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Indoleamine 2,3-dioxygenase (IDO) is essential for dendritic cell activation and chemotactic responsiveness to chemokines

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Cell Research 2005年第3期15卷 167-175页

作者： Shih Ling HWANG,Nancy Pei-Yee CHUNG,Jacqueline Kwai-Yi CHAN,Chen-Lung Steve LIN Department of Surgery Kaohsiung Medical University Kaohsiung Taiwan China Department of Surgery The University of hong Kong Medical Centre Queen Mary Hospital Pokfulam Road hong kongsar China Department of Surgery The University of hong Kong Medical Centre Queen Mary Hospital Pokfulam Road hong kongsar China Department of Surgery The University of hong Kong Medical Centre Queen Mary Hospital Pokfulam Road hong kongsar China

Indoleamine 2, 3-dioxygenase (IDO) is a rate-limiting enzyme for the tryptophan catabolism. In human and murine cells, IDO inhibits antigen-specific T cell proliferation in vitro and suppresses T cell responses to fetal alloantigens during murine pregnancy. In mice, IDO expression is an inducible feature of specific subsets of dendritic cells (DCs), and is important for T cell regulatory properties. However, the effect of IDO and tryptophan deprivation on DC func- tions remains unknown. We report here that when tryptophan utilization was prevented by a pharmacological inhibitor of IDO, 1-methyl tryptophan (1MT), DC activation induced by pathogenic stimulus lipopolysaccharide (LPS) or inflam- matory cytokine TNF-α was inhibited both phenotypically and functionally. Such an effect was less remarkable when DC was stimulated by a physiological stimulus, CD40 ligand. Tryptophan deprivation during DC activation also regu- lated the expression of CCR5 and CXCR4, as well as DC responsiveness to chemokines. These results suggest that tryptophan usage in the microenvironment is essential for DC maturation, and may also play a role in the regulation of DC migratory behaviors.

关键词： Indoleamine 2 3-dioxygenase (IDO) dendritic cells activation T cell tryptophan chemokine.

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Modulation of Neuroimmune Responses on Glia in the Central Nervous System： Implication in Therapeutic Intervention against Neuroinflammation

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Cellular & Molecular Immunology 2009年第5期6卷 317-326页

作者： Raymond Chuen-Chung Chang Kin Chiu Yuen-Shan Ho Kwok-Fai So Laboratory of Neurodegenerative Diseases Depamnent of Anatomy LKSFaculty of Medicine University of Hong Kong Pokfulam Hong KongSAR China Research Centre of Heart Brain Hormone and Healthy Aging LKSFaculty of Medicine University of Hong Kong Pokfulam Hong KongSAR China State Key Laboratory for Brain and Cognitive Sciences University of HongKong. Pokfulam Hong Kong SAR China Department of Anatomy LKS Faculty of Miedicine The University of Hong Kong Rm.

It has long been known that the brain is an immunologically privileged site in normal conditions. Although the cascade of immune responses can occur as long as there is a neuronal injury or a potent immune stimulation, how the brain keeps glial cells in a quiescent state is still unclear. Increasing efforts have been made by several laboratories to elucidate how repression oi~ immune responses is achieved in the neuronal environment. The suppression factors include neurotransmitters, neurohormones, neurotrophic factors, anti-inflammatory factors, and cell-cell contact via adhesion molecules or CD200 receptor. This review discusses how these factors affect the cascade of cerebral immune responses because no single factor listed above can fully account for the immune suppression. While several factors contribute to the suppression of immune responses, activation of glial cells and their production of pro-inflammatory factors do occur as long as there is a neuronal injury, suggesting that some neuronal components facilitate immune responses. This review also discusses which signals initiate or augment cerebral immune responses so that stimulatory signals override the suppressive signals. Increasing lines of evidence have demonstrated that immune responses in the brain are not always detrimental to neurons. Attempt to simply clear off inflammatory factors in the CNS may not be appropriate for neurons in neurological disorders. Appropriate control of immune cells in the CNS may be beneficial to neurons or even neuroregeneration. Therefore, understanding the mechanisms underlying immune suppression may help us to reshape pharmacological interventions against inflammation in many neurological disorders.

关键词： neural cell adhesion molecule neurotrophins potassium ions microglia neuroinflammation

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Microproteinuria for detecting calcineurin inhibitor-related nephrotoxicity after liver transplantation

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World Journal of Gastroenterology 2009年第23期15卷 2913-2917页

作者： Jing Li Bin Liu Lu-Nan Yan Lan-Lan Wang Wan Y Lau Bo Li Wen-Tao Wang Ming-Qing Xu Jia-Yin Yang Fu-Gui Li Department of Anesthesiology and Critical CareMedicine West-China Hospital Sichuan University Chengdu610041 Sichuan Province China Division of Liver Transplantation West-China Hospital Sichuan University Chengdu 610041Sichuan Province China Department of Clinical ImmunologicalLaboratory West-China Hospital Sichuan University Chengdu610041 Sichuan Province China Faculty of Medicine The Chinese Universityof Hong Kong Prince of Wales Hospital Shatin Hong KongSAR China

AIM： To investigate whether microproteinuria could be used as an early and sensitive indicator to detect calcineurin inhibitor （CNI）-related nephrotoxicity after liver transplantation.METHODS： All liver transplant recipients with normal serum creatinine （SCr） and detectable microproteinuria at baseline were included in this study. The renal function was monitored by the blood clearance of 99mTc-diethylenetriaminepentaacetic acid every 6 mo. Microproteinuria, SCr and blood urea nitrogen （BUN） were measured at entry and at subsequent follow-up visits. The patients were divided into different groups according to the mean values of glomerular filtration rate （GFR） at the follow-up time points： Group 1, GFR decreased from baseline by 0%-10%; Group 2, GFR decreased from baseline by 11%-20%; Group 3, GFR decreased from baseline by 21%-40%; Group 4, GFR decreased from baseline by 〉 40% and/or SCr was increasing.RESULTS： A total of 143 patients were enrolled into this study （23 females and 120 males）. The mean follow-up was 32 mo （range 16-36 mo）. Downward trends in renal function over time were observed in the study groups. SCr and BUN increased significantly only in Group 4 patients （P 〈 0.001）. β2-microglobulin （β2m） and al-microglobulin （αlm） significantly increased with the subtle change of renal function in recipients who were exposed to CNI-based immunosuppression regimens. The reductions in GFR were closely correlated with elevated cclm （P = -0.728, P 〈 0.001） and β2m （r2 = -0.787, P 〈 0.001）.CONCLUSION： β2m and α1m could be useful as early and sensitive indicators of CNI-induced nephrotoxicity.

关键词： Microproteinuria Liver transplantation Calcineurin inhibitors Nephrotoxicity

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