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경구면역을 통한 항원 특이적 IgA 항체 합성에 있어 Cholera Toxin과 Alginate-Microsphere의 효과
송민형,유진수,권명상,성승룡,김용희,권익찬,정서영,양재명,김평현 大韓免疫學會 1996 大韓免疫學會誌 Vol.18 No.3
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.
Transforming growth factor-β1 regulates macrophage migration via RhoA
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>
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>
Pyeung-Hyeun Kim,박석래,김현아,Sung-Ki Chun,Jae-Bong Park 한국분자세포생물학회 2005 Molecules and cells Vol.19 No.3
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, Pyeung-Hyeun The Microbiological Society of Korea 1990 微生物과 産業 Vol.16 No.3
IgA is the predominant immunoglobulin isotype in mucosal secretions(1). It has been reported that a population of Peyer's patch T cells can selectively induce IgM bearing B cells to switch to surface IgA bearing B cells(2,3). Further, IL-4, IL-5, and IL-6 alone and in combination, can significantly influence murine IgA B cell differentiation in vitro(4-7). However, it remains an open question which cytokines have a major role in class switching to the IgA isotype. Recently, it has been reported that transforming growth factor .betha.1(TGF .betha.1) alone, or in combination with IL-2 increases IgA secretion by LPS-activated surface IgA negative (sIgA$\^$-/) murine spleen B cells while concurrently downregulating IgM and IgG secretion by such cells(8-11). In the present study, limiting dilution analysis was used to demonstrate, at the clonal level, that TGF .betha.1 has siginificant activity as an IgA isotype switch factor.