Biomedical subjects

M Daibata

Publications and source records attributed to M Daibata.

45 records · Page 3Linked to original sources

PubMed1991

Relating homology between the Epstein-Barr virus BOLF1 molecule and HLA-DQw8 beta chain to recent onset type 1 (insulin-dependent) diabetes mellitus.

A role for the Epstein-Barr virus in initiating Type 1 (insulin-dependent) diabetes mellitus has been proposed since Epstein-Barr virus BOLF1 (497-513) AVTPL RIFIVPPAAEY has an 11 amino acid identity with HLA-DQw8 beta (49-60) AVTPL GPPAAEY. Rabbit antisera to the BOLF1 (496-515) peptide crossreacted with the homologous DQw8 beta (44-63) peptide but not with the related DQw7 beta (44-63) peptide, which differed from the DQw8 peptide only in an ALA to ASP substitution in position 57. Antisera to DQw8 beta (49-60) reacted with the DQw8 beta (44-63) peptide and BOLF1 (496-515), but not with DQw7 beta (44-63). The antiserum to the BOLF1 peptide bound to denatured class II major histocompatibility complex beta chains from Epstein-Barr virus-transformed DQw8-positive lymphocytes in an immunoblotting analysis. Epstein-Barr virus antibodies were detected at equal frequencies and similar titres in sera of 30 patients with Type 1 diabetes (16 of 30; 63%) and in sera of 20 non-diabetic control subjects (13 of 20; 65%). Sera from diabetic patients did not bind to DQw8 beta (44-63) or BOLF1 (496-515) peptides. From these data we conclude that there is no simple relationship between serological evidence of Epstein-Barr virus infection and crossreactions between homologous Epstein-Barr virus and class II major histocompatibility complex peptides.

Adolescent↗

PubMed1991

Early events in Epstein-Barr virus genome expression after activation: regulation by second messengers of B cell activation.

RNA transcription from the BamHI Z and BamHI R and HindIII G regions of the Epstein-Barr virus (EBV) genome was studied after treatment of Akata cells with anti-immunoglobulin G (IgG), with second messenger agonists or antagonists to determine how latent EBV activation is regulated by B cell second messengers. Northern gel analysis demonstrated that BZLF1, BZLF1 + BRLF1, and BMLF1 + BSLF2 transcripts were induced at 2 hr and increased in concentration at 4 hr after induction with anti-IgG; transcripts from BRRF1, BaRF1, BMLF1, and BMRF1 were initiated at 4 hr; a transcript from BRRF2 appeared at 6 hr. The patterns of transcription from these genes after repeated stimulations with calcium ionophore A23187 + dioctanoylglycerol paralleled those with anti-IgG except that times of initiation were delayed by about 2 hr. Nuclear run-off assay of BZLF1 gene showed rapid increases in their transcriptions from 30 to 60 min after anti-IgG treatment. The protein kinase C antagonist, staurosporine, completely blocked the appearance of these transcripts, while 8-bromo cAMP + theophylline suppressed the transcription by about 40%. The regulation of EBV activation in Akata cells with anti-IgG or with second messenger agonists or antagonists can be explained by regulation at the level of transcription of immediate-early genes of EBV.

Alkaloids↗

PubMed1990

Activation of latent EBV via anti-IgG-triggered, second messenger pathways in the Burkitt's lymphoma cell line Akata.

Anti-IgG treatment activated latent EBV genomes in 50 to 70% of the cells of the Burkitt's lymphoma cell line Akata. The EBV-activating role of intracellular Ca2+, as potentiated by diacylglycerol (DAG) and suppressed by cAMP, was analyzed in the cells through effects of agonists and antagonists of these second messenger pathways. Early Ag (EA) was induced in 10% of cells with the calcium ionophore A23187 (A23187). EA induction with anti-IgG or A23187 was blocked by a calmodulin antagonist, trifluoperazine. The DAG pathway had a potentiating but not direct effect on EBV activation because: 1) the DAG analog, dioctanoylglycerol (diC8), an agonist for protein kinase C, alone induced only 2% EA-positive cells, 2) diC8 synergized with A23187 for EA induction, and 3) the protein kinase C antagonist, staurosporine, almost completely inhibited EA induction by anti-IgG. When cells were reincubated in medium with fresh diC8 and A23187 at 3, 6, 9, and 12 h, EA induction at 24 h reached the levels seen with anti-IgG stimulation. A cAMP-mediated pathway suppressed EBV activation because dibutyryl cAMP or 8-bromo-cAMP, plus blockage of phosphodiesterase by theophylline, or use of forskolin, inhibited EA induction with anti-IgG. Although the principal stimulatory role in EBV activation of a Ca2(+)-mediated, second messenger pathway, as synergized by DAG and inhibited by cAMP, was established, we did not explain the significant lag in EA induction by A23187 and diC8 as compared with anti-IgG induction of EA. We conclude that EBV genome activation with anti-IgG is mediated by Ca2+/calmodulin and DAG pathways in Akata cells, that the cAMP pathway suppresses EA induction by anti-IgG, and that a mechanism regulating the speed of EA induction remains unexplained.

Alkaloids↗

PubMed1989

The establishment of Epstein-Barr virus nuclear antigen-positive (SP-50B) and Epstein-Barr virus nuclear antigen-negative (SP-53) cell lines with t(11;14)(q13;q32) chromosome abnormality from an intermediate lymphocytic lymphoma.

Two lymphoma cell lines, SP-50B and SP-53, were established from peripheral blood of a 58-year-old woman with leukemic conversion of intermediate lymphocytic lymphoma. These cell lines grew in suspension with or without forming clumps of cells. SP-50B was morphologically similar to the common Epstein-Barr (EB) virus-transformed lymphoblastoid cell lines and was positive for EB virus nuclear antigen (EBNA), whereas SP-53 closely resembled the patient's lymphoma cells and was negative for EBNA. Both cell lines expressed the same phenotypic markers as original lymphoma cells (CpIg+, SmIg+, OKIa1+, Leu12+) and possessed t(11;14)(q13;q32) chromosome translocation. These results indicate that although morphologically different, SP-50B and SP-53 were both derived from patient's lymphoma cells. The long-term cultivation of EBNA-positive and EBNA-negative B-cell lymphoma lines from a single donor has not been previously reported. These cell lines would provide useful tools for studying the oncogenic role of EB virus and bcl-1 oncogene that is located on chromosome 11q13.

Antigens, Viral↗

PubMed1988

Generalized lymph node metastasis of early uterine cancer in an HTLV-I carrier.

Generalized lymphadenopathy due to metastases of keratinizing squamous cell carcinoma developed in a 68-year-old woman who was a carrier of human T-cell leukemia Type I (HTLV-I). On her 74th hospital day, she died of massive metastases of the superficial and deep-seated lymph nodes, thyroid, lungs, pleura, liver, spleen, pancreas, kidneys, and retroperitoneum. At autopsy, the primary tumor was found in the uterine cervix. The depth of stromal invasion was approximately 4.0 mm. Such an extensive dissemination usually does not occur in cervical cancer with this type of early stromal invasion. It is conceivable that the chronic HTLV-I infection compromised the immunosurveillance against cancer and accelerated progression of the disease in this patient.

Carrier State↗

PubMed1988

Serial transplantation of an HTLV-I-transformed hamster lymphoid cell line into hamsters.

A hamster lymphoid cell line, HCT-2, transformed by human T-cell leukemia virus type I (HTLV-I) was serially transplanted for 9 passages in newborn hamsters. A total of 34 newborn hamsters inoculated intraperitoneally (i.p.) with 0.2-2 X 10(7) HCT-2 cells developed fatal lymphomas with dissemination to various organs within 5-10 days. The growth of i.p. inoculated HCT-2 cells was found to be dependent on the age of recipients: all 21 suckling hamsters inoculated when aged 5-10 days succumbed to disseminated lymphomas within 6-7 days, while 4 of 12 older hamsters inoculated at the age of 15-25 days developed less extensive disease with signs of tumor regression. To investigate the effect of immunosuppression on host resistance, 3 adult hamsters treated with anti-thymocyte serum were inoculated i.v. with 2-4 X 10(7) HCT-2 cells; all 3 developed fatal leukemias in 5-7 days. Irrespective of whether HCT-2 cells were inoculated into newborn, suckling, or adult hamsters, histopathological findings were similar, with frequent involvement of liver, spleen, lungs, kidneys, lymph nodes, blood, and bone marrow. Cells harvested from tumors and peripheral blood of some tumor-bearing hamsters could be readily recultured as cell lines. Chromosome analysis and Southern blot hybridization showed that tumors were caused by growth of HCT-2 cells.

Age Factors↗

PubMed1987

Gastric lymphoma associated with human T-cell leukemia virus type I.

A 41-year-old woman presented with a gastric lymphoma. A total gastrectomy was performed, and the tumor was found to consist of T cells of the helper/inducer (E+, Leu-1+, Leu-2a-, Leu-3a+) phenotype. The patient was seropositive for T-cell leukemia virus type I, and the tumor cells contained the proviral genome.

Adult↗

PubMed1987

Establishment of a new human B cell line carrying t(11;14) chromosome abnormality.

A new human cell line, SP-49, was established from the peripheral blood of a patient with leukemic conversion of diffuse lymphoma, medium-sized cell type. SP-49 cells were shown to have intracytoplasmic and surface immunoglobulin and Leu-12 antigen, but were negative for Epstein-Barr virus nuclear antigen. Chromosome analysis demonstrated that SP-49 had t(11;14) chromosome translocation involving 11q13 and 14q32, where oncogene bcl-1 and immunoglobulin heavy chain gene, respectively, were reportedly located.

B-Lymphocytes↗

PubMedDate not supplied

Lymphoblastoid cell lines with integrated human herpesvirus type 6.

OBJECTIVE: Attempts were made to establish stable in vitro cell lines latently infected with human herpesvirus type 6 (HHV-6). STUDY DESIGN/METHODS: We previously studied a patient with B-cell acute lymphoblastic leukemia infected with HHV-6. The peripheral blood mononuclear cells (PBMCs) from this patient were immortalized by infection with Epstein-Barr virus (EBV) and herpesvirus saimiri (HVS). RESULTS: Infection of the PBMCs with EBV and HVS gave rise to B- and T-lymphoblastoid cell lines, respectively. Both cell lines were positive for HHV-6 DNA, as confirmed by polymerase chain reaction (PCR) and Southern blot hybridization. Fluorescence in situ hybridization (FISH) demonstrated integration of HHV-6 in these cell lines. Only one integrated site of viral DNA was detected in metaphase chromosome spreads, and it was preferentially located at the long arm of chromosome 1 (1q44). HHV-6 appeared latent in the infected cells, since neither the HHV-6 immediate-early gene transcript nor virion-associated protein was detected. CONCLUSIONS: The HHV-6-positive lymphoblastoid cell lines would be useful for study of the mechanism of HHV-6 integration.

Aged↗