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Biomedical subjects

Kazuo Oshimi

Publications and source records attributed to Kazuo Oshimi.

At least 37 records · Page 2Linked to original sources
PubMed2005

[Diffuse large B-cell lymphoma expressing surface immunoglobulin heavy chain (Ig alpha) and lacking light chains].

A 59-year-old woman with goiter complained of nausea, vomiting and weight loss in April 2000. She underwent an endoscopic examination and was admitted to our hospital because gastric biopsy specimens revealed that she had diffuse large B-cell lymphoma. A thyroid biopsy also detected the diffuse infiltration of lymphoma cells, which were positive for CD19, CD20, CD38 and HLA-DR. Although the cells expressed surface immunoglobulin a chain, they lacked expressions of the kappa and lambda light chains. Chromosomal analysis of the thyroid cells showed 47, XX, t(2 ; 3)(q31 ; q13), + 3, t(8 ; 22)(q24 ; q11). After five courses of biweekly CHOP chemotherapy, she received autologous peripheral blood stem cell transplantation in October 2000. Currently, she has maintained complete remission for more than 4 years.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2004

Epstein-Barr virus (EBV)-encoded RNA promotes growth of EBV-infected T cells through interleukin-9 induction.

EBV associates with various T-cell-proliferating diseases such as chronic active EBV infection and nasal lymphoma. In contrast to B cells, which are highly susceptible to EBV infection in vitro, T cells are refractory to EBV infection in vitro, and it has been difficult to examine the effects of EBV infection on T cells. We recently generated EBV recombinants with a selectable marker, which made it possible to select EBV-infected cells even when the efficiency of infection was low. Using the recombinant virus, we found that a human T-cell line, MT-2, was susceptible to EBV infection, and we succeeded in isolating EBV-infected cell clones with type II EBV latency, which was identical with those seen in EBV-infected T cells in vivo. EBV-infected MT-2 cell clones had shorter cell doubling times and higher saturation density than non-EBV-infected counterparts. We found that EBV-positive MT-2 cells expressed higher levels of interleukin (IL)-9 than EBV-negative MT-2 cells at the transcriptional level. It was also demonstrated that EBV-encoded small RNA was responsible for IL-9 expression. Addition of recombinant IL-9 accelerated the growth of MT-2 cells, whereas growth of the EBV-converted MT-2 cells was blocked by treatment with an anti-IL-9 antibody. These results suggest that IL-9 induced by EBV-encoded small RNA acts as an autocrine growth factor for EBV-infected T cells. Analysis of nasal lymphoma biopsies indicated that three of four specimens expressed IL-9. The present findings suggest that EBV directly affects the pathogenesis of EBV-associated T-cell diseases.

Biopsy↗
PubMed2004

Epstein-Barr virus infection of human natural killer cell lines and peripheral blood natural killer cells.

Although considerable part of natural killer (NK) cell neoplasms possess EBV genome, there has been no direct evidence that EBV infects human NK cells in vitro. In this study, we demonstrated EBV entry into NK cells using a recombinant EBV, which contains enhanced green fluorescent protein (EGFP) gene in its genome (EGFP-EBV). After 48 h of exposure to EGFP-EBV, we detected EGFP signals in approximately 30% of NK-92 and NKL cells and >40% of peripheral blood NK cells from three healthy volunteers. Reverse transcription-PCR analysis of various EBV-associated genes confirmed EBV infection. In situ hybridization for EBERs and BHLFs showed that latent and lytic infections coexisted at the early phase of EBV infection in two NK cell lines. Although BHLF-positive cells in the early lytic phase were round-shaped, EBER-positive cells in latent EBV infection tended to show a bizarre shape. Flow cytometric analysis of EGFP-EBV-exposed NK cell lines showed that most of EBV-infected cells entered early apoptosis after 72 h of EBV exposure, which explains the difficulties to establish EBV-carrying NK clones. Flow cytometry and reverse transcription-PCR analysis indicated that two NK cell lines may fuse with EBV using HLA class II after binding to the virus through a distinct molecule from CD21. We established two EBV-carrying NKL clones showing latency types I and II, both of which are recognized in EBV-associated NK cell neoplasms. Because EBV-infected NKL cells showed only type I latency during the early phase of infection, the temporal profile of latent gene expression is similar to that of T cells. We first report in vitro EBV infection of human NK cells and establishment of EBV-carrying NK clones, which should contribute to elucidate the role of EBV in the development of NK cell neoplasms.

Apoptosis↗
PubMed2004

Gammadelta T-cell large granular lymphocyte (LGL) leukemia with spontaneous remission.

T-cell large granular lymphocyte (LGL) leukemia is a clonal disorder with an indolent clinical course. In July 1995, a 46-year-old Japanese man was admitted to our hospital because his anemia had progressed. He had a white blood cell count of 3.9 x 10(9)/L with 75% lymphocytes, which were intermediate to large and had almost round nuclei and azurophilic granules, and anemia with a red blood cell count (RBC) of 2.69 x 10(12)/L, hemoglobin (Hb) of 9.5 g/dL, and hematocrit (Hct) of 28.3%. Electron microscopic examination showed that most of the lymphocytes had a parallel tubular array and dense core granules in their cytoplasm. Flow cytometry and Southern blotting of the T-cell antigen receptor (TCR) genes using the peripheral blood species showed monoclonal proliferation of LGLs with a CD3+, TCRgammadelta+, CD4-, CD8-, CD16+, CD56-, CD57-, HLA-DR+ phenotype, and a TCR gamma gene rearrangement, respectively, suggesting that the patient was diagnosed as having gammadelta T-cell LGL leukemia. He had no symptoms, organomegaly, or skin lesions. About 1.5 years after diagnosis, the anemia gradually improved with disappearance and appearance of a rearranged band in the TCR-gamma gene and TCR-beta gene, respectively. About 7 years after diagnosis, the anemia improved completely with a RBC of 5.01 x 10(12)/L, Hb of 14.8 g/dL, and Hct of 44.3%, and he was in complete remission without TCR-beta and -gamma gene rearrangements. He had received no therapy. This is the first report of spontaneous remission of gammadelta T-cell LGL leukemia.

Blotting, Southern↗
PubMed2004

Successful high-titer immunoglobulin therapy for persistent parvovirus B19 infection in a lymphoma patient treated with rituximab-combined chemotherapy.

A 40-year-old female diagnosed with follicular lymphoma was treated with rituximab-combined chemotherapy. Although she achieved complete remission, she developed progressive anemia and reticulocytopenia. Bone marrow examination revealed features of pure red cell aplasia and hemophagocytosis. In addition, the appearance of large pronormoblasts suggested that she was infected with parvovirus B19. Excess viral DNA in her bone marrow confirmed that her illness was caused by persistent parvovirus B19 infection. Serum immunoglobulin levels decreased beyond the lower normal limit, which indicated that her humoral immunity was impaired after rituximab-combined chemotherapy. Although she had been infected with parvovirus B19, she was re-infected and failed to control the viral expansion. High-titer immunoglobulin against parvovirus B19 was intravenously administrated and resulted in remarkable reticulocytosis and improvement of anemia. High-titer immunoglobulin, which contained a sufficient amount of neutralizing antibodies against parvovirus B19, likely inactivated most viruses in vivo. We successfully eradicated the virus after 2 courses of high-dose therapy at 0.5 g/kg/day every week followed by 8 courses of maintenance therapy at 0.1 g/kg/day every other week. It is important to consider that parvovirus B19 infection is a possible cause of progressive anemia in B-cell lymphoma patients treated with rituximab-combined chemotherapy. We propose that the use of high-titer immunoglobulin against parvovirus B19 may enable such immunocompromised patients to eradicate the virus before sufficient immune system reconstruction.

Adult↗
PubMed2004

Enteropathy-type T-cell lymphoma expressing NK-cell intraepithelial lymphocyte (NK-IEL) phenotype.

Enteropathy-type T-cell lymphoma (ETL) is an intraepithelial T-lymphocyte (T-IEL) tumor. The tumor cells are usually CD3+, CD4-, CD8+, and contain cytotoxic granule associated proteins. We report on a CD3-negative CD56-positive enteropathy-associated lymphoma (ETL). This is the first case report of CD3-negative, CD56-positive, CD94-negative, and CD161-positive ETL. ETL cells originate from intraepithelial T-lymphocytes of the intestine. CD3-negative intraepithelial lymphocytes are known as natural killer (NK)-IELs. The phenotype of NK-IELs is also CD3-negative, CD56-positive, CD94-negative, and CD161-positive, while most normal NK cells express CD56 and CD94. CD3-negative lymphoma cells in this report also expressed CD56 and CD161, but not CD94. Because Southern blotting analysis showed a rearrangement of T-cell receptor (TCR) Cbeta in this case, the tumor is classified as an ETL. Based on the findings, NK-IELs may originate from T-cells, not NK-cells.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2004

[Case of malignant lymphoma arising from the posterior mediastinum, with pleural effusion].

We report a rare case of malignant lymphoma arising from the posterior mediastinum with bilateral pleural effusion. A 71-year-old man was admitted to our hospital for evaluation of a posterior mediastinal tumor and bilateral pleural effusion revealed on a chest CT scan. Because no tumor tissue could be obtained by fiberbronchoscopy, video-assisted thoracoscopic surgery was performed. The tumor sample was composed of large, atypical lymphocytes positive for CD20 on immunohistochemical analysis. A diagnosis of diffuse large B cell lymphoma was made from the typical histological features. The patient was treated with combination chemotherapy (CHOP) and rituximab and improved dramatically.

Aged↗
PubMed2003

Leukemia and lymphoma of natural killer lineage cells.

Natural killer (NK) cells are lymphocytes with a large granular lymphocyte morphology, a CD3- CD56+ phenotype, a non-major histocompatibility complex-restricted cytotoxicity, and germline configuration T-cell receptor genes. NK cell lineage tumors originate from either precursor NK cells or mature NK cells. Tumors originating conceivably from precursor NK cells include myeloid/NK cell precursor acute leukemia, precursor NK cell acute lymphoblastic leukemia, and blastic NK cell lymphoma. However, because the developmental pathway of normal NK cells and the characteristics of these NK precursors are not fully understood, the definition and characterization of the tumors are only provisional. Tumors of mature NK cell origin include aggressive NK cell leukemia/lymphoma, nasal-type NK cell lymphoma, and chronic NK lymphocytosis, but the last disorder seems to be reactive in most cases. Because NK cell tumors are rare and difficult to manage, vigorous studies are required for their understanding and management.

Cell Lineage↗
PubMed2003

Ursodeoxycholic acid treatment of idiopathic thrombocytopenic purpura with liver dysfunction.

Ursodeoxycholic acid (UDCA) is known to reduce immunoglobulin from B cells and cytokine production from T cells. We found that UDCA increased the platelet count in two idiopathic thrombocytopenic purpura (ITP) patients who have liver dysfunction. UDCA was tolerated and did not cause diarrhea in the amounts used. Further investigation is needed to evaluate the effectiveness of UDCA in ITP patients.

Adult↗
PubMed2003

Pure red cell aplasia associated with expansion of CD3+ CD8+ granular lymphocytes expressing cytotoxicity against HLA-E+ cells.

T-cell granular lymphocyte-proliferative disorder (T-GLPD) is characterized by the proliferation of cytotoxic T lymphocytes, and is often associated with pure red cell aplasia (PRCA). The mechanism involved in the development of PRCA in T-GLPD is unknown. Peripheral blood mononuclear cells were isolated from 20 patients with T-GLPD. Ten patients had associated PRCA. Granular lymphocytes (GLs) of T-GLPD are positive for CD94, but not NKG2A. To clarify the functional role of CD94 in T-GLPD, we performed a cytotoxicity assay against the trophoblast cell line, BeWo, which is known to express human leucocyte antigen (HLA)-E, a natural ligand of CD94, and is deficient in other HLA class I and class II antigens. GLs isolated from T-GLPD with PRCA patients killed BeWo cells more significantly than GLs from T-GLPD without PRCA patients. Furthermore, GLs from T-GLPD with PRCA were significantly stimulated by a monoclonal antibody against CD94, whereas those of T-GLPD without PRCA were not. Taken together, HLA-E, a ligand of CD94, was suggested to stimulate CD94+ cells to kill HLA-E+ cells in T-GLPD with PRCA. GLs of T-GLPD with PRCA have a potential positive activity against HLA-E+ cells, whereas GLs from T-GLPD without PRCA do not. CD94 may play a key role in the pathogenesis of PRCA in T-GLPD.

Adult↗
PubMed2003

Multifocal motor neuropathy caused by a B-cell lymphoma producing a monoclonal IgM autoantibody against peripheral nerve myelin glycolipids GM1 and GD1b.

Various data support the pathogenetic significance of serum IgM autoantibodies against glycolipid GM1 in patients with multifocal motor neuropathy. Although some patients with this neuropathy have an extraneural lymphoma, IgM anti-GM1 glycolipid autoantibodies have not been investigated in these cases. We found IgM anti-GM1 autoantibody in the serum of a 52-year-old man who developed multifocal motor neuropathy that was associated with an extraneural diffuse large B-cell lymphoma. An autopsy showed severe widespread demyelination without lymphoma cell infiltration in the peripheral nerves. Immunofluorescent flow cytometry and thin-layer chromatographic immunostaining demonstrated that most of the anti-GM1 antibody in the serum was monoclonal IgM of lambda type, which was also demonstrable in secretory form on lymphoma cells. The antibody showed affinity for the Galbeta1-3GalNAc terminal disaccharide of glycolipids GM1 and GD1b, which both are widespread in peripheral nerve myelin. Enzyme-linked immunosorbent assay demonstrated that this antibody was much more abundant in lymphoma cell culture supernatant than in normal lymphocyte culture supernatant. Thus, our patient's B-cell lymphoma cells produced a monoclonal IgM lambda autoantibody against this terminal disaccharide residue. This antibody bound to glycolipids GM1 and GD1b in peripheral motor nerve myelin, presumably initiating formation of destructive immune complexes that caused multifocal motor neuropathy.

Antigen-Antibody Complex↗
PubMed2003

B-cell marker negative (CD7+, CD19-) Epstein-Barr virus-related pyothorax-associated lymphoma with rearrangement in the JH gene.

Pyothorax-associated lymphoma (PAL) develops decades after receiving artificial pneumothorax for pulmonary tuberculosis. The lymphomas, develop in tissue affected by long-standing severe inflammatory process. Most cases demonstrate diffuse large B-cell lymphoma. We present a patient with T-cell phenotype-positive and B-cell phenotype-negative (CD7+, CD43+, CD19-, and CD20-) PAL. Southern blot hybridization using immunglobulin heavy chain J region (IgH) gene probe revealed a monoclonal rearrangement, and hybridization using T-cell receptor beta chain (TCR) gene probe revealed a germline configuration. This indicates that the tumor origin was of B-lymphocytes. Chromosomal abnormality of the lymphoma was complicated. It suggested that many transformations occurred. In the transformation process, probably B-cell antigens were lost, and T-cell antigens were aberrantly expressed.

Aged↗
PubMed2003

[Zygomycosis: two case reports and review of reported cases in the literature in Japan].

This article reports two cases of zygomycosis and analyzes the zygomycosis cases reported in the literature in Japan. Case 1 was a 43-year-old male with malignant lymphoma who presented complications of pneumonia and cerebral bleeding, leading to his death. Autopsy findings showed pulmonary lesions were due to zygomycosis. Cerebral lesion was presumed to be due to zygomycosis without pathological examination. Case 2 was a 52-year-old male with acute lymphocytic leukemia from whom 4 sputum cultures were taken that were positive for Cunninghamella elegans. Combination therapy of itraconazole and amphotericin B (AMPH) was begun, and AMPH was changed to liposomal amphotericin B. During the neutropenic period after receiving premedication for a peripheral blood stem cell transplantation performed for his underlying disease, high fever was recognized and Staphylococcus epidermidis was isolated from the blood culture. Despite the change in antibiotics administered, pneumonia also developed as a complication, causing his death. Two hundred four cases of zygomycosis have been reported in the literature in Japan: 55 cases were rhinocerebral zygomycosis, including 29 cases with no underlying disease. A premortem diagnosis was made in 34 cases by pathological findings of operation materials or drainage samples, and 24 cases were postmortem. Pulmonary, disseminated, cardiovascular, gastrointestinal and thyroidal zygomycoses were found in 144 cases, including 66 cases with leukemia. A premortem diagnosis was made in 39 cases and 120 cases were postmortem. Prognosis of rhinocerebral type was better in operated or drainage cases, and for resected cases in all other types. Five cases with allergic zygomycosis were all alive. There were only 14 cases in which isolated fungi were identified (Cunninghamella spp. from 5 cases, Mucor spp. from 2, Rhizomucor spp. from 2, and Rhizopus spp. from 5).

Adult↗
PubMed2003

[The chimerism and GVT effects on murine mini-transplantation model].

We established a murine mini-transplantation model to examine chimerism and graft versus tumor effects(GVT) using with C57BL/6(donor) and(C57BL/6 x BALB/c) (CBF1) (recipient) combination and a IgE producing plasmacytoma cell clone (B53) of BALB/c origin. The chimerism and graft versus tumor effects(GVT) were observed. Two experimental groups were prepared. One is mini-transplantation group (G2): recipients irradiated with 200 rad were inoculated with B53 cells, along with donor cells, the other is bone marrow transplantation group(G4): recipients irradiated with 800 rad were inoculated with B53, along with donor cells. The full chimera was observed one week after transplantation in G4, but that was seen 3 week after transplantation. The GVT effects were observed in both groups. However, GVT effects on G4 is stronger than that on G2 in pathological findings and serum IgE level.

2,4-Dinitrophenol↗