Akito Toshitani
Kyushu University
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Featured researches published by Akito Toshitani.
International Archives of Allergy and Immunology | 1997
Yumiko Kubota; Shuhei Imayama; Akito Toshitani; Hiroko Miyahara; Tomoko Tanahashi; Yoko Uemura; Tetsuya Koga; Naoto Sugawara; Fumihiko Kurimoto; Keishi Hata
There is a great need to develop a method for making an accurate and reliable in vitro diagnosis of adverse hypersensitivity reactions to drugs. We measured the amount of sulfidoleukotriene (sLT) released from the peripheral blood leukocytes obtained from 25 patients who developed hypersensitivity reactions following the administration of nonsteroidal anti-inflammatory drugs (NSAIDs); 12 patients demonstrated reactions to Voltaren, 8 patients to Bufferin, and 5 patients to Sedes G. The stimulation index, the ratio of the amounts of sLT (pg/ml) incubated with and without drugs, was considerably higher in the patients than in the controls, which consisted of 5 nonallergic healthy subjects. The sensitivity of the CAST (cellular antigen stimulation test) was evaluated to range from 62.5 to 80%, while the specificity was 70-100%. The CAST may thus be useful as a novel in vitro test system in order to screen for possible hypersensitive reactions to NSAIDs with both reliability and safety.
Journal of Dermatological Science | 1999
Akito Toshitani; Shuhei Imayama; Yuji Shimozono; Takaaki Yoshinaga; Masutaka Furue; Yoshiaki Hori
Coupled with the previous finding that sIgA excretion was reduced onto the surface of the skin, we demonstrated that sIgA secretion in the tears of patients with atopic dermatitis (AD) was significantly lower than that of normal subjects, using a small stick made of nitrocellulose membrane. In the bacterial cultures, we have also detected a higher frequency of Staphylococcus aureus in the tears from patients with AD compared to normal subjects. These findings suggested reduced sIgA secretion on the mucous membrane might play a crucial role in the pathomechanisms of the ocular lesions, such as abnormal bacterial flora and ocular complications as well as the establishment of skin lesions in AD.
British Journal of Dermatology | 1992
Juichiro Nakayama; Yoichi Moroi; Akito Toshitani; Shun'ichiro Taniguchi; M. Okamoto-Inoue; Yoshiaki Hori
The cytolytic and/or cytostatic effects of hyperthermia, lymphokine‐activated killer cells (LAK cells) and the combination of both were assayed using F1 and F10 B16 melanoma cell lines. F10 cells with a high metastatic potential showed a greater sensitivity to hyperthermia than F1 cells which have low metastatic potential. The F10 cells were lysed to a lesser extent by LAK cells than the F1‐B16 cells. When the cell lines were subjected to hyperthermia at 43°C for 3 h and then interacted with LAK cells, the maximum cytolysis reached almost 100%. When the interaction with LAK cells was followed by hyperthermia at 43°C, the total release of 51Cr from the cell lines was 75–85%. The extent of 51Cr release from the B16 melanoma cell lines was inversely correlated with the survival rate as calculated by the plating efficiency of the incubated cells. The survival rate of mice intravenously injected with B16‐F10 cells and subjected to hyperthermia at 41°C for 3 h in vitro increased compared to that of controls. This was further increased by the simultaneous administration of LAK cells.
Cellular Immunology | 1987
Akito Toshitani; Kazuto Taniguchi; Yoh-Ichi Kawano; Kikuo Nomoto
We investigated the manner in which rIL-2 induced effectors in vitro (LAK cells), which, like NK cells, lyse targets nonspecifically and discriminate nonself, and how H-2 as the self-marker affects the LAK cell killing mechanism. NK cells showed an appreciably higher killing activity to B16 melanoma H-2- cells than to H-2+ cells. In contrast, LAK cells lysed more efficiently to H-2+ cells. The in vivo experiments showed that the NK cells prevented pulmonary metastasis of B16 H-2- cells in the normal syngeneic host, whereas the transferred LAK cells had a preferential inhibitory effect on the pulmonary metastasis of B16 H-2+ cells in the immunodeficient syngeneic hosts. Taken together, these results show that the H-2-encoded or H-2-associated molecules contribute to the triggering signal in the lysis by LAK cells, whereas the NK cells recognize the reduced self H-2 expression on the targets, thereby contributing to a trigger of the lysis.
European Journal of Clinical Pharmacology | 1995
Ichiro Ieiri; W. Goto; Shun Higuchi; Kentaro Hirata; Akito Toshitani; Shuhei Imayama; Yukiko Ohyama; Hiroaki Yamada; Kenji Ohtsubo
The purpose of this study was to assess the possible role of the (R)- and (S)- enantiomers of the phenytoin metabolite p-HPPH in the pathogenesis of gingival hyperplasia (GH). About 98% of circulating p-HPPH is in the (S)-form. There were significant differences between patients with and without GH in (R)-p-HPPH level (0.055 vs 0.042 μg·ml−1), both enantiomer/racemate level ratios, and R/S enantiomeric ratio (0.0313 vs 0.0232); an increase in serum (R)-p-HPPH level was observed in patients with GH. In separate experiments, the effect of p-HPPH enantiomers on the proliferation of the normal human dermal fibroblast was studied. The in vitro study showed that (R)-p-HPPH selectively stimulated fibroblast growth. The results suggest that the least abundant metabolite, (R)-p-HPPH, is the most toxic with respect to gingival hyperplasia.
Cellular Immunology | 1988
Atsushi Karashima; Kazuto Taniguchi; Kunisuke Himeno; Yoh-Ichi Kawano; Akito Toshitani; Kikuo Nomoto
B6-lpr/lpr mice develop massive T cell lymphoproliferation, as associated with autoimmune disease. We found a reduced NK activity in the spleen of B6-lpr/lpr mice. Neonatal thymectomy markedly retarded the development of lymphoproliferation and the development of autoantibodies in the B6-lpr/lpr mice. These animals had a higher level of NK activity in the spleen. When the neonatally thymectomized B6-lpr/lpr mice were given anti-asialo GM1 serum (30 microliter) four times at 6-day intervals, initiated at the 8th-10th postnatal week, these mice developed lymphoproliferative disorders and splenomegaly, concomitantly with depression of NK activity. It is therefore tempting to speculate that NK cells are involved in the regulation of the occurrence of lymphoproliferative disorders.
Cellular Immunology | 1988
Akito Toshitani; Kazuto Taniguchi; Kunisuke Himeno; Yoh-Ichi Kawano; Kikuo Nomoto
We investigated whether the adoptive transfer of H-2-incompatible lymphokine-activated killer (LAK) cells would efficiently demonstrate antitumor activity without damaging the normal host cells. Allogeneic LAK cells (5 X 10(7] did not cause graft-versus-host disease (GVHD) in irradiated recipients, whereas more than half of the mice transferred with the same dose of fresh allogeneic spleen cells developed GVHD. Repeated transfer (three times at 4-day intervals, 1.2 X 10(8) cells/mouse) did not result in GVHD. Graft-versus-host reaction (GVHR), which is detectable by spleen enlargement of recipients transferred with allogeneic lymphoid cells was also absent in LAK cell-transferred mice of all strain combinations tested. Host immune responses were not affected in these mice. Therefore, it is feasible to transfer allogeneic LAK cells. With the antitumor efficacy of allogeneic LAK cells, they preferentially lysed allogeneic tumor targets. Adoptive transfer of the allogeneic LAK cells led to a significant decrease in the lung-colonizing foci of intravenously inoculated B16 melanoma cells. Allogeneic LAK cells and syngeneic ones were equally active, in vivo. The use of allogeneic LAK cells may prove to be a valuable method for effective clinical antitumor immunotherapy.
Cellular Immunology | 1988
Yoh-Ichi Kawano; Kazuto Taniguchi; Klas Kärre; Akito Toshitani; Kikuo Nomoto
The mechanisms of host H-2-associated resistance against metastasis of tumor cells were evaluated in relation to the H-2 phenotype of tumor cells. We used H-2 heterozygous H-2a/b and H-2d/b, and H-2 homozygous H-2b/b hosts, and H-2-associated variant lines of B16 cells (H-2b+, H-2b-). In H-2b/b hosts, H-2+ cells were highly metastatic in vivo, and were resistant to host NK effectors in vitro. Therefore, H-2a/b and H-2d/b hosts showed resistance to metastasis of H-2+ cells and their effectors showed killing activity to these cells in vitro. Though the host resistance was reduced by anti-asialo GM1 serum treatment, these hosts continued to demonstrate a considerable resistance against early survival and metastasis of the B16 cells. To evaluate this natural resistance, aside from the NK system, radiation bone marrow chimeras of F1-parental combinations were used. The data suggest that host MHC-associated resistance involves not only the NK defense system but also the host environmental resistance. Both exert resistance by recognizing the H-2 mismatch in relation to the host.
Journal of Dermatology | 1993
Juichiro Nakayama; Akito Toshitani; Toshio Hattori; Yoichi Moroi; Yoshiaki Hori
Three adult T‐cell leukemia/lymphoma‐derived cell lines, MT‐2, MJ, and HUT102, were investigated to determine how they responded to hyperthermia, lymphokine‐activated killer (LAK) cells, or a combination of both in vitro. All three cell lines showed a similar sensitivity to LAK cells, but revealed varying degrees of sensitivity to hyperthermia (MT‐2
Cellular Immunology | 1989
Kazuto Taniguchi; Yoh-Ichi Kawano; Akito Toshitani; Atsushi Karashima; Kikuo Nomoto
We attempted to investigate if the in vivo administration of concanavalin A (Con A), a potent T cell stimulator, would render anti-metastatic activity in hosts. Assays of activity were performed 20 days after iv inoculation of two clones of the B16 melanoma, B16-H (H-2+, highly metastatic), B16-L (H-2-, low metastatic), or 3LL cells into C57BL mice by enumerating lung colonies. In some experiments, hosts treated with anti-asialo GM1 Ab were used to evaluate effector mechanisms other than NK cells. While the injection of Con A alone had no significant effect on anti-metastatic activity, in nonimmunized hosts the effect by Con A was displayed when the mice were preimmunized with B16-H cells but not in those immunized with B16-L cells. Immunization with B16-H or B16-L cells alone resulted in the generation of killer cells with promiscuous lytic activity and induced an anti-metastatic effect against B16-H, B16-L, and 3LL cells. Con A treatment significantly augmented the killer activity of spleen cells of mice preimmunized with B16-H cells but not of those immunized with B16-L cells. The effectors from mice immunized with B16-H alone or given both Con A and B16-H were mainly of Thy 1+ Lyt2+ asialo GM1- cells, on the other hand, those from mice immunized with B16-L cells expressed asialo GM1 antigen. We showed the efficacy of Con A on the anti-metastatic effect in relation to the host immune response.