Search PubMed⌕ Search

Biomedical subjects

H Shiku

Publications and source records attributed to H Shiku.

At least 289 records · Page 16Linked to original sources
PubMed1985

Production and analysis of HH 10 monoclonal antibodies reactive to immature hematopoietic cells and their use for monitoring acute leukemia cells.

A clone of murine monoclonal antibody HH 10 (IgM) was raised by fusing NS-1 myeloma cells and spleen cells of a mouse hyperimmunized with acute promyelocytic leukemia cells. Serological analysis by means of immune adherence assays showed that HH 10 reacts with immature hematopoietic cells including thymocytes and myeloid precursor cells (defined as colony-forming units in culture assays). The antibodies were not reactive to either peripheral blood cells or bone marrow cells obtained from normal individuals. Lymphoid blasts induced with phytohemagglutinin, pokeweed mitogen, or concanavalin A were also non-reactive, and all non-hematopoietic cultured cells examined were also negative. The antibodies were, however, reactive to leukemia cells in 67 cases out of 91 cases (74%) of acute leukemia. In patients with acute lymphoblastic leukemia, 43 out of 52 cases (83%) were positive and, in particular, all of 12 T-cell-type acute leukemias were reactive to HH 10. Comparison of percent HH 10 positive cells in the bone marrow of patients with acute leukemia with the results of cytological studies showed a good correlation. Analysis of sequentially collected bone marrow cells of acute leukemia patients using HH 10 revealed its usefulness for monitoring leukemia cells.

Acute Disease↗
PubMed1984

[Therapeutic effect of ceftizoxime on severe infectious complications in blood disorders. Tohkai Research Group on Infections in Hematopoietic Disorders].

Ceftizoxime (CZX) was given by intravenous injection in daily doses of 2-8 g to 103 patients with severe infections complicating hematopoietic disorders. The clinical effect was evaluated in 95 of the 103 patients. The causative organisms were identified in 22 patients but were unknown in the remaining 73. Infected sites were the respiratory tract, urinary tract, soft tissue, and blood. The overall effectiveness rate (inclusive of marked and moderate) was 61.1% (58/95). The effectiveness rate was 63.6% (14/22) in patients in whom the causative organisms were identified and 60.3% (44/73) in patients in whom the causative organisms could not be identified and 60.0% (18/30) in 30 patients with less than 100 neutrophils per mm3 before treatment. No side effects were noted except drug fever in 1 patient. Abnormal hepatic function was seen in 6 patients but was not attributed to the drug in any case. The results indicate that CZX is a safe and useful antibiotic for the treatment of severe infectious complications in hematopoietic disorders.

Adolescent↗
PubMed1983

Autologous and allogeneic typing of human leukemia cells: definition of surface antigens restricted to lymphocytic leukemia cells.

Serum from a patient (CO) with acute lymphoblastic leukemia was reactive in immunoadherence assays with autologous leukemia cells but not with autologous blood lymphocytes or bone marrow cells during complete remission. Extensive absorption tests with an array of leukemia cells and normal cells were performed in order to define the specificity of the reaction. The autologous leukemia reactivity was either completely or partially absorbed with acute lymphoblastic leukemia cells obtained from 10 of 14 patients but not with acute nonlymphoblastic leukemia cells or normal hematopoietic cells. Some cultured lymphocytic leukemia lines also showed expression of the antigen. The absence of alloantibodies in CO's serum detectable in our assay allowed direct testing of CO's serum on allogeneic target cells. The results of these tests correlated with the results of absorption tests, indicating that small populations of antigen-positive cells were not missed with absorption tests. In addition, absorption tests with CO-positive allogeneic leukemia target cells showed the same pattern of antigen distribution as tests with autologous targets. CO reactivity was not removed by absorption with cell lines expressing human T-cell leukemia virus, nor did CO's serum react with adult T-cell leukemia cells from three patients.

Antigens, Neoplasm↗
PubMed1983

[Human monoclonal antibodies with human-mouse hybridomas].

Our trial to produce human monoclonal antibodies with human-mouse hybridomas is described. Human spleen cells, in comparison with peripheral blood lymphocytes, bone marrow cells and lymphnode lymphocytes, seem to be the best partner to fuse with myeloma line NS-1 to obtain hybridomas. About sixty percent of hybridomas derived from human spleen cells at first produce human Ig which in most cases belong to either IgG or IgM. Fifty percent of hybridomas which had initially produced human Ig continued to do so after 4 months. One of the clones of human monoclonal antibodies reacted with a cell surface antigen expressed on three out of 5 B cell lines, 14 out of 38 Epstein-Barr virus transformed B cell lines and null cell type lymphocytic leukemia cells obtained from one patient out of 34 tested. Other normal or malignant cells, hematopoietic or nonhematopoietic cells examined were negative. The antigen does not seem to be related to EBNA, early antigen and VCA of EB virus, or certain haplotype specificity of HLA-A, B, C, and DR loci. Reports by others on production of monoclonal antibodies with similar approaches were also reviewed.

Animals↗
PubMed1982

Human melanoma antigen AH is an autoantigenic ganglioside related to GD2.

AH antigen, initially defined by an antibody present in a melanoma patient, is a cell surface antigen found on approximately 65% of melanoma cell lines. Absorption analysis indicates that AH is a differentiation antigen marking normal and malignant cells of neuroectodermal origin. The AH determinant has been found to be related to GD2 ganglioside.

Antigens↗
PubMed1982

Serological response of melanoma patients receiving melanoma cell vaccines. I. Autologous cultured melanoma cells.

Our past studies have defined Class 1 (unique), Class 2 (shared) and Class 3 (widely distributed) melanoma cell surface antigens by serological typing with autologous antibody. These definitions provide the basis for determining the immunogenicity of a series of melanoma vaccines in patients with malignant melanoma. The first vaccine we tested in this way was prepared from autologous melanoma cell lines, and the results of our trial are the basis of this report. Thirteen patients with metastatic malignant melanoma were vaccinated with irradiated, cultured autologous melanoma cells mixed with BCG in an attempt to induce a serological response to Class 1 or 2 melanoma antigens. Antibodies were measured by protein A (PA), mixed hemadsorption (MHA), immune adherence (IA), C3-mixed hemadsorption (C3-MHA) and antibody-dependent cell-mediated cytotoxicity (ADCC) assays. The specificity of observed reactions was defined by absorption analysis. Eight patients showed an increase in the titer of antibodies to autologous melanoma cell surface antigens after vaccination. In two of these patients, the antibodies had specificity for shared melanoma antigens. In six patients, the antibodies were directed solely against antigens related to the fetal calf serum (FCS) used in growing cells for serological testing and vaccine preparation. We conclude that unmodified autologous cultured melanoma cells, administered as they were in this trial, induce a serological response to melanoma cell surface antigens only in exceptional cases.

Adult↗
PubMed1982

Production and characterization of monoclonal antibody against 10S DNA polymerase alpha from calf thymus.

One hybridoma cell line that produces an antibody directed against 10S DNA polymerase alpha purified from calf thymus was obtained. The monoclonality of the antibody was tested by sodium dodecyl sulfate polyacrylamide gel electrophoresis, isoelectrofocusing and antibody subclass determination. The antibody specifically recognized the 10S DNA polymerase alpha and 6.5S DNA polymerase alpha-2 from calf thymus, but not 6.5S DNA polymerase alpha-1. The antibody precipitated both polypeptides of 140-150,000 and 46-50,000 dalton of 10S DNA polymerase alpha. The antibody also recognized the DNA polymerase alpha purified from human cells, but did pig DNA polymerase alpha only partially. The antibody did not crossreact with rat DNA polymerase alpha, calf DNA polymerase beta, virus DNA polymerase and E. coli DNA polymerase I. This antibody will be a useful tool for studying the mechanism of DNA replication in eukaryotic cells.

Animals↗
PubMed1980

Tumor-specific antigens.

Based on autologous serological typing of cultured astrocytoma cells from 30 patients, three classes of surface antigens have been defined. Class I antigens are restricted to autologous astrocytoma cells. Class II antigens are shared by autologous as well as certain allogeneic tumors, but are not detected on normal cells. Class III antigens are not tumor-specific and are found on both normal and malignant cells. This analysis of human astrocytoma, with the recognition of three classes of surface antigens recognized by autologous sera, resembles the results of autologous typing of human malignant melanoma, acute leukemia, and renal carcinoma.

Antigens, Neoplasm↗
PubMed1980

Comparison of multiple rosetting assays for detecting antibody reactivity of different immunoglobulin classes against surface antigens of benign and malignant tissue culture cells.

Four serological assays for detection of antibody reactivity against surface antigens of benign and malignant cells have been evaluated. In all four assays, antibody attached to the surface of a target cell is detected by a rosette of indicator red blood cells. Of the four assays (antibody mixed hemadsorption assay, immune adherence assay, anti-C3 mixed hemadsorption assay and protein A assay), the anti-C3 mixed hemadsorption assay showed highest sensitivity. By using purified IgM and IgG fractions we could demonstrate that, except for the protein A assay, all assays show reactivity both with IgG and IgM. Protein A assay detected only the IgG fraction, with high sensitivity. The optimization of the four assays is described and the importance of using multiple assays is emphasized.

Antigen-Antibody Reactions↗
PubMed1980

Alloantigen-induced T-cell proliferation: Lyt phenotype of responding cells and blocking of proliferation by Lyt antisera.

Cytotoxic T cells of the mouse express Lyt-1 as well as Lyt-2 and -3 on their surface, and T-cell cytotoxicity can be blocked by Lyt-2 and Lyt-3 (but not Lyt-1) antisera in the absence of added complement [Nakayama, E., Shiku, H., Stockert, E., Oettgen, H. F. & Old, L. J. (1979) Proc. Natl. Acad. Sci. USA 76, 1977-1981]. This analysis has now been extended to the study of the Lyt phenotype of T cells responding to alloantigens, concanavalin A (Con A), and phytohemagglutinin (PHA) and the effect of Lyt antibody on T-cell proliferation and the generation of H-2-specific killer T cells. H-2 (D/K and I), Con A, and PHA stimulation was abolished by pretreating responding cell populations with Lyt-1 antiserum and complement. Pretreatment with Lyt-2 or -3 antiserum and complement did not decrease alloantigen or Con A stimulation but did abolish PHA stimulation. Cytotoxic cells were not generated in H-2 alloantigen-primed cultures pretreated with Lyt-1, -2, or -3 antiserum and complement. When responding cells were cultured with Lyt antiserum in the absence of added complement, Lyt-2 or -3 antiserum (but not Lyt-1 antiserum) blocked alloantigen-induced proliferation and delayed generation of killer cells. Under similar conditions, Con A and PHA stimulation was not blocked by Lyt-1,-2, or -3 antiserum. Evidence from these Lyt elimination and blocking tests and from direct Lyt phenotyping of responding cells leads to the following conclusions. Two populations of Lyt(+) cells are involved: Lyt-1(+)2(-)3(-) and Lyt-1(+)2(+)3(+). Current evidence does not favor the existence of Lyt-1(-)2(+)3(+) cells but indicates that pre-killer and killer cells derive from the Lyt-1(+)2(+)3(+) population and have a Lyt-1(+)2(+)3(+) phenotype. H-2 (D/K and I) and PHA stimulation ordinarily activate the Lyt-1(+)2(+)3(+) population, whereas Con A and I region or Mls locus antigens activate the Lyt-1(+)2(-)3(-) population. However, when Lyt-1(+)2(+)3(+) cells are eliminated or blocked by Lyt-2 or -3 antiserum, H-2 alloantigen stimulation leads to proliferation of the Lyt-1(+)2(-)3(-) population. Blocking of H-2-induced proliferation by Lyt-2 or -3 antiserum adds further support to the possibility that molecules bearing Lyt-2 and -3 determinants are involved in T-cell recognition.

Animals↗
PubMed1979

Cell surface antigens of human renal cancer defined by autologous typing.

Sera from 28 patients with renal cancer were tested for reactivity with surface antigens of cultured autologous renal cancer cells. Four serological assays were used to survey sera for autologous antibody. Immune adherence, protein A, and C3-mixed hemadsorption assays detected reactivity in a high percentage of patients (80-100%), whereas mixed hemadsorption assays were negative with sera from all but one patient. Reactive sera from six patients were analyzed by absorption tests with autologous, allogeneic, and restricted to autologous renal cancer cells; class 2 antigens, present on certain allogeneic renal and nonrenal cancer cells; and class 3 antigens, found on a wide variety of normal and malignant cell types. The sera of one patient detected class 1, 2, and 3 antigens, the sera of three patients detected class 2 antigens, and the sera of two patients detected class 3 antigens. This analysis of renal cancer, with the recognition of three classes of surface antigens recognized by autologous sera, resembles the results of autologous typing of three other human malignancies: malignant melanoma, acute leukemia, and astrocytoma. Evidence provided by autologous typing of these cancers indicates that class 1 and class 2 antigens are tumor-restricted and that under certain circumstances these antigens are immunogenic for the autologous host.

Adult↗
PubMed1979

Cell-mediated cytotoxicity for cultured autologous melanoma cells.

Peripheral blood lymphocytes from 32 patients with malignant melanoma were tested for cell-mediated cytotoxicity (CMC) against cultured autologous melanoma cells. Effector cells were prepared from venous blood by defibrination, gel sedimentation, nylon column filtration, and lysis of remaining erythrocytes with NH4Cl. Melanoma cells prelabelled with [3H])proline were used as target cells in a 40-h assay and CMC was evaluated against standards obtained with blood lymphocytes from the least reactive normal donor. Reproducible autologous CMC was detected in 18 of 32 patients in a series of 367 total tests. CMC correlated with tumor volume (5-500 cm3) but not with tumor stage or DNCB reactivity. Preliminary results indicated that autologous CMC was not affected by treatment with DTIC, dexamethasone, intralesional BCG, radiation therapy, or partial surgical excision. Lack of consistent CMC in 14 patients could not be attributed to a measurable decrease in general immune capacity or to increased resistance of the patients' melanoma cells to CMC in general. Fibroblasts were more resistant to CMC than melanoma cells, and therefore of questionable value for defining specificity in direct tests.

Adult↗
PubMed1979

Cytotoxic T cells: Lyt phenotype and blocking of killing activity by Lyt antisera.

WE REEXAMINED TWO QUESTIONS CONCERNING LYT ANTIGENS OF CYTOTOXIC T CELLS OF THE MOUSE: is Lyt-1 antigen expressed on cytotoxic effector cells and can cytotoxicity be blocked by antibody to Lyt antigens in the absence of added complement? A 3-hr (51)Cr-release assay with splenic effector cells and leukemia or myeloma target cells was used to measure cell-mediated cytotoxicity. The cytotoxic activity of effector cells against allogeneic targets was abolished by exposure to Lyt-1, Lyt-2, or Lyt-3 antiserum and complement. Specificity was established by tests with C57BL/6 Lyt congenic mice and absorption studies with thymocytes. Similarly, the cytotoxicity of effector cells directed against semisyngeneic myeloma targets was reduced by Lyt-1, -2, or -3 antiserum and complement. Effector cell cytotoxicity against another semisyngeneic target was only marginally affected by Lyt-1 antiserum and complement, but was abolished by Lyt-2 or -3 antiserum and complement. It appears likely that cytotoxic T cells are a heterogeneous population with regard to Lyt-1 expression and that past studies indicating an apparent absence of Lyt-1 on cytotoxic T cells revealed a quantitative, not qualitative, feature of these cells. With regard to the activity of Lyt antisera in the absence of added complement, selective blocking of effector cell cytotoxicity for allogeneic and semisyngeneic targets was found with Lyt-2 and Lyt-3 antisera but not with Lyt-1 antiserum. The specificity of blocking was established by tests with Lyt congenic mice and absorption studies with thymocytes. With the exception of blocking by antisera to the H-2 haplotype expressed by the target cell, no effector cell blocking was observed with alloantisera or heteroantisera to a range of other cell surface molecules present on mouse lymphoid cells. One possibility to account for the selective blocking by Lyt-2 and Lyt-3 antisera is that Lyt-2,3 determinants on the surface of cytotoxic T cells have a close spatial relation to the T cell receptor.

Animals↗