http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
개별검색 DB통합검색이 안되는 DB는 DB아이콘을 클릭하여 이용하실 수 있습니다.
통계정보 및 조사
예술 / 패션
<해외전자자료 이용권한 안내>
- 이용 대상 : RISS의 모든 해외전자자료는 교수, 강사, 대학(원)생, 연구원, 대학직원에 한하여(로그인 필수) 이용 가능
- 구독대학 소속 이용자: RISS 해외전자자료 통합검색 및 등록된 대학IP 대역 내에서 24시간 무료 이용
- 미구독대학 소속 이용자: RISS 해외전자자료 통합검색을 통한 오후 4시~익일 오전 9시 무료 이용
※ 단, EBSCO ASC/BSC(오후 5시~익일 오전 9시 무료 이용)
Secretory (S-IgA) isotype antibody (Ab) is known to play an essential role in the primary defense against various infectious agents in mucosal tissue. However, it has been mostly unsuccessful in the induction of antigen (Ag)-specific IgA Ab response in this site by peroral vaccination. In the present study, we investigated the effect of cholera toxin (CI) as a mucosal adjuvant and alginates-microspheres as a carrier on BSA-specific IgA Ab response in gut-associated lymphoid tissue`(GALT). Peroral immunization of BSA plus CT conferred a great BSA-specific IgA response but IgG response on intestinal fluid (IF). In contrast, intraperitoneal immunization of BSA with Freund's adjuvant readily induced BSA-specific IgG response but IgA response in IF. Further, number of CT specific IgA-secreting cells was substantially increased in mesenteric lymph node when CT-encapsulated-VI alginates-microspheres was administered perorally. Taken together, these results indicate that peroral immunization of soluble antigen in combination of CT or microspheres significantly enhances antigen-specific IgA response in GALT.
Activation-induced cytidine deaminase (AID) is needed for Ig class switch recombination (CSR). We explored the effect of LPS on the expression of AID during B cell differentiation, and the role of AID in IgA isotype expression. In normal spleen B cells, LPS increased AID transcription up to 48 h post-stimulation, i.e. around the time of Ig CSR. TGF-β1 and AID were requiredfor IgA expression, and LPS contributed toTGFβ1-induced IgA production largely by inducing AID. Interestingly, LPS repressed AID transcription in sIgA+ B cells but still stimulated IgA production mainly by increasing the rate of IgA secretion. Our data indicate that LPS contributes to TGFβ1-induced IgA isotype expression in at least two ways: by stimulating AID transcription before CSR and by enhancing the IgA secretion rate after CSR.
Kim, Seong-Ryeol,Song, Jae-Hyoung,Ahn, Jae-Hee,Lee, Geun-Shik,Ahn, Huijeong,Yoon, Sung-il,Kang, Seung Goo,Kim, Pyeung-Hyeun,Jeon, Sang-Min,Choi, Eun-Ji,Shin, Sooyoung,Cha, Younggil,Cho, Sungchan,Kim, Elsevier 2018 Antiviral research Vol.151 No.-
<P>Human rhinovirus (HRV) infection causes more than 80% of all common colds and is associated with severe complications in patients with asthma and chronic obstructive pulmonary disease. To identify antiviral drug against HRV infection, we screened 800 FDA-approved drugs and found budesonide as one of the possible drug candidates. Budesonide is a corticosteroid, which is commonly used to prevent exacerbation of asthma and symptoms of common cold. Budesonide specifically protects host cells from cytotoxicity following HRV infection, which depend on the expression of glucocorticoid receptor. Intranasal administration of budesonide lowered the pulmonary HRV load and the levels of IL-1 beta cytokine leading to decreased lung inflammation. Budesonide regulates IL-1 beta production following HRV infection independent of inflammasome activation. Instead, budesonide induces mitochondrial reactive oxygen species followed by activation of autophagy. Further, the inhibition of autophagy following chloroquine or bafilomycin Al treatment reduced the anti-viral effect of budesonide against HRV, suggesting that the antiviral activity of budesonide was mediated via autophagy. The results suggest that budesonide represents a promising antiviral and anti-inflammatory drug candidate for the treatment of human rhinovirus infection.</P>
'스콜라' 이용 시 소속기관이 구독 중이 아닌 경우, 오후 4시부터 익일 오전 9시까지 원문보기가 가능합니다.
Cholera toxin (CT) and its B subunit (CTB) are potent immonogens and adjuvants that, either alone or linked to protein Ags, can stimulate mucosal immune responses, modulate the induction of oral tolerance, and stimulate IgA isotype switching. The present studies addressed the mechanisms by which CT and CTB promote IgA switching. CT and rCTB, in the presence of IL-2, significantly increased IgA isotype switching at the clonal level in populations of purified and LPS-activated murine surface IgA￣spleen B cells, as determined by ELISA, enzyme linked immunospot assays, and limiting dilution analysis. The IgA stimulatory effects of CT and CTB were independent of the a subunit of CT.CTB and CT dld not increase the secretory rate of IgA-producing cells or the clonal burst size of IgA clones. and did inhibit B cell growth. Because TGF-β1 also Inhibits B cell growth and promotes IgA switching, further studies tested whether the activity of CTB and CT on IgA isotype switching was mediated through TGF-β1. Anti-TGFβ Ab and soluble TGF-β1 type ILR inhibited CTB-and CT-stimulated IgA isotype switching. Furthermore increased TGF-β1 mRNA levels and bioactive TGF-β1, within a range shown to induce IgA isotype switching, were detected in cultures of surface IgA￣B cells stimulated with CT or CTB and IL-2. These data indicate that CTB-and CT-stimulated IgA isotype switching are mediated through TGF-β1. The finding that CTB up-regulates TGF-β1 activity has important implications for understanding the mechanisms by which CTB promotes both IgA mucosal immunity and oral tolerance.
Kim, Jun-Sub,Kim, Jae-Gyu,Moon, Mi-Young,Jeon, Chan-Young,Won, Ha-Young,Kim, Hee-Jun,Jeon, Yee-Jin,Seo, Ji-Yeon,Kim, Jong-Il,Kim, Jaebong,Lee, Jae-Yong,Kim, Pyeung-Hyeun,Park, Jae-Bong American Society of Hematology 2006 Blood Vol.108 No.6
<B>Abstract</B><P>Brief treatment with transforming growth factor (TGF)-β1 stimulated the migration of macrophages, whereas long-term exposure decreased their migration. Cell migration stimulated by TGF-β1 was markedly inhibited by 10 μg/mL Tat-C3 exoenzyme. TGF-β1 increased mRNA and protein levels of macrophage inflammatory protein (MIP)-1α in the initial period, and these effects also were inhibited by 10 μg/mL Tat-C3 and a dominant-negative (DN)-RhoA (N19RhoA). Cycloheximide, actinomycin D, and antibodies against MIP-1α and monocyte chemoattractant protein-1 (MCP-1) abolished the stimulation of cell migration by TGF-β1. These findings suggest that migration of these cells is regulated directly and indirectly via the expression of chemokines such as MIP-1α and MCP-1 mediated by RhoA in response to TGF-β1. TGF-β1 activated RhoA in the initial period, and thereafter inactivated them, suggesting that the inactivation of RhoA may be the cause of the reduced cell migration in response to TGF-β1 at later times. We therefore attempted to elucidate the molecular mechanism of the inactivation of RhoA by TGF-β1. First, TGF-β1 phosphorylated RhoA via protein kinase A, leading to inactivation of RhoA. Second, wild-type p190 Rho GTPase activating protein (p190RhoGAP) reduced and DN-p190RhoGAP reversed the reduction of cell migration induced by TGF-β, suggesting that it inactivated RhoA via p190 Rho GAP.</P>