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CIS controls the functional polarization of GM-CSF-derived macrophages

Cellular & Molecular Immunology 2023年第1期20卷 65-79页

作者： Shengbo Zhang Jai Rautela Naiara G.Bediaga Tatiana B.Kolesnik Yue You Junli Nie Laura F.Dagley Justin Bedo Hanqing Wang Li Sun Robyn Sutherland Elliot Surgenor Nadia Iannarella Rhys Allan Fernando Souza-Fonseca-Guimaraes Yi Xie Qike Wang Yuxia Zhang Yuekang Xu Stephen L.Nutt Andrew M.Lew Nicholas D.Huntington Sandra E.Nicholson Michaël Chopin Yifan Zhan Walter and Eliza Hall Institute of Medical research ParkvilleVICAustralia Department of Medical Biology University of MelbourneParkvilleVICAustralia Department of Biochemistry and Molecular Biology Biomedicine Discovery InstituteMonash UniversityClaytonVICAustralia oNKo-Innate Pty Ltd Moonee PondsVICAustralia Department of Computing and Information Systems University of MelbourneParkvilleVICAustralia Department of Respiratory Medicine Guangzhou Institute of PediatricsGuangzhou Women and Children’s Medical CentreState Key Laboratory of Respiratory DiseasesGuangzhou Medical UniversityGuangzhouGuangdongChina College of Biological Science Anhui Normal UniversityHefeiChina University of Queensland Diamantina Institute University of QueenslandTranslational Research InstituteBrisbaneQLDAustralia Program in Cardiovascular and Metabolic Disorders Duke-NUS Medical SchoolDukeSingapore Drug Discovery Shanghai Huaota BiopharmShanghaiChina

The cytokine granulocyte-macrophage-colony stimulating factor (GM-CSF) possesses the capacity to differentiate monocytes into macrophages (MØs) with opposing functions, namely, proinflammatory M1-like MØs and immunosuppressive M2-like MØs. Despite the importance of these opposing biological outcomes, the intrinsic mechanism that regulates the functional polarization of MØs under GM-CSF signaling remains elusive. Here, we showed that GM-CSF-induced MØ polarization resulted in the expression of cytokine-inducible SH2-containing protein (CIS) and that CIS deficiency skewed the differentiation of monocytes toward immunosuppressive M2-like MØs. CIS deficiency resulted in hyperactivation of the JAK-STAT5 signaling pathway, consequently promoting downregulation of the transcription factor Interferon Regulatory Factor 8 (IRF8). Loss- and gain-of-function approaches highlighted IRF8 as a critical regulator of the M1-like polarization program. In vivo, CIS deficiency induced the differentiation of M2-like macrophages, which promoted strong Th2 immune responses characterized by the development of severe experimental asthma. Collectively, our results reveal a CIS-modulated mechanism that clarifies the opposing actions of GM-CSF in MØ differentiation and uncovers the role of GM-CSF in controlling allergic inflammation.

关键词： CIS GM-CSF Macrophage M2 M1

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CCR2 enhances CD25 expression by FoxP3^(+) regulatory T cells and regulates their abundance independently of chemotaxis and CCR2^(+) myeloid cells

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Cellular & Molecular Immunology 2020年第2期17卷 123-132页

作者： Yifan Zhan Nancy Wang Ajithkumar Vasanthakumar Yuxia Zhang Michael Chopin Stephen L.Nutt Axel Kallies Andrew M.Lew The Walter&Eliza Hall Institute of Medical research ParkvilleVIC 3052Australia Department of Medical Biology University of MelbourneParkvilleVIC 3010Australia Guangzhou Institute of Paediatrics Guangzhou Women and Children’s Medical CentreGuangzhou Medical University510623 GuangzhouGuangdongChina Department of Microbiology and Immunology Peter Doherty Institute for Infection and ImmunityUniversity of MelbourneParkvilleVIC 3010Australia

A wide array of chemokine receptors,including CCR2,are known to control Treg migration.Here,we report that CCR2 regulates Tregs beyond chemotaxis.We found that CCR2 deficiency reduced CD25 expression by FoxP3^(+) Treg cells.Such a change was also consistently present in irradiation chimeras reconstituted with mixed bone marrow from wild-type(WT)and CCR2−/−strains.Thus,CCR2 deficiency resulted in profound loss of CD25 ^(hi) FoxP3^(+) Tregs in secondary lymphoid organs as well as in peripheral tissues.CCR2−/−Treg cells were also functionally inferior to WT cells.Interestingly,these changes to Treg cells did not depend on CCR2+monocytes/moDCs(the cells where CCR2 receptors are most abundant).Rather,we demonstrated that CCR2 was required for TLR-stimulated,but not TCR-or IL-2-stimulated,CD25 upregulation on Treg cells.Thus,we propose that CCR2 signaling can increase the fitness of FoxP3^(+) Treg cells and provide negative feedback to counter the proinflammatory effects of CCR2 on myeloid cells.

关键词： CCR2 CD25 organs

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Functional regulation of monocyte-derived dendritic cells by microRNAs

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Protein & Cell 2012年第7期3卷 497-507页

作者： Yifan Zhan Li Wu The Walter and Eliza Hall Institute of Medical research Parkville 3052Australia Department of Medical Biology University of MelbourneParkville 3010Australia Tsignhua University and Peking University Joint Center for Life Sciences and Tsinghua University School of Medicine Beijing 100084China

Dendritic cells(DCs)as a rare type of leukocytes play an important role in bridging the innate and adaptive immune system.A subset of DCs,monocyte-derived dendritic cells(moDCs),exists in very low numbers at steady state but become abundant in inflammatory states.These inflammation-associated DCs are potent producers of pro-inflammatory cytokines and potent inducers of T helper differentiation.They behave as a“double-edge”sword so that they not only mediate protective immunity but also immuno-pathology.It is still incompletely understood how their function is regulated.Emerging evidence indicates that microR-NAs(miRNAs),as a new class of gene regulators,potently regulate the function of moDCs.Here we summarize recent progress in this area.

关键词： dendritic cells microRNA function

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