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Biomedical subjects

T Kishida

Publications and source records attributed to T Kishida.

At least 271 records · Page 15Linked to original sources
PubMed1982

Production and characterization of human T leukemic lymphoblastoid cell interferon.

Although human lymphoblastoid cells (Namalva and BALL-1 cells) which have the characteristics of B lymphocytes are known to be good producers of human lymphoblastoid interferon (Hu IFN-alpha (Ly) ), there is only one report on IFN production by human T lymphoblastoid cells. The present study showed that Sendai virus could induce human T lymphoblastoid cells (RPMI 8402 cells) to produce IFN. On incubation with virus, IFN was detected after 9 h, and increased until 24 h. The IFN yield depended on the dose of Sendai virus. No superinduction was observed on treatment with BUdR or antimetabolites or on irradiation with ultraviolet light. The T cell line produced IFN even in serum-free medium. The IFN produced by RPMI 8402 cells (8402-IFN) was as stable at pH 2 and on heating at 60 C for 30 min as Hu IFN-alpha and Hu IFN-beta. 8402-IFN, Hu IFN-alpha and Hu IFN-beta showed the same kinetics of induction of the antiviral state of FL cells. The 8402-IFN was neutralized by anti-Hu IFN-beta serum, but not anti-Hu IFN-alpha serum, indicating that it was antigenically identical with Hu IFN-beta. MDBK cells were very sensitive to Hu IFN-alpha, but not to this IFN or Hu IFN-beta, but L929 and RK-13 cells were equally sensitive to 8402-IFN, Hu IFN-alpha and Hu IFN-beta. The molecular weight of this IFN was estimated as 21,000 and 16,500 daltons by SDS-PAGE and Sephadex G-100 gel chromatography, respectively.

Cell Line↗
PubMed1982

[Antigenic types of interferons produced by several human lymphoblastoid cells].

There are two antigenic types of human virus-induced interferons (IFNs): one is a human leukocyte IFN (Hu IFN-alpha and the other is a human fibroblast IFN (Hu IFN-beta). We examined the antigenic types of IFNs produced in several human T and B lymphoblastoid cell lines through the induction by Sendai virus. We could produce IFNs in the several human T lymphoblastoid cells (RPMI 8402, Peer, JM and CCRF-CEM) and in several human B lymphoblastoid cells (BALL-1, B35M, DG-75 and ARH-77), and examined antigenic types of the IFNs produced. The results showed that all T lymphoblastoid cells produced Hu IFN-beta. On the other hand, the antigenic types of IFN were dependent on each cell line in human B lymphoblastoid cell lines. The IFN produced in BALL-1 cell was only one type of Hu IFN-alpha. The IFNs produced in ARH-77 and DG-75 cells contained two types of the Hu IFN-alpha and Hu IFN-beta. The IFN produced in B35M cell was only one type of Hu IFN-beta. It was concluded that human T lymphoblastoid cell produced Hu IFN-beta, and that the first type of human B lymphoblastoid cell produced only Hu IFN-alpha, the second type produced Hu IFN-alpha and Hu IFN-beta and the third type produced only Hu IFN-beta.

B-Lymphocytes↗
PubMed1982

[Degenerative change in tumor cells caused by human fibroblasts and its enhancement by human interferons].

The target cells (KB, HeLa, FL, human hepatoma and murine L929) were cocultured with human embryonic fibroblasts in the Petri dish. The degenerative changes of the target cells except L929 cells by the human fibroblasts were found. Human leukocyte interferon (HuIFN-alpha) and human fibroblast interferon (HuIFN-beta) enhanced these changes, but mouse IFN (MuIFN-alpha, beta) did not. The other human fibroblasts also caused the degenerative changes of the target cell, and HuIFN-alpha enhanced these changes. It was concluded that human fibroblasts play a certain role in the suppression of the human tumor cell.

Animals↗
PubMed1982

Antigenic types of various human lymphoblastoid cell interferons.

There are two antigenic types of human virus-induced interferon (IFN): human leukocyte IFN (Hu IFN-alpha) and human fibroblast IFN (Hu IFN-beta). Production of IFNs in various human T, B and non-T non-B lymphoblastoid cell lines were induced with Sendai virus and the antigenic types of these IFNs were determined. All the IFNs produced in human T lymphoblastoid cell lines (RPMI 8402, Peer, JM and CCRF-CEM cells) were antigenically identical to Hu IFN-beta. On the other hand, the antigenic type of IFN produced in human B lymphoblastoid cell lines was different in each cell line. IFNs produced in BALL-1 and RPMI 6410 cells were Hu IFN-alpha, but IFN produced in B35M cell was Hu IFN-beta. IFNs produced in DG-75 and ARH-77 cells consisted of both Hu IFN-alpha and Hu IFN-beta. IFNs produced in non-T non-B lymphoblastoid cell lines (NALM-16 and U-937 cells) also consisted of Hu IFN-alpha and Hu IFN-beta. Thus the antigenic types of IFNs produced in human lymphoblastoid cells reflect certain characteristics of the producer cells. The factors that determine which antigenic type of IFN is produced have not yet been clarified.

B-Lymphocytes↗
PubMed1982

Assessment of anti-tumor cell effect of human leukocyte interferon in combination with anticancer agents by a convenient assay system in monolayer cell culture.

Cell growth inhibition by anticancer agents was determined by a simple dye-uptake method. This technique could be performed more easily and rapidly than the cell counting method, the method for measurement of 3H-thymidine incorporation, or other dye-uptake methods. The number of viable cells was linearly correlated with the amount of dye taken by the surviving cells, so that the method described in this article could be applied to the assessment of anti-tumor cell effects of human leukocyte interferon (Hu IFN-alpha) in combination with anticancer agents. In combinations of Hu IFN-alpha with anticancer agents such as bleomycin, mitomycin C, and cytosine arabinoside in certain concentration ranges, antagonism was noticed when Hu IFN-alpha and anticancer agents were added simultaneously to the cell culture. However, outside those ranges of concentration, additive effects were observed. Furthermore, the treatment of the cell with IFN followed by the anticancer agents and vice versa showed additive effects.

Antibiotics, Antineoplastic↗
PubMed1982

The preventive effect of human interferon-alpha on influenza infection; modification of clinical manifestations of influenza in children in a closed community.

A double-blind, controlled trial to ascertain the preventive effect of human interferon-alpha (Hu IFN-alpha) on upper respiratory viral infections was performed on children in a closed community. Drops of Hu IFN-alpha were instilled into the nasal cavity of 13 healthy children aged one to three years. Fourteen children were given placebos as controls. Administration of the interferon and clinical observations were carried out in the winter of 1980. Serological examination revealed that this was the period of outbreaks of influenza type A epidemics in the community. Clinical manifestations referable to influenza virus infection were milder in the interferon-treated group than in the controls. However, there was no significant difference in the serological responses of the two groups after infection with influenza virus type A.

Administration, Intranasal↗
PubMed1981

Effects of intralesional interferon on neuroblastoma: changes in histology and DNA content distribution of tumor masses.

Local injections of interferon, 30 X 10(4) IU, ten times, were found to reduce masses of neuroblastoma. Histologic findings and nuclear DNA measurements of cells from tumors in which interferon has been injected compared with cells from tumors that did not receive injections demonstrated that the reduction of neuroblastoma masses by interferon did not depend on increased cell differentiation or on interruption of tumor cell production. Although the mechanism of interferon's action on reducing neuroblastoma is unknown, the disappearance of tumor cells may be caused by high levels of interferon in tumor tissues.

Adult↗
PubMed1981

Preparation of anti-Gm sera by immunization of rabbits with protein A-fractionated normal IgG proteins from Japanese: further study.

A method is described for the production of rabbit anti-Gm sera using normal IgG proteins and fragments thereof as the immunogens. Anti-G3m(16) and anti-G3m(21) were readily producible by immunizations with protein A-purified IgG3 proteins of G3m(13, 15, 16) and G3m(21) type, respectively. Anti-G1m(2), anti-G1m(3), and anti-G3m(5) were obtained by immunizations with type Gm(1, 2, 21) Fc fragments, type Gm(1, 3, 5, 13) IgG1-rich IgG, and type G3m(5, 13, 21) IgG3, respectively. These immune sera can distinguish the 9 Gm phenotypes in the Japanese.

Animals↗
PubMed1981

Induction of pulmonary indoleamine 2,3-dioxygenase by interferon.

Pulmonary indoleamine 2,3-dioxygenase [indoleamine: oxygen 2,3-oxidoreductase(decyclizing)] has been found to be induced (30- to 100-fold) in the mouse after a single intraperitoneal administration of bacterial endotoxin [Yoshida, R. & Hayaishi, O. (1978) Proc. Natl. Acad. Sci. USA 75, 3998-4000] or during in vivo virus infection [Yoshida, R., Urade, Y., Tokuda M. & Hayaishi, O. (1979) Proc. Natl. Acad. Sci. USA 76, 4084-4086]. In the present study, an in vitro system with mouse lung slices was developed in which bacterial endotoxin (5 micrograms/ml)produced an induction (approximately 10-fold) of indoleamine 2,3-dioxygenase. The endotoxin was substituted by interferon from mouse L cells or mouse brain. The pulmonary enzyme activity increased almost linearly for 48 hr after addition of mouse interferon (10(4) units/ml) to lung slices. Interferon from mouse L cells or mouse brain produced a 10- to 15-fold increase in the enzyme activity, whereas that from human leukocytes was all but ineffective. The effect also was observed using highly purified L-cell interferon, prepared by poly(U) affinity column chromatography. When interferon was treated either by heat, alpha-chymotrypsin, or anti-interferon serum, such increase in the enzyme activity was diminished essentially to the same extent as seen in the antiviral activity. The increase in the enzyme activity was blocked when actinomycin D or cycloheximide was added to the slices before interferon treatment. These results suggest that the enzyme induction was produced by interferon and not by possible contaminants in the interferon preparations.

Animals↗
PubMed1981

Inhibition of interferon-mediated induction of indoleamine 2,3-dioxygenase in mouse lung by inhibitors of prostaglandin biosynthesis.

Inhibitors of fatty acid cyclooxygenase such as indomethacin (0.1 mM), phenylbutazone (0.3 mM), and aspirin (1 mM) were found to suppress almost completely the interferon-mediated induction of indoleamine 2,3-dioxygenase in mouse lung slices. However, phenacetin, an anti-inflammatory agent devoid of cyclooxygenase inhibitory activity, and sodium salicylate, a weak inhibitor of cyclooxygenase, were much less active under identical conditions. Glucocorticoids including dexamethasone, betamethasone, and cortisone, all of which are inhibitors of phospholipase A2, blocked induction of the dioxygenase by interferon in the nanomolar range, whereas other steroid hormones, such as aldosterone, testosterone, and 17 beta-estradiol, were all but ineffective. These results suggest that the enzymes phospholipase A2 and fatty acid cyclooxygenase, both of which are essential for the biosynthesis of prostaglandins, play an important role in the induction of indoleamine 2,3-dioxygenase by interferon.

Animals↗
PubMed1981

Combined protective effects on interferon and interferon induction on herpes simplex and ectromelia virus infections in mice.

Mouse interferon or the induction of mouse interferon with polyriboinosinic acid-polyribocytidylic acid significantly protected mice against herpes simplex and ectromelia viral infections. When polyriboinosinic acid-polyribocytidylic acid was administered 24 h before herpes simplex or ectromelia viral infection and mouse interferon was administered shortly before and 24 h after infection, a combined protective effect against either herpes simplex or ectromelia viral infection in mice was evident. There was a significant decrease in the mortality rate with the combined treatment as compared either with the rate in group treated with interferon or polyriboinosinic acid-polyribocytidylic acid.

Animals↗
PubMed1981

[Effect of interferon on the inhibition of malignant cell growth by human peripheral leukocytes. III. Effect of systemic administration].

Human leukocyte interferon preparation (HuIFN-alpha LE) was given to the patients with cancer or with chronic hepatitis. Spontaneous tumor cell growth inhibition by human peripheral lymphocytes (STGI) and NK activity were enhanced by the systemic administration of HuIFN-alpha LE, although there were differences in the kinetics between the two activities after one time administration or by the repeated administration. This suggests that IFN acts indirectly on the tumor cells by the medium of normal lymphocytes or NK cells, and that tumor cell growth inhibition is different from NK activity.

Cell Division↗
PubMed1981

New simple dye-uptake assay for interferon.

Using the spectrophotometer that the authors developed, the amounts of human leukocyte and mouse L cell interferons on FL cells and L929 cells were measured and values were compared with those measured by the cytopathogenic effect (CPE) reduction method (CPE method). The spectrophotometric method, which was simpler than the original dye-uptake method, was found to be more sensitive than the latter. When Sindbis virus was used instead of vesicular stomatitis virus (VSV), there were no significant differences in the sensitivities of the two methods or the interferon titers estimated. When FL cells or L929 cells were treated with interferon at the time of their dispersion, their interferon titers were almost the same as those of cells treated with interferon 2 days after dispersion. It is concluded that this new dye-uptake method is useful for assay of human and mouse interferons.

Biological Assay↗