Koda A, Yanagihara Y, Matsuura N
Department of Pharmacology, Gifu Pharmaceutical University, Japan.
Agents Actions Suppl. 1991;34:369-78.
IPD-1151T [(+/-)-[2-[4-(3-ethoxy-2-hydroxypropoxy)phenylcarbamoyl]-ethyl] dimethylsulfonium p-toluenesulfonate] inhibits not only antigen-induced histamine release from mast cells but also IgE antibody formation. The present paper describes the inhibitory effect of IPD-1151T on the IgE antibody formation. The IgE antibody formation in BALB/c mice which had been immunized with dinitrophenylated ascaris extract (DNP.As) plus alum was inhibited dose-dependently by IPD-1151T given p.o. The formations of anti-DNP.IgM and IgG antibodies, however, were unaffected in this case. Ongoing IgE antibody formation was also inhibited by this agent. The total IgE in sera of atopic patients including asthma and atopic dermatitis showed a tendency to decrease when IPD-1151T was given p.o. for 6 to 12 weeks, though the titer of specific IgE antibody against Dermatophagoides pteronyssinus or D. farinae clearly decreased. In these cases, the ratio of B cell expressing low-affinity Fc receptor for IgE (Fc epsilon RII) also decreased. Antigen-induced production of interleukin 4 (IL-4) from a helper T-cell line (TCL) prepared from peripheral blood lymphocytes of an allergic patient sensitive to Japanese cedar pollen was reduced with the addition of IPD-1151T. This agent also decreased antigen-induced IgE synthesis by autologous B cell concomitant with the TCL and antigen presenting cell. The consideration was done on the mechanism regarding the inhibition of IgE antibody formation by IPD-1151T.
IPD - 1151T[（±）-[2 - [4 - （3 - 乙氧基 - 2 - 羟基丙氧基）苯基氨基甲酰基] - 乙基]对甲苯磺酸二甲硫鎓盐]不仅能抑制抗原诱导的肥大细胞组胺释放，还能抑制IgE抗体的形成。本文描述了IPD - 1151T对IgE抗体形成的抑制作用。经二硝基苯基化蛔虫提取物（DNP.As）加明矾免疫的BALB/c小鼠，口服给予IPD - 1151T后，IgE抗体的形成呈剂量依赖性受到抑制。然而，在这种情况下，抗DNP.IgM和IgG抗体的形成未受影响。该药物也抑制了正在进行的IgE抗体形成。口服给予IPD - 1151T 6至12周后，包括哮喘和特应性皮炎在内的特应性患者血清中的总IgE呈下降趋势，尽管针对粉尘螨或户尘螨的特异性IgE抗体滴度明显下降。在这些情况下，表达低亲和力IgE Fc受体（FcεRII）的B细胞比例也下降。加入IPD - 1151T后，来自对日本雪松花粉过敏患者外周血淋巴细胞制备的辅助性T细胞系（TCL）的抗原诱导白细胞介素4（IL - 4）产生减少。该药物还降低了TCL和抗原呈递细胞伴随的自体B细胞的抗原诱导IgE合成。对IPD - 1151T抑制IgE抗体形成的机制进行了探讨。
