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정두현,박인애,함의근,Chung, Doo-Hyun,Park, In-Ae,Ham, Eui-Keun 대한세포병리학회 1991 대한세포병리학회지 Vol.2 No.1
The diagnosis of carcinoma in situ of urinary bladder is difficult in that the symptoms and cystoscopic findings are nonspecific. The cytology of urine could be helpful for diagnosis of carcinoma in situ of urinary bladder. We present a case of bladder washing cytology of carcinoma in situ. A 54-year-old man presented with dysuria for 1 year. Cystoscopic findings revealed multifocal reddish trabeculated lesions. The bladder washing cytology revealed rather uniform tumor cells which were singly scattered of forming syncytium in the clean back-ground. The nuclei were round to oval with inconspicious nucleoli. The cystoscopic biopsy revealed typical histologic features of carcinoma in situ of urinary bladder.
정두현,박효진,김혜성 대한면역학회 2010 Immune Network Vol.10 No.1
Hypersensitivity pneumonitis (HP) is an interstitial lung disease that develops following repeated exposure to inhaled particulate antigens. The family of Fcγ receptors (FcγRs) has emerged as central regulators for modulating both pro-and anti-inflammatory responses. However,the role of FcγRs in the development of HP has not been investigated yet. Methods: To explore the functional roles of FcγRs in HP, FcγR−/− and B6 mice were challenged with Saccharopolyspora rectivirgula (SR) antigen intranasally,and compared these mice in terms of the histological change,infiltrated immune cells in BALF and in vitro immune responses. Results: FcγR−/− mice exhibited attenuation of HP in terms of histological alterations, and reduced numbers of neutrophils and macrophages in and the increased CD4:CD8 ratio of bronchoalveolar lavage fluid. The lungs of FcγR−/− mice showed high production of Th2 cytokine such as IL-4 and slightly low production of Th1 cytokine,INF-γ compared to those of B6 mice. However, SR-specific adaptive immune responses of FcγR−/− mice were similar to those of B6 mice. Conclusion: These results demonstrate that activating Fcγ receptors play an important role in activating neutrophils and macrophages in pulmonary inflammation and inducing Th1 differentiation by regulating cytokine expression in SR-induced HP.
IL-4-deficient Mice Aggravate Hypersensitivity Pneumonitis
황수진,정두현 대한면역학회 2008 Immune Network Vol.8 No.3
Background: Hypersensitivity pneumonitis (HP) comprises a group of lung diseases resulting from repeated inhalation of various antigens such as Saccharopolyspora rectivirgula (SR). HP is categorized as a Th1 disease. Therefore, it has been suggested that IL-4, Th2 type cytokine, plays a protective role in the development of HP. However, the functional role of IL-4 in HP has not been extensively investigated in vivo. Therefore, we investigated the functional role of IL-4 in HP using IL-4 knockout (KO) mice. Methods: HP was induced by repeated exposure to SR in C57BL/6 (B6) and IL-4 KO (C57BL/6 background) mice. Results: IL-4 KO mice aggravated HP in terms of histological alteration, SR-specific immune responses, and inflammatory cell infiltration in the lungs compared with B6 mice. IL-4 KO mice produced high levels of IFN-γ, TGF-β and TNF-α in the lungs, whereas B6 mice showed the enhanced production of IL-4. Moreover, chemokines such as MIP-1α, MCP-1, and RANTES were highly expressed in IL-4 KO mice. IFN-γ-secreting CD4, CD8 T cells, and neutrophils were enhanced in the bronchoalveolarlavage fluid (BALF) of IL-4 KO mice than those of B6 mice. The administr ation of recombinant(r) IL-4 restored these immunologic parameters in IL-4 KO mice. Conclusion: These results indicate that IL-4 plays a suppressive role in SR-induced HP by attenuating Th1-dominant immune responses. Background: Hypersensitivity pneumonitis (HP) comprises a group of lung diseases resulting from repeated inhalation of various antigens such as Saccharopolyspora rectivirgula (SR). HP is categorized as a Th1 disease. Therefore, it has been suggested that IL-4, Th2 type cytokine, plays a protective role in the development of HP. However, the functional role of IL-4 in HP has not been extensively investigated in vivo. Therefore, we investigated the functional role of IL-4 in HP using IL-4 knockout (KO) mice. Methods: HP was induced by repeated exposure to SR in C57BL/6 (B6) and IL-4 KO (C57BL/6 background) mice. Results: IL-4 KO mice aggravated HP in terms of histological alteration, SR-specific immune responses, and inflammatory cell infiltration in the lungs compared with B6 mice. IL-4 KO mice produced high levels of IFN-γ, TGF-β and TNF-α in the lungs, whereas B6 mice showed the enhanced production of IL-4. Moreover, chemokines such as MIP-1α, MCP-1, and RANTES were highly expressed in IL-4 KO mice. IFN-γ-secreting CD4, CD8 T cells, and neutrophils were enhanced in the bronchoalveolarlavage fluid (BALF) of IL-4 KO mice than those of B6 mice. The administr ation of recombinant(r) IL-4 restored these immunologic parameters in IL-4 KO mice. Conclusion: These results indicate that IL-4 plays a suppressive role in SR-induced HP by attenuating Th1-dominant immune responses.