http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Ryu, Yun-Kyoung,Lee, Mi-Hee,Lee, Jiyoung,Lee, Jae-Wook,Jang, Su-Jin,Kang, Joo-Hyun,Moon, Eun-Yi Society for Leukocyte Biology 2015 Journal of Leukocyte Biology Vol.97 No.4
<P>RT is commonly used to treat malignant tumors. However, tumor regrowth is a major limitation to RT as an antitumor treatment. In the present study, we investigated the tumor-promoting effects of high-dose (or ablative) RT treatments on tumor-bearing mice. We focused on the role of macrophages that interact with IR-CCs in the TME, which cause tumor regrowth. We observed that CT26(H-2(d)) tumor growth was enhanced by i.v. injection of IR-CT26 cells compared with NR control CT26 cells. The levels of iNOS gene expression and NO production from RAW264.7 macrophages (H-2(d)) in response to the interaction with IR-CT26 cells were higher than with NR-CT26 cells. When CT26 tumor-bearing mice were treated i.v. with L-NMMA, a NOS inhibitor, the reduction in in vivo tumor growth was higher in the IR-CT26-injected group compared with the NR-CT26-injected control group. In vivo CT26 tumor growth was decreased after transplanting PEM extracted from L-NMMA-treated, tumor-bearing mice. Although iNOS activity was reduced by inhibiting TLR1 expression with TLR1-siRNA, it was enhanced by TLR1 overexpression. Transcriptional activation and protein expression levels of iNOS were also decreased in the presence of TLR1-siRNA but increased as a result of TLR1 overexpression. These results demonstrate that postradiotherapeutic tumor regrowth may be caused by interaction of IR-CCs with macrophages that induce TLR1-mediated iNOS expression and NO production. Our data suggest that iNOS in macrophages could be a useful target to regulate postradiotherapeutic responses in hosts and subsequently limit tumor regrowth.</P>
Lee, Seon-Yeong,Jung, Young Ok,Ryu, Jun-Geol,Oh, Hye-Jwa,Son, Hye-Jin,Lee, Seung Hoon,Kwon, Jeong-Eun,Kim, Eun-Kyung,Park, Mi-Kyung,Park, Sung-Hwan,Kim, Ho-Youn,Cho, Mi-La Society for Leukocyte Biology 2016 Journal of Leukocyte Biology Vol.100 No.3
<P>EGCG attenuates arthritis and osteoclastogenesis by inhibition of Th17 and reciprocal induction of T-reg. The green tea polyphenol epigallocatechin-3-gallate is a potent antioxidant. Here, we describe the effects of epigallocatechin-3-gallate on T cell differentiation and osteoclast differentiation in an animal model of arthritis. Mice with collagen-induced arthritis were injected intraperitoneally with epigallocatechin-3-gallate, 3 times/wk after the primary immunization. Surface markers of T helper 17 cells and regulatory T cells were analyzed by flow cytometry. Flow cytometry, Western blotting, and enzyme-linked immunosorbent assays were used to evaluate the effect of epigallocatechin-3-gallate on cell signaling in the collagen-induced arthritis model. Epigallocatechin-3-gallate decreased the arthritis index and showed protective effects against joint destruction in collagen-induced arthritis mice. The expression of cytokines, oxidative stress proteins, and phosphorylated-signal transducer and activator of transcription-3, 705 and 727, were significantly less in mice treated with epigallocatechin-3-gallate than it was in controls. Epigallocatechin-3-gallate reduced the expression of osteoclast markers in vitro and in vivo relative to the control, and the antiosteoclastic activity was observed in epigallocatechin-3-gallate-treated, interferon- knockout mice. The proportion of forkhead box protein 3-positive regulatory T cells was increased in the spleens of mice treated with epigallocatechin-3-gallate compared with control mice, whereas the proportion of T helper 17 cells was reduced. In vitro, the expression of nuclear respiratory factor 2, heme oxygenase-1, and extracellular signal-regulated kinase was increased significantly by epigallocatechin-3-gallate. We demonstrated that the administration of epigallocatechin-3-gallate attenuated the symptoms of arthritis, inhibited osteoclastogenesis and T helper 17 cell activation, and increased the number of regulatory T cells. At the molecular level, the antiarthritic effects of epigallocatechin-3-gallate may be due to induction of phosphorylated-extracellular signal-regulated kinase, nuclear respiratory factor 2, and heme oxygenase-1 and inhibition of signal transducer and activator of transcription-3 activation.</P>
Seo, Goo-Young,Jang, Young-Saeng,Kim, Hyun-A,Lee, Mi-Ra,Park, Mi-Hee,Park, Seok-Rae,Lee, Jeong-Min,Choe, Jongseon,Kim, Pyeung-Hyeun Society for Leukocyte Biology 2013 Journal of leukocyte biology Vol.94 No.2
<P>Retinoic acid, in cooperation with TGF-β1, increases IgA class switching and expression of gut-homing molecules CCR9 and α4β7, on mouse B cells.</P>
Kim, Jong-Seok,Kim, Woo Sik,Choi, Han-Gyu,Jang, Byungki,Lee, Keehoon,Park, Jong-Hwan,Kim, Hwa-Jung,Cho, Sang-Nae,Shin, Sung Jae Society for Leukocyte Biology 2013 Journal of leukocyte biology Vol.94 No.4
<P>RpfB regulates innate immunity and activates adaptive immunity through TLR4; a potential design for more effective vaccines.</P>
Kim, Hyun-Ju,Yoon, Kyung-Ae,Yoon, Hye-Jin,Hong, Jung Min,Lee, Min-Jung,Lee, In-Kyu,Kim, Shin-Yoon Society for Leukocyte Biology 2013 Journal of leukocyte biology Vol.94 No.1
<P>Liver X receptors may have potential as therapeutic targets for bone resorption-associated diseases.</P>
Woo, Sun-Je,Im, Jintaek,Jeon, Jun Ho,Kang, Seok-Seong,Lee, Mi-Hee,Yun, Cheol-Heui,Moon, Eun-Yi,Song, Man Ki,Kim, Hong-Hee,Han, Seung Hyun Society for Leukocyte Biology 2013 Journal of leukocyte biology Vol.93 No.3
<P>In human intestinal epithelial cells, IFN-γ induces BAFF expression through the signaling pathway of JAK/STAT and GAS, in the promoter region of the BAFF gene.</P>
Park, Ok-Jin,Han, Ji Young,Baik, Jung Eun,Jeon, Jun Ho,Kang, Seok-Seong,Yun, Cheol-Heui,Oh, Jong-Won,Seo, Ho Seong,Han, Seung Hyun Society for Leukocyte Biology 2013 Journal of leukocyte biology Vol.94 No.6
<P><I>E. faecalis</I> lipoteichoic acid induces chemokine expression via TLR2/CD14/MyD88 and PAFR/JAK/STAT1 signaling pathways, without induction of IFN-β in murine macrophages.</P>
Negative role of inducible PD-1 on survival of activated dendritic cells
Park, Seong Jeong,Namkoong, Hong,Doh, Junsang,Choi, Jong-Cheol,Yang, Bo-Gie,Park, Yunji,Chul Sung, Young Society for Leukocyte Biology 2014 Journal of Leukocyte Biology Vol.95 No.4
<P>PD-1 expressed on activated DCs suppresses T cell activation via decreasing DC survival.</P>