Suppression of IgE production by suplatast (suplatast tosilate), a new dimethylsulfonium agent: (1). Regulation of murine IgE response
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- Yanagihara Yukiyoshi
- Clinical Research Center for Allergy, National Sagamihara Hospital
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- Kiniwa Mamoru
- Clinical Research Center for Allergy, National Sagamihara Hospital
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- Ikizawa Koichi
- Clinical Research Center for Allergy, National Sagamihara Hospital
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- Yamaya Hidetoshi
- Clinical Research Center for Allergy, National Sagamihara Hospital
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- Shida Takao
- Clinical Research Center for Allergy, National Sagamihara Hospital
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- Matsuura Naosuke
- Department of Pharmacology, Gifu Pharmaceutical University
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- Koda Akihide
- Department of Pharmacology, Gifu Pharmaceutical University
書誌事項
- タイトル別名
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- Suppression of IgE Production by IPD-1151T (Suplatast Tosilate), a New Dimethylsulfonium Agent: (1). Regulation of Murine IgE Response.
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抄録
The effect of IPD-1151T, a new dimethylsulfonium compound, on the IgE response was investigated in the mouse system. The oral administration of IPD-1151T to immunized BALB/c mice suppressed the primary IgE antibody response and depressed the elevation of serum IgE levels, whereas the same treatment did not affect the IgG antibody response. The enhanced expression of low-affinity IgE receptor (Fc ε RII/CD23) on the spleen cells of immunized mice was also inhibited by IPD-1151T administration. It was further demonstrated from the adoptive transfer experiment that IPD-1151T, administered to hapten-primed B cell donors, but not to carrier-primed T cell donors, exerted its suppressive influence on the hapten-specific secondary IgE antibody response in irradiated syngeneic recipients. Interestingly, IPD1151T concentration-dependently inhibited the production of interleukin 4 (IL-4) by D10G4.1, known to be a typical Th2 clone. However, IPD-1151T did not suppress the production of IgE and IgGI by normal splenic B cells stimulated with lipopolysaccharide and IL-4. Moreover, IL-4-induced expression of Fc ε RII on normal spleen cells was not inhibited by the agent. These results strongly suggest that the IgE-suppressive activity of IPD-1151T is most likely due to the inhibition of IL-4 production at the T cell level.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 61 (1), 23-30, 1993
公益社団法人 日本薬理学会
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詳細情報
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- CRID
- 1390001204285583104
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- NII論文ID
- 130000840211
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- NII書誌ID
- AA00691188
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- COI
- 1:CAS:528:DyaK3sXhtl2ntrk%3D
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- ISSN
- 13473506
- 00215198
- http://id.crossref.org/issn/00215198
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- PubMed
- 8382322
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可