• 제목/요약/키워드: T&B cell mitogenesis

검색결과 4건 처리시간 0.017초

Pycnogenol Supplementation Retards Immune Dysfunction in Murine AIDS (MAIDS) After LP-BM5 Leukemia Virus Infection by Modulating Cytokine Secretion

  • Lee, Jeong-Min;Park, Kun-Young;Hwang, Kwon-Tack;Watson, Ronald R.
    • Preventive Nutrition and Food Science
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    • 제10권2호
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    • pp.161-166
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    • 2005
  • We investigated the effect of pycnogenol (PYC) supplementation on retarding the immune dysfunction of CS7BL/6 mice after murine AIDS (MAIDS) development. Dysfunction of T and B cell mitogenesis from primary cultured splenocytes has been observed with retrovirus infection and PYC supplementation partially recovered the dysfunction of T and B cells. There was an abnormal shift of cytokine pattern with retrovirns infection, which was designated by the decreased secretion of Th1 cytokines and increased secretion of Th2 cytokines. PYC supplementation increased IL-2 and $IFN-\gamma$ secretion and decreased IL-4, IL-6, and $TNF-\alpha$ secretion, but it was not sufficient enough to maintain the normal level of these cytokines. Hepatic vitamin E level was significantly decreased by retrovirns infection, in accordance with increased hepatic lipid peroxidation level, whereas PYC supplementation normalized the hepatic level of vitamin E and lipid peroxidation. This study suggests that PYC supplementation may partially help retard the incidence of symptoms during MAIDS.

자외선에 의한 면역반응의 억제를 회복시키는 면역조절물질을 생산하는 토양 Streptomyces sp.의 분리 및 동정 (Isolation And Identification Of Soil Streptomyces sp. Producing An Immunomodulator That Restores Ultraviolet B Radiation-Induced Suppression Of The Immune Response)

  • 모영근;신영근;박동진;김창진;이종길;한성순
    • 약학회지
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    • 제39권6호
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    • pp.585-592
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    • 1995
  • Soil microorganisms producing immunomoduators that can restore ultraviolet B (UVB) radiation-induced suppression of the immune response were screened in vitro. Exposure of freshly isolated murine epidermal cells (EC) to $180{\;}J/m^{2}$ of UVB radiation resulted in approximately 90% impairtnent of accessory cell function, as measured by their ability to support anti-CD3 monoclonal antibody-induced T-cell mitogenesis. When the culture supenmtants of 150 actinomycete strains were exanuned for their capacity to prevent or repair the UVB-induced impairment of accessory cell function, 4 of them were identified to contain immunomodulators that can restore the decreased accessory cell finiction. The soil isolate that showed the most effective restorative activity, G40025. was selected and fturther characters Addition of 10.mu.l of the culture supernatant of G40025 grown in G-media to cultures of UVB-irradiated EC right after UVB-irradiation restored the decreased accessory cell function by 58%. The immunomodtdator produced by G40025 appeared to be stable at 100.deg. C for 10 min. Taxonomical studies by cultural, morphological, and physiological characterization showed that the soil isolate, G40025, belongs to the genus Streptomyces.

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Role of Shc and Phosphoinositide 3-Kinase in Heregulin-Induced Mitogenic Signaling via ErbB3

  • Kim, Myong-Soo;Koland, John G.
    • The Korean Journal of Physiology and Pharmacology
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    • 제4권6호
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    • pp.507-513
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    • 2000
  • ErbB3/HER3 is a cell surface receptor which belongs to the ErbB/HER subfamily of receptor protein tyrosine kinases. When expressed in NIH/3T3 cells, ErbB3 can form heterodimeric coreceptor with endogenous ErbB2. Among known intracellular effectors of the ErbB2/ErbB3 are mitogen-activated protein kinase (MAPK) and phosphoinositide (PI) 3-kinase. In the present study, we studied relative contributions of above two distinct signaling pathways to the heregulin-induced mitogenic response via activated ErbB3. For this, clonal NIH-3T3 cell lines expressing wild-type ErbB3 and ErbB3 mutants were stimulated with $heregulin{\beta}_1$. While cyclin D1 level was markedly high and further increased by treatment of heregulin in cells expressing wild-type ErbB3, the elimination of either Shc binding or PI 3-kinase binding lowered both levels. This result was supported by the reduction of cyclin $D_1$ expression by preteatment with MAPK kinase inhibitor or PI 3-kinase inhibitor before stimulation with heregulin. In accordance with the cyclin $D_1$ expression, elimination of either Shc binding or PI 3-kinase binding reduced the heregulin-induced DNA synthesis and cell growth rate. Our results obtained by the comparison of wild-type and ErbB3 mutants indicate that the full induction of the cell cycle progression through $G_1/S$ phase by ErbB3 activation is dependent on both Shc/MAPK and PI 3-kinase signal transduction pathways.

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LP-BM5 Leukemia Retrovirus 감염으로 유발된 Murine AIDS에서 Dehydroepiandrosterone Sulfate의 Th1/Th2 Cytokines의 발현 조절 및 산화적 스트레스 억제 효과 연구 (Dehydroepiandrosterone Sulfate Inhibited Immune Dysfunction Induced by LP-BM5 Leukemia Retrovirus Infection through Regulating Th1/Th2 Type Cytokine mRNA Expression and Oxidative Stress in Murine AIDS Model)

  • 이정민
    • 한국식품영양과학회지
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    • 제35권10호
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    • pp.1329-1335
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    • 2006
  • AIDS로의 진행과정은 단순히 몇몇 기작에 의한 것이 아니라 여러 경로를 거쳐 발생하며 그 진행속도도 개개인에 따라 다양하게 나타나고 있다. 본 연구에서는 쥐 AIDS 모델을 이용하여 항산화호르몬으로 알려진 DHEAS의 면역조절 효과를 확인하고자 하였다. DHEAS의 투여는 LP-BM5 retrovirus 감염으로 인한 T와 B 임파구의 mitogenesis를 증가시켰으며 Th1/Th2 type cytokines의 발현에도 영향을 미쳤는데 주로 전사수준에서 작용한 것으로 생각된다/ 또한 retrovirus 감염으로 인한 간조직의 지질과산화 유발을 억제하여 조직 내의 항산화제인 vitamin E의 함량을 유지시킴으로 NF-kB의 활성화를 통한 retrovirus의 복제를 억제시켜 Th1/Th2 type cytokines의 불균형적인 발현을 저해하였을 것으로 여겨진다. 따라서 쥐 AIDS모델에 있어서 DHEAS의 면역조절 효과를 확인한 본 연구는 향후 HIV감염 이후 AIDS로의 진행 과정 시 항산화제의 역할과 기작 규명에 대한 가능성을 제시할 수 있을 것으로 생각된다.