated that lymphocytes at the site of inflammation in acute viral myocarditis carried antigenic markers that differed from those of peripheral lymphocytes and suggested that Thy 1.2+ (pan T) cells, especially the Lyt 1+, 23+ subset (immature T cells and T-cell subset precursors) were involved in the development of myocarditis in these animals.

Animals↗
PubMed1987

Selective IgM deficiency in adults: phenotypically and functionally altered profiles of peripheral blood lymphocytes.

Peripheral blood lymphocytes from four patients with selective IgM deficiency were examined phenotypically and functionally. Although B cell subpopulations determined by surface immunoglobulins were within normal or nearly normal range, T8+ cells were significantly increased and T4/T8 ratios were inverted in three patients. IgM specific hyporesponsiveness in the PWM-driven immunoglobulin production system was observed in all four patients. Ia-like antigen positive T cells were increased in two patients; both had increased Leu2a+ Leu15+ suppressor-effector cells. In addition, Leu3a+ Leu8+ suppressor-inducer cells were increased in one of these two patients. Excessive (either IgM-specific or isotype non-specific) suppressor activity of T cells and IgM specific hyporesponsiveness of non-T cells were observed in these two patients in the recombination plaque assay. Although these results showed the complexity of the pathogenesis of this syndrome, they suggested that suppressor-associated T cells may play a role in some patients with selective IgM deficiency.

Adult↗
PubMed1986

Animal model of silent myocarditis in athymic mice.

To clarify the role of the immune system in the development of myocarditis, BALB/c-nu/nu mice (group 1), BALB/c-nu/+ mice (group 2), BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice treated with rat anti-Thy-1.2 monoclonal antibody with complement (group 4) were inoculated with encephalomyocarditis virus. There were no significant differences in the incidence of myocarditis among the four groups. Virus titrations of the heart and serum neutralising antibody titres in the four groups did not show any significant differences. Fifty two per cent (26/50) of group 2 and 43% (20/46) of group 3 died on days 9-15, when congestive heart failure developed. Only 9% (5/54) of group 1 and 8% (1/12) of group 4, however, died on days 9-15. Pathological examination confirmed congestive heart failure in groups 2 and 3 but not in groups 1 and 4. Dilatation of the ventricular cavities, pleural effusion, ascites, and congestion of the lungs and liver were present in groups 2 and 3 but not in groups 1 and 4. Cellular infiltration and myocardial necrosis were severe in groups 2 and 3 but minimal in groups 1 and 4. Thus the severity of myocarditis may be regulated by T cells. So-called silent myocarditis seen in clinical settings may be similar to myocarditis in BALB/c-nu/nu mice.

Animals↗
PubMed1986

Primary gastric lymphoma with intranuclear inclusions. An immunohistochemical and ultrastructural study.

Two patients with primary gastric lymphoma, diffuse lymphoma, a plasmacytoid variant of small cell type, with numerous intranuclear inclusions, are reported. In both cases, biopsy and surgical specimens showed diffuse proliferation of lymphoid cells having plasmacytoid features at different steps of maturation in lamina propria and submucosal layer. The cytoplasm of the lymphoma cells was stained with anti-IgM, anti-kappa chain, and anti-J chain antibodies by avidin-biotin peroxidase complex technique. A number of intranuclear inclusions in the lymphoma cells were diastase-resistant PAS positive, and also stained with anti-IgM, anti-kappa chain, and anti-J chain antibodies, suggesting a monoclonal situation. In an ultrastructural study of the first case, the inclusions were round and composed of amorphous materials surrounded by a single membrane. In many lymphoma cells, the perinuclear cisternal space was dilated and filled with materials similar to those within both inclusions and rough endoplasmic reticulum. A direct communication between the perinuclear space and the inclusion was demonstrated in some cells, suggesting the perinuclear cisternal origin of these inclusions.

Adult↗
PubMed1986

Decreased NK activity of nude mice receiving long-term ultraviolet irradiation: in relation to tumor induction.

We have serially evaluated the basal and poly I: C-enhanced NK activity of BALB/c X C57BL/6 F1 nude mice (CB6F1-nu/nu) receiving repeated ultraviolet (UV) exposures with the interval of 2-5 weeks until overt skin tumor(s) developed. Chronic UV exposure induced a dose dependent suppression of basal splenic NK activity. The latent period between the initial UV treatment and the appearance of the first overt skin tumor was 19 weeks. After that time, incidence of tumor development gradually increased until it became 69% at the last inspection (27th week). 89% of the tumors inspected were fibrosarcoma and the remaining revealed squamous cell carcinoma. The UV-induced suppression of NK activity was restored by poly I:C treatment before the tumor appearance; however, this restorative effect was significantly reduced thereafter.

Animals↗
PubMed1985

Organ-specific autoimmune diseases induced in mice by elimination of T cell subset. I. Evidence for the active participation of T cells in natural self-tolerance; deficit of a T cell subset as a possible cause of autoimmune disease.

Organ-specific autoimmune diseases such as oophoritis, gastritis, thyroiditis, and orchitis were induced in female or male nude (nu/nu) mice by the transfer of nu/+spleen cells from which particular Lyt T cell subset(s) had been removed: nu/+spleen cells treated with anti-Lyt-1 plus complement (C) caused disease in recipient nude mice; anti-Lyt-2 plus C-treated spleen cells, in contrast, did not. The cells responsible for disease induction are believed to be Thy-1+, Lyt-1-, 2,3- (Thy-1, Lyt-1, 2,3), since spleen cells treated with mixed antisera, including anti-Lyt-1 and anti-Lyt-2, plus C, could induce the disease with almost the same incidence as anti-Lyt-1 plus C-treated cells (oophoritis 50%, gastritis 25%, thyroiditis 10-20%, and orchitis 40%). Cells treated with mixed antisera of anti-Thy-1, anti-Lyt-1, and anti-Lyt-2, plus C, could not induce autoimmune disease. Each induced autoimmune disease could be adoptively transferred to other nude mice via spleen cells, with resulting histological lesion of corresponding organs and development of specific circulating autoantibodies. Since anti-Thy-1 plus C treatment of donor spleen cells abrogated the capacity to transfer the disease, we conclude that T cells are required as effector cells, and that these may develop from Lyt-1-, 2,3- cells. Lyt-1+, 2,3- cells were demonstrated to have suppressive activity upon the development of the diseases; induction of autoimmunity was completely inhibited by the cotransfer of Lyt-1+, 2,3- cells with Lyt-1-, 2,3- cells. When anti-Lyt-2 plus C-treated cells (i.e., Lyt-1+, 2,3- and Lyt-1-, 2,3- cells) were mixed with anti-Lyt-1 and anti-Lyt-2 plus C-treated cells (i.e., Lyt-1-, 2,3- cells) in various ratios, then transferred to nude mice, the development of each autoimmune disease was clearly inhibited, even by small doses of Lyt-1+, 2,3- cells. The autoimmune disease we were able to induce was quite similar to human organ-specific autoimmune disease in terms of the spectrum of organs involved, histopathological features, and the development of autoantibodies to corresponding organ components (oocytes, parietal cells, thyroid colloid, including thyroglobulin, and sperm).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Familial occurrence of oligomeganephronia.

Oligomeganephronia (OMN) is a rare, renal hypoplasia, consisting of a reduced number of hypertrophied nephrons. This disorder has been considered to be a congenital but not a genetic disease. We describe the first report, to the best of our knowledge, of familial cases of OMN; two male siblings ran rapidly downhill courses and died 11 and 8 days after birth, respectively. In addition, the two patients had similar multiple anomalies; microcephaly, prominent glabella, hypertelorism, antimongoloid slant, epicanthal folds, broad nose, cleft lip and palate, down-turned mouth, short philtrum, micrognathia, low set ears, hypospadias, and cryptorchism. Although the patients and the parents had normal G-banded karyotypes, 4p monosomy syndrome is suggested from clinical features. The implications of this are discussed briefly.

Abnormalities, Multiple↗
PubMed1985

Immunologic behavior of lymphocytes in experimental viral myocarditis: significance of T lymphocytes in the severity of myocarditis and silent myocarditis in BALB/c-nu/nu mice.

To clarify the immune mechanism in myocarditis, we examined by immunofluorescence techniques the serial changes in percentages of T and B lymphocytes in the heart, spleen, and peripheral blood of DBA/2 mice inoculated with encephalomyocarditis (EMC) virus (experiment I). B cells were demonstrated by staining with fluorescein isothiocyanate (FITC)-labeled rabbit antimouse immunoglobulin (Ig). T cells were demonstrated with rat anti-Thy1.2 monoclonal antibody plus FITC-labeled antimouse Ig. There was a marked decrease in T cells in peripheral blood and a moderate decrease in the cells in the spleen on day 14. There were no significant changes in B cells in peripheral blood or spleen throughout the entire period and T cells accounted for approximately 80% of the cells in the myocardium on days 7 and 14. To confirm the involvement of T cells in the development of myocarditis, we also carried out studies in which BALB/c-nu/nu mice (group 1, n = 58), BALB/c-nu/+ mice (group 2, n = 54), and BALB/c-nu/nu mice injected with 5 X 10(7) spleen cells from BALB/c-nu/+ mice (group 3, n = 50) were inoculated with EMC virus (experiment II). Four mice from each of the three groups were killed on day 6 for virologic studies. In experiment II, there were no significant differences in the incidence of myocarditis among the three groups. Virus titrations of the heart and serum neutralizing antibody titers did not show any significant differences between the three groups on days 6 and 16.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗