Search PubMed⌕ Search

Biomedical subjects

T Masuda

Publications and source records attributed to T Masuda.

At least 739 records · Page 41Linked to original sources
PubMed1982

Studies on effects of forphenicinol on immune responses.

The oral administration of forphenicinol, S-2-(3-hydroxy-4-hydroxymethylphenyl)glycine which was synthesized during the study of derivatives and analogs of forphenicine, augmented delayed-type hypersensitivity to sheep red blood cells and oxazolone in mice. The treatment with forphenicinol restored DTH in mice immuno-suppressed by cyclophosphamide to normal response. Forphenicinol neither augmented antibody-formation nor stimulated proliferation of lymphocytes in the presence or absence of lectins. Phagocytosis by peritoneal macrophages was enhanced by forphenicinol in vivo and in vitro. Forphenicinol was effective in increasing the production of CFU-C in the presence of colony stimulating factor and partially prevented the reduction of leucocyte counts caused by mitomycin C.

Adjuvants, Immunologic↗
PubMed1982

Antitumor effect of forphenicinol, a low molecular weight immunomodifier, on murine transplantable tumors and microbial infections.

The antitumor activities of forphenicinol against murine transplantable tumors were examined. Ehrlich carcinoma was suppressed by treatment with 0.08 approximately 0.31 mg/kg/day of forphenicinol given for 10 days starting 5 days after tumor inoculation. IMC carcinoma was also suppressed by treatment with 0.5 approximately 5 mg/kg/day given for 5 days starting 8 days after the inoculation. The antitumor activity was dependent on the number of tumor cells inoculated, schedule of administration and dose. However, even in case of fast growing tumors such as L1210 and inoculation with a large number of tumor cells, forphenicinol markedly enhanced the antitumor effect of 6-mercaptopurine, aclacinomycin and cyclophosphamide. Forphenicinol showed a protective effect on Pseudomonas infection in mice.

Adjuvants, Immunologic↗
PubMed1982

Feedback regulation of immune responses by immune complexes; possible involvement of a suppressive lymphokine by FcR gamma-bearing B cell.

Inoculations of antigen-antibody complexes (immune complexes) with the intact Fc portion generates suppressor cells in vivo by binding to FcR gamma on B cells via Fc portions. The cell type responsible for the suppression appears to be B cells bearing FcR gamma. Neither T cells nor macrophages participate in both the inductive and effective phases of this type of regulation. The suppression caused by splenic B cells, previously stimulated with immune complexes in vivo, is mediated by humoral factor(s) released from them. The suppressive factor(s) have H-2 gene product(s) coded by the right-hand side of the H-2 gene complex, but not for FcR gamma themselves or immunoglobulins. It has shared component(s) with suppressive B cell factor (SBF) released from FcR gamma + B cells stimulated with immune complexes in vitro, and it resembles SBF in its mode of action. These findings indicate that immune complexes, the final products of antibody responses, control the immune responses by stimulating surface FcR gamma on B cells. It is of interest that this type of regulation functions in vivo.

Animals↗
PubMed1982

Ontogeny of 'macrophage' function. III. Manifestation of high accessory cell activity for primary antibody response by Ia+ functional cells in newborn mouse spleen in collaboration with Ia- macrophages.

The ontogenesis of the responsiveness of murine whole spleen cells in the in vitro primary antibody response paralleled not only the development of competent lymphoid cells but also that of the accessory cell (A-cell) activity of spleen adherent cells (SAC). The Ia+ cell content of SAC (and also peritoneal exudate cells) was very low until 2 weeks of age. The phagocytic activity of macrophages in SAC was higher in newborns than in adults, though no significant difference was observed between Ia- and Ia+ macrophages in phagocytic activity. We attempted to reveal a high A-cell activity using cells in newborn spleen by means of our experimental strategy documented previously in adult mice (Inaba, Nakano & Muramatsu, 1981): though neither Ia- macrophage population (Ia- SAC) nor a temporarily adherent spleen cell population containing few phagocytic macrophages (crude non-macrophage cell fraction, CF) serves as an autonomous A-cell source, the collaboration of Ia+ non-macrophage cells in CF with Ia- SAC causes the manifestation of A-cell activity. Adult CF collaborated as well with newborn SAC as with adult Ia- SAC, indicating that newborn Ia- macrophages are functionally comparable with adult Ia- macrophages in the ability to collaborate with Ia+ non-macrophage cells. On the other hand, a high A-cell activity was generated by the combination of adult Ia- SAC with a large number of newborn CF cells, indicating that there exist competent Ia+ cells in newborn spleen, though much fewer than in adult spleen.

Animals↗