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The selective retinoic acid receptor-α agonist AM580 fails to control autoimmune neuroinflammation

Cellular & Molecular Immunology 2019年第8期16卷 727-729页

作者： Qing Wang rodolfo thome Abdolmohamad Rostami Cun-Gen Ma Guang-Xian Zhang Department of Neurology Thomas Jefferson University900 Walnut StreetSuite 300PhiladelphiaPA 19107USA The Key Research Laboratory for the Study of Beneficial Qi and the Blood Circulation Activation Method in Treating Multiple Sclerosis State Administration of Traditional Chinese MedicineResearch Center of NeurobiologyShanxi University of Chinese MedicineTaiyuan 030024China

Environmental cues provided by products from the diet,gut microbiota metabolism,and exposure to sunlight are sensed by specific receptors that drive a specific genomic profile in immune cells and influence the outcome of multiple sclerosis(MS),an autoimmune disease of the central nervous system(CNS),1 which affects approximately 2.3 million people worldwide.2 Among these receptors,the ligand-activated transcription factor retinoic acid receptorα(RAR-α)senses retinoic acid and other ligands to promote the transcription of genes that have retinoic acid receptor elements in their promoter region.3 Supplementation with all-trans retinoic acid(ATRA),a metabolite of vitamin A,ameliorates inflammation in MS and the corresponding animal model,experimental autoimmune encephalomyelitis(EAE),by shifting the balance between Th17/regulatory T cells(Tregs)and inducing tolerogenic dendritic cells.4,5 To overcome the weaknesses associated with ATRA agonists,e.g.,instability,poor bioavailability and nonselective binding to a broad range of retinoid receptors,a variety of synthetic agonists specifically targeting RAR have been developed.6 One of them,AM80,inhibits Th17 cells and suppress acute neuroinflammation;however,continuous AM80 treatment is ineffective,most likely because AM80 also inhibits Tregs and IL-10 production.6 AM580,a stable benzoic derivative of retinoic acid and a selective RAR-αagonist,has been recently shown to significantly reduce the production of Th1 cytokines but promote Th2 cytokines in human PBMCs7 and to inhibit microglial activation,thus acting beneficially in Alzheimer’s disease treatment.8 In addition,AM580 protects retinal cells against diabetes-induced apoptosis by inducing neurotrophic factors.9 However,whether it has a protective effect on neuroinflammation is unknown.

关键词： inflammation autoimmune metabolism

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Chloroquine reduces Th17 cell differentiation by stimulating T-bet expression in T cells

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Cellular & Molecular Immunology 2021年第3期18卷 779-780页

作者： rodolfo thome Alexandra Boehm Larissa Lumi Watanabe Ishikawa Giacomo Casella Jaqueline Munhoz Bogoljub Ciric Guang-Xian Zhang Abdolmohamad Rostami Department of Neurology Thomas Jefferson UniversityPhiladelphiaPAUSA

Chloroquine(CQ)is a weak base that was originally used to treat malaria infection.1 However,recent findings have pinpointed the modulatory effect of CQ in models of chronic inflammation and viral *** antiviral effect of CQ and its derivative hydroxychloroquine has attracted great attention due to the recent Sars-CoV-2 virus outbreak.

关键词： Th17 stimulating inflammation

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Nitric oxide plays a key role in the suppressive activity of tolerogenic dendritic cells

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Cellular & Molecular Immunology 2015年第3期12卷 384-386页

作者： Liana Verinaud Luidy Kazuo Issayama Fabio Zanucoli Ana Carolina de Carvalho Thiago Alves da Costa Rosaria Di Gangi Amanda Pires Bonfanti Isadora Tassinari Ferreira Alexandre Leite Rodrigues de Oliveira Dagmar Ruth Stach Machado rodolfo thome Department of Structural and Functional Biology Institute of Biology University of Campinas SP Brazil

Tolerogenic dendritic cells （DCs） are widely studied for their possible use in the treatment of inflammatory disorders, such as autoimmune diseases. One of the obstacles for the use of this cell-based therapy is the characterization of drugs that are able to modulate DCs. We have previously shown that chloroquine （CQ）, an antimalarial agent, has the ability to modulate DCs towards a tolerogenic phenotype.1 These tolerogenic DCs are able to suppress the development of experimental autoimmune encephalomyelitis （EAE）, a T cell-driven mouse model of human multiple sclerosis. In addition, several studies have proposed that nitric oxide （NO） plays a major role in the dif- ferentiation of regulatory T cells （Tregs） and the suppression of Thl/Th17 cells.2＂3 However, little is known about the role of DC-derived NO in the modulation of inflammatory auto- immune responses. Thus, we aimed to evaluate whether NO plays a role in the tolerogenic activity of CQ-treated DCs （CQ- DCs）. We found that CQ induces DC production of NO and expression of indoleamine 2,3-dioxygenase （IDO）, as well as inducible nitric oxide syrtthase （iNOS）.

关键词： suppressive activity tolerogenic

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Mdivi-1,A Mitochondrial Fission Inhibitor,Modulates T Helper Cells and Suppresses the Development of Experimental Autoimmune Encephalomyelitis

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神经药理学报 2019年第4期 59-59页

作者： LI Yan-hua XU Fang rodolfo thome GUO Min-fang SUN Man-luan SONG Guo-bin LI Rui-lan CHAI Zhi Bogoljub Ciric A.M.Rostami MA Cun-gen ZHANG Guang-xian Department of Neurology Thomas Jefferson University Institute of Brain Science Shanxi Key Laboratory of Inflammatory Neurodegenerative DiseasesShanxi Datong University “2011” Collaborative Innovation Center/Research Center of Neurobiology Shanxi University of Traditional Chinese Medicine

Background:Unrestrained activation of Th1 and Th17 cells is associated with experimental autoimmune encephalomyelitis( EAE),an animal model of multiple sclerosis. While inactivation of dynamin-related protein 1( Drp1),a GTPase that regulates mitochondrial fission,is known to protect myelin from demyelination and to reduce severity of EAE,its effect on T cells is not yet known. Methods:We investigated the effect of Mdivi-1,a small molecule inhibitor of Drp1,on EAE. Clinical scores,inflammation,demyelination and p-Drp1 expression in the central nervous system( CNS),and T cell responses in both CNS and periphery were determined. Results:Mdivi-1 effectively suppressed EAE severity by reducing demyelination and cellular infiltration in the CNS. Mdivi-1 treatment decreased the phosphorylation of Drp1( ser616) on CD4+ T cells,reduced the numbers of Th1 and Th17 cells and increased Foxp3+ regulatory T cells in the CNS. Moreover,Mdivi-1 treatment effectively inhibited IFN-γ+,IL-17+ and GM-CSF+ CD4+ T cells,while it induced CD4+ Foxp3+,CD4+ IL-10+ regulatory T cells in the spleen. Conclusions:Together,our results demonstrate that Mdivi-1 has therapeutic potential in EAE by modulating the balance between Th1/Th17 and regulatory T cells.

关键词： experimental autoimmune encephalomyelitis dynamin-related protein 1 Mdivi-1 T cells

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