http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
질내투여 인정장(人精漿)의 인정자(人精子) 및 면양적혈구에 대한 면역반응 억제작용
이헌구,김용탁,하대유 大韓免疫學會 1987 大韓免疫學會誌 Vol.9 No.1
A number of evidence has been accumulated to show that human seminal plasma (HSP) can suppress the immune responeses in vitro and in vivo. Several immunosuppressive factors have been identified from HSP and it has been proposed that these factors play a critical role in preventing sensitization of females to spermantigens after insemination. The purpose of the present study is to answer the q question whether HSI' is able to suppress in vivo immune responses induced by some antigens such as human sperms and sheep red blood cells(SRBC) which are introduced into the vagina of females. In this study the author used an experimental model in which mice were immunized intravaginally with human sperms and SRBC, and delayed-type hypersensitivity reacion (DTH) to these antigens was eva- luated by footpad swelling reaction. Repeated simultaneous intravaginal administrations of HSP with human sperms or SRBC significantly suppressed the DTH but failed to suppress the antibody formation to these antigens. However, intravaginal administration of a high molecular weigt fraction(G― 200 F, greater than 200 KD) which was partially purified by ammonium sulfate precipitation, DEAE- cellulose and Sephadex G -200 chromatography from HSP resulted in a significant suppression of DTH as well as antibody formation to SRBC. Furthermore, when various concentrations of G―200 F were ad-ministered intraperitoneally, a dose-dependent suppression of both DTH and antibody formation to SR BC was observed. These results provide the evidence that in vivo immunosuppressive activity of HSP is mediated by a high molecular weight fraction of greater than 200 KD and strongly support the concept that HSP can prevent sensitization of females to sperm antigens after insemination.
IL-4와 다른 여러가지 cytokines이 사람 편도 단핵세포의 IgE 생산에 미치는 영향
이헌구,송원재,하대유 大韓免疫學會 1995 大韓免疫學會誌 Vol.17 No.3
The present study was desinged to compare IgE producing ability of cultured human tonsillar mononuclear cells (TMNC) stimulated by rhIL-4 between complete Iscove's modified Dulbeco's medium (C-IMDM, which was composed of IMDM enriched with bovine serum albumin, fetal calf serum, transferrin, insulin, and mixture of saturated and unsaturated fatty acids) and RPMI-1640 supplemented with FCS (RPMI-1640), as well as to investigate a single or combined effects of IL-4 and 7 different human cytokines (IL-2, IL-5, IL-6, IL-7, TNF-a, IFN- 7' and TGF-fi ) in a culture system on IgE production of human TMNC. It was found that C-IMDM was superior to RPMI 1640 as a culture medium for supporting the synthesis of IgE by TMNC stimulated with rhIL-4. In fact, RPMI-1640 failed to induce significant IgE synthesis by TMNC cultured for 21 days in the presence of rhlL-4 (100 U / ml). In addition, 7 different cytokines other than IL-4 failed to induce the significant IgE synthesis by TMNC cultured in C-IMDM when tested alone. However, IL-2 or IL-6, which was ineffective in inducing IgE production when tested alone, enhanced IL-4-mediated IgE production, indicating - that IL-2 or IL-6 acts synergistically with IL-4. In contrast, IFN- Y . or TGF-J1 demonstrated the inhibition of IL-4 dependent IgE synthesis by TMNC. Interestingly, IL-5, IL-7 and TNF-a had no modulatory effect on the IL-4 dependent IgE response in the applied experimental conditions. Taken together, the present results strongly suggested that 1) C-IMDM may be superior to RPMI-1640 as a culture _medium for IgE production, 2) Only IL-4 had the ability to stimulate in vitro with IgE synthesis by TMNC when tested alone. 3) IL-2 and IL-6 may be synergistic with IL-4 in IgE synthesis, 4) IFN- F and TGF-P may have the antagonistic effects on IL-4 dependent IgE synthesis and 5) IL-5, IL-7 and TNF-a may have no modulatory effects. This study also suggested that increased insight into various mechanisms of IgE regulation by cytokines may eventually lead to improve therapeutic strategies in the clinical management of IgE-mediated allergy.
Lee, Kyung Sun,Park, Seoung Ju,Kim, So Ri,Min, Kyung Hoon,Jin, Sun Mi,Lee, Hern Ku,Lee, Yong Chul American Association of Immunologists 2006 Journal of Immunology Vol.177 No.8
<P>Toluene diisocyanate (TDI) is a leading cause of occupational asthma. Although considerable controversy remains regarding its pathogenesis, TDI-induced asthma is an inflammatory disease of the airways characterized by airway remodeling. Peroxisome proliferator-activated receptor gamma (PPARgamma) has been shown to play a critical role in the control of airway inflammatory responses. However, no data are available on the role of PPARgamma in TDI-induced asthma. We have used a mouse model for TDI-induced asthma to determine the effect of PPARgamma agonist, rosiglitazone, or pioglitazone, and PPARgamma on TDI-induced bronchial inflammation and airway remodeling. This study with the TDI-induced model of asthma revealed the following typical pathophysiological features: increased numbers of inflammatory cells of the airways, airway hyperresponsiveness, increased levels of Th2 cytokines (IL-4, IL-5, and IL-13), adhesion molecules (ICAM-1 and VCAM-1), chemokines (RANTES and eotaxin), TGF-beta1, and NF-kappaB in nuclear protein extracts. In addition, the mice exposed to TDI developed features of airway remodeling, including thickening of the peribronchial smooth muscle layer, subepithelial collagen deposition, and increased airway mucus production. Administration of PPARgamma agonists or adenovirus carrying PPARgamma2 cDNA reduced the pathophysiological symptoms of asthma and decreased the increased levels of Th2 cytokines, adhesion molecules, chemokines, TGF-beta1, and NF-kappaB in nuclear protein extracts after TDI inhalation. In addition, inhibition of NF-kappaB activation decreased the increased levels of Th2 cytokines, adhesion molecules, chemokines, and TGF-beta1 after TDI inhalation. These findings demonstrate a protective role of PPARgamma in the pathogenesis of the TDI-induced asthma phenotype.</P>