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Identification of CM1 as a Pathogenic Factor in Inflammatory Diseases and Cancer
배세연,강재승,이왕재,김혜민,유연실,이나은,공주명,김항래,황영일,송영욱 대한면역학회 2011 Immune Network Vol.11 No.3
Background: CM1 (centrocyte/-blast marker 1) was defined by a mAb against concavabalin-A (ConA) activated PBMC. It is expressed in germinal center of human tonsil and on the surface of activated PBMC as well as cancer cells. Recently,increased productions of pro-inflammatory mediators were detected from activated PBMC by CM1 ligation. Methods:However, there is a limitation to explain the exact role of CM1 on inflammation and its related mechanisms, since the identity of CM1 is still not clarified. In our previous study, we have already confirmed that soluble form of CM1 was produced by Raji. Therefore, we performed Q-TOF analysis after immunoprecipitation of concentrated Raji culture supernatant using anti-CM1 mAbs. Results: As a result, we found that CM1 is identical to enolase-1(ENO1), a glycolytic enzyme,and we confirmed that results by silencing ENO1 using siRNA. It was also confirmed through competition assay between anti-CM1 and anti-ENO1 mAbs. Finally, we investigated the possible role of CM1 in inflammatory response and cancer. The ligation of CM1 on Raji cells with anti-CM1mAbs induces the extensive production of prostaglandin E2(PGE2). In addition, the increased activity of matrix metalloproteinase (MMP)-2/9 was shown in NCI-N87, stomach cancer cell line by CM1 stimulation. Conlusion: CM1 is identical to ENO1 and it might be an important role in the regulation of inflammatory responses.
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김예진,강재승,이왕재,김혜민,배세연,최지원,임선영,이나은,공주명,황영일 대한면역학회 2013 Immune Network Vol.13 No.2
L-ascorbic acid (vitamin C) is one of the well-known antiviral agents, especially to influenza virus. Since the in vivo antiviral effect is still controversial, we investigated whether vitamin C could regulate influenza virus infection in vivo by using Gluo (-/-) mice, which cannot synthesize vitamin C like humans. First, we found that vitamin C-insufficient Gluo (-/-)mice expired within 1 week after intranasal inoculation of influenza virus (H3N2/Hongkong). Viral titers in the lung of vitamin C-insufficient Gluo (-/-) mice were definitely increased but production of anti-viral cytokine, interferon (IFN)-α/β, was decreased. On the contrary, the infiltration of inflammatory cells into the lung and production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-α/β, were increased in the lung. Taken together,vitamin C shows in vivo antiviral immune responses at the early time of infection, especially against influenza virus,through increased production of IFN-α/β.
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