陈小平
从事CD8 T细胞分化的分子调节机制、及其在I型自身免疫型糖尿病发病机理中的作用的研究。
个性化签名
- 姓名:陈小平
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学术头衔:
博士生导师
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学科领域:
人体免疫学
- 研究兴趣:从事CD8 T细胞分化的分子调节机制、及其在I型自身免疫型糖尿病发病机理中的作用的研究。
陈小平,1987年7月毕业于上海医科大学医疗系,获医学学士学位。1997年6月毕业于美国犹他大学,获得实验病理学免疫专业博士学位,导师是Dr. Raymond Daynes。1998年至2001年,在美国匹兹堡大学医学院神经内科系Dr. David Fink实验室作博士后工作。从2001年8月至回国前,在美国匹兹堡大学医学院免疫学教研室担任研究助理。从事CD8 T细胞分化的分子调节机制、及其在I型自身免疫型糖尿病发病机理中的作用的研究。自2004年9月至今,任职同济大学医学院免疫教研室,教授。
博士论文研究T细胞表达细胞因子IL-4的调节机制。博士工作期间,发表论文四篇,包括有以第一作者发表在Journal of Immunology上,获得专利一项。自博士毕业后,一方面的工作为研究人类单纯疱疹病毒在神经细胞中分布的广泛程度及其只在神经细胞中潜伏存在的分子机制和免疫机制,发表论文三篇,其中有以第一作者发表在Journal of Virology。由于创造性地把原位杂交、激光显微捕获和单细胞real-time PCR相结合,用来检测病毒在单细胞中的分布,被邀为著名的分子生物技术丛书撰写一章。另一部分工作则是研究激活的CD8 T细胞不产生II型细胞因子如IL-4和IL-5的分子机制。并发现CD8 T细胞产生IFN- 或IL-4的能力可能对I型糖尿病的早期有重要作用。部分工作已在European Journal of Immunology上发表。工作的结果被选在2005年的美国免疫学会年会上及2005年的亚洲及太平洋地区免疫联盟会上选作口头报告。
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陈小平, XIAO-PING CHEN, , JIA LI, MARINA MATA, JAMES GOSS, DARREN WOLFE, JOSEPH C. GLORIOSO, AND DAVID J. FINK, *
JOURNAL OF VIROLOGY, Nov. 2000, p. 10132-10141 Vol. 74, No.21,-0001,():
-1年11月30日
Infected-cell protein 0 (ICP0), the product of the herpes simplex virus (HSV) immediate-early (IE) a0 gene, is a promiscuous transactivator of viral early (E) and late (L) gene expression. HSV mutants lacking ICP0 function are severely deficient in viral growth and protein synthesis, particularly at low multiplicities of infection. Early in the infectious process in vitro, ICP0 protein accumulates in distinct domains within the nucleus to form characteristic structures active in the transcription of viral genes. However, following infection of primary trigeminal ganglion cells in vitro with a recombinant HSV mutant that expresses only ICP0, we observed that ICP0 protein accumulated in the characteristic intranuclear distribution only in the nuclei of Schwann cells; neurons in the culture did not accumulate ICP0 despite expression of ICP0 RNA in those cells. The same phenomenon was observed in PC12 cells differentiated to assume a neuronal phenotype. In primary neurons in culture, the amount of ICP0 protein could be increased by pharmacologic inhibition of calciumactivated protease (calpain) activity or by inhibition of protein phosphatase 2B (calcineurin). The failure of ICP0 protein to accumulate in the nucleus of neurons suggests that one mechanism which may impair efficient replication of the virus in neurons, and thus favor the establishment of viral latency in those cells, may be found in the cell-specific processing of that IE gene product.
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陈小平, By Ting Liu, * Kamal M. Khanna, * XiaoPing Chen, ‡ David J. Fink, ‡§ and Robert L. Hendricks*§
Volume 191, Number 9, May 1, 2000 1459-1466,-0001,():
-1年11月30日
Recurrent herpes simplex virus type 1 (HSV-1) disease usually results from reactivation of latent virus in sensory neurons and transmission to peripheral sites. Therefore, defining the mechanisms that maintain HSV-1 in a latent state in sensory neurons may provide new approaches to reducing susceptibility to recurrent herpetic disease. After primary HSV-1 corneal infection, CD8+T cells infiltrate the trigeminal ganglia (TGs) of mice, and are retained in latently infected ganglia. Here we demonstrate that CD8 1 T cells that are present in the TGs at the time of excision can maintain HSV-1 in a latent state in sensory neurons in ex vivo TG cultures. Latently infected neurons expressed viral genome and some expressed HSV-1 immediate early and early proteins, but did not produce HSV-1 late proteins or infectious virions. Addition of anti-CD8 a monoclonal antibody 5 d after culture initiation induced HSV-1 reactivation, as demonstrated by production of viral late proteins and infectious virions. Thus, CD8+T cells can prevent HSV-1 reactivation without destroying the infected neurons. We propose that when the intrinsic capacity of neurons to inhibit HSV-1 reactivation from latency is compromised, production of HSV-1 immediate early and early proteins might activate CD8+T cells aborting virion production.
cytotoxic T lymphocytes, trigeminal ganglion, mice, HSV-1 immediate early genes, HSV-1 late genes
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【期刊论文】GANGLIOSIDE CONTROL OVER IL-4 PRIMING AND CYTOKINE PRODUCTION IN ACTIVATED T CELLS
陈小平, Xiao-Ping Chen, , Xiaohong Ding, Raymond A. Daynes
CYTOKINE, Vol. 12, No.7 (July), 2000: pp 972-985,-0001,():
-1年11月30日
Our previous studies have shown that the enzymatic activities of Neu-1, an endogenous sialidase encoded in the murine MHC, are involved in promoting IL-4 synthesis by naive CD4+T cells. Our present studies have characterized responsible sialoconjugate targets of Neu-1 and questioned possible biochemical mechanisms responsible for their regulatory influences on IL-4 gene expression. These studies determined that treatment of T cells with the naturally occurring ganglioside GM3 inhibited the production of IL-4 without affecting the production of IL-2. An analysis of IL-4-primed CD4+ T cells further demonstrated that GM3 treatment specifically inhibited the restimulated production of IL-4, IL-5 and IL-13, without inhibiting the production of IL-2 and IFN-. The inhibitory effects of GM3 could be overcome by treatment with thapsigargin or ionomycin, suggesting ganglioside regulation occurs upstream of activationinduced calcium mobilization. GM3 treatment attenuated the level of calcium influx following CD3 crosslinking, and CD4+T cells from Neu-1-deficient B10.SM strain mice (neu-1a and IL-4-deficient) expressed reduced levels of intracellular calcium following activation. Our results indicate that activities by membrane gangliosides can influence the cytokine programs in CD4+T cells, possibly through the modulation of calcium responses induced by T cell activation.
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陈小平, Xiao-Ping Chen, * Elena Yu. Enioutina, * and Raymond A. Daynes*+
The journal of Immunology, 1997, 158: 3070-3080,-0001,():
-1年11月30日
IL-4 is important in controlling the development of immune responses. Following activation with anti-CD3e under serum-free conditions, splenocytes from most normal (neu-7') mouse strains directly produced IL-4 and other T cell cytokines. However, splenic T cells from SM/J and B1O.SM (H-21; neu-1") strain mice, deficient in neu-7 sialidase activity, failed to produce IL-4 but produced normal levels of IL-2 following activation. Moreover, sialidase-deficient mice produced markedly less IgE and lgGl Abs following immunization with protein Ags than did mouse strains with normal neu-7 sialidase activity. Enriched T cells from newla mice failed to be effectively primed with exogenous murine 11-4 to become IL-4-producing cells. Treatment of splenocytes or enriched T cells from neu-V mice with bacterial sialidase prior to activation or IL-4 priming promoted their subsequent capacity to produce IL-4. In contrast, activation of T cells from neu-7' mice in the presence of a sialidase inhibitor almost completely blocked subsequent IL-4 production. The presence of IL-4 during priming enhanced T cell expression of neu-7-specific sialidase activity and increased the membrane expression of asialo-G,, compared with T cells activated without 1L-4. These results suggest that T cell-associated neu-1 sialidase is required for early IL-4 production by splenic T cells and is involved in the 11-4 priming process of conventional T cells to become active IL-4 producers.
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陈小平, Matthew E. Poynter, * Hong-Hua Mu, * Xiao-Ping Chen, * and Raymond A. Daynes*, †
CELLULAR IMMUNOLOGY 179, 22-29 (1997),-0001,():
-1年11月30日
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陈小平, Jon D. Hennebold, Hong-Hua Mu, Matthew E. Poynter, Xiao-Ping Chen and Raymond A. Daynes,
International Immunology, Vol. 9, No.1, pp. 105-115,-0001,():
-1年11月30日
The results from the present study demonstrate that the innate defense mechanisms which control the progressive growth of Listeria monocytogenes in normal animals in vivo are dependent upon the active catabolism of endogenous glucocorticoids by the enzyme 11b-hydroxysteroid dehydrogenase (11b-HSD). When 11b-HSD activity was pharmacologically inhibited in vivo, host susceptibility to progressive bacterial disease was markedly increased. Depressed natural resistance following 11b-HSD inhibition correlated with changes in the patterns of inducible cytokines by macrophages and T cells. Similar changes were observed when normal adult animals were treated with low doses of dexamethasone prior to experimental infection with Listeria.
11b-hydroxysteroid dehydrogenase,, corticosterone,, cytokines,, glucocorticoids,, Listeria monocytogenes
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