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      • Heligmosomoides polygyrus 감염 마우스의 면역반응 잠재력

        하대유,고유승,한병갑 大韓免疫學會 1996 大韓免疫學會誌 Vol.18 No.2

        Heligmosomoides polygyrus(=Nematospiroides dubis) is gastrointestinal parasitic nematoda which is common parasite of wild rodents in North America, Western Europe and the CIS. The experimental infection with this parasite has been studied extensively in models of host-parasite interaction. The present study was undertaken to investigate the effect of H. polygyrus infection on the humoral and cellular immune responses in mice. It was found that H. polygyrus infection suppressed delayed-type hypersensitivity(DTH) to SRBC, contact hypersensitivity to dinitroflurobenzene (DNFB) and hemagglutinin response to SRBC. Surprisingly, H. polygyrus infection suppressed active systemic anaphylaxis(ASA) induced by ovalbumin(OVA), but elicited marked increase of the total IgE antibody and total IgG production compared with uninfected mice. In a histological examination of the mucosal mast cell(MMC) response in vivo in ICR mice, H. polygyrus infection elicited a enhance MMC response 14 days post-infection, but did not show any difference 21 days post-infection, but did not show any difference 21 days post-infection compared with uninfected controls, suggesting mucosal mastocytosis response may depend on certain stage of life cycle of H. polygyrus. Taken together, the present study strongly suggested that H. polygyrus infection in mice in-creased the total IgE and IgG antibody production, but suppressed cellular immune response to SRBC and DNFB, hemagglutinin respose and OVA-induced anaphylaxis, and that mucosal mastocytosis may be decreased or increased depending on certain stage of life cycle H. polygyrus.

      • Heligmosomoides polygyrus 감염 마우스의 비장세포로 부터 만든 Conditioned Supernatant의 면역억제작용

        하대유,한병갑,김명선,고유승 大韓免疫學會 1996 大韓免疫學會誌 Vol.18 No.3

        Heligmosomoides polygyrus is gastrointestinal parasitic nematoda which is common parasire of wild rodents. The experimental infection with this parasite has been studied extensively in models of host-parasite interaction. The present study was undertaken to investigate both the effects of administration of conditioned supernatant or conditioned medium(CM) prepared from H. polygyrus-infected mice on the humoral and cellular immune responses in mice. Normal conditioned supernatant(NCM) was prepared from uninfected mouse splenocytes stimulated with Con A. Supematants conditioned by Con A-stimulated splenocytes of H. polygyrus -infected mice were prepared on different days post-infection, namely on day 6(HCM-D6), day 14 (HCMD14) and day 18 (HCM-D18) post-infection with H. polygyrus L3 larvae. Effects of NCM, HCM-D6, HCM-D14 and HCM-D18 on delayed-type hypersensitivity(DTH) to sheep red blood cells (SRBC), contact hypersensitivity to dinitrofluorobenzene (DNFB), hemagglutinin response to SRBC, ovalbumin (OVA)-induced active systemic anaphylaxis(ASA), and anti-OVA specific IgE were investigated. Effect of anti-IL-4 antibody (11B11) on immunoinhibitory action of HCMD18 in OVA-induced ASA was also investigated. It was found that the administration into mice of HCM-D6, HCM-D14 or HCM-D18 significantly suppressed DTH to SRBC, contact hypersensitivity to DNFB, hemagglutinin response compared with NCM. The degree of immunosuppressive activity of HCM was less marked in HCM-D6 than HCM-D14 and HCM-D18. Interestingly, HCM-D18 prepared from ICR mouse strain also showed the profound suppression of OVA-induced ASA in BALB/c and C57BL/6 mouse strains as well as in ICR mice. ASA-inhibitory activity of HCM-D18 was Somewhat abrogated in terms of mouse mortality when mice were treated in the combination of HCM-D18 and anti-IL-4 antibody, indicating that IL-4 may play a role, at least in part, in the inhibitory activity of HCM. Taken together, the present study may be the first to demonstrate that conditioned supernatants prepared from the spleen cells of H. polygyrus-infected mice may suppress the in vivo humoral and cellular immyne responses to heterologous antigens, particularly fatal anaphylaxis induced by OVA, strongly suggesting that

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