TIGIT negatively regulates inflammation by altering macrophage phenotype

Chen, Xi; Lu, Puhan; Liu, Lei; Fang, Zemin; Wu, Du-An; Liu, Zhe-Long; Wang, Cong Yi; Zhou, Ping; Yu, Xuefeng; Wang, He

doi:10.1016/j.imbio.2015.08.003

Cited by 48 publications

(42 citation statements)

References 36 publications

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“…TIGIT binding of CD155 (Poliovirus receptor, PVR) on the surface of DCs induces production of the anti-inflammatory IL-10 in these DCs [ 208 ]. This process has also been reported after TIGIT binding to macrophage-bound CD155 [ 213 ]. In addition to its inhibitory effects on myeloid cells, TIGIT can also intrinsically suppress T cell function.…”

Section: Extrinsic Mediators Of T Cell Exhaustionsupporting

confidence: 71%

Cellular and Molecular Mechanisms of CD8+ T Cell Differentiation, Dysfunction and Exhaustion

Verdon

Mulazzani

Jenkins

2020

IJMS

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T cells follow a triphasic distinct pathway of activation, proliferation and differentiation before becoming functionally and phenotypically “exhausted” in settings of chronic infection, autoimmunity and in cancer. Exhausted T cells progressively lose canonical effector functions, exhibit altered transcriptional networks and epigenetic signatures and gain constitutive expression of a broad coinhibitory receptor suite. This review outlines recent advances in our understanding of exhausted T cell biology and examines cellular and molecular mechanisms by which a state of dysfunction or exhaustion is established, and mechanisms by which exhausted T cells may still contribute to pathogen or tumour control. Further, this review describes our understanding of exhausted T cell heterogeneity and outlines the mechanisms by which checkpoint blockade differentially engages exhausted T cell subsets to overcome exhaustion and recover T cell function.

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Section: Extrinsic Mediators Of T Cell Exhaustionsupporting

confidence: 71%

Cellular and Molecular Mechanisms of CD8+ T Cell Differentiation, Dysfunction and Exhaustion

Verdon

Mulazzani

Jenkins

2020

IJMS

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“…Moreover, the ability of TIGIT‐Fc to relieve T cell‐mediated delayed‐type hypersensitivity symptoms in wild‐type but not Il10 −/− mice suggested that this mechanism of action is conserved across species. The regulatory role of TIGIT as a ligand that promotes suppressive functions of CD155‐expressing myeloid cells was confirmed by another group . This second study indicated that, in mice, TIGIT promotes the polarization of CD155‐expressing type 1 proinflammatory macrophages into IL‐10‐secreting type 2 macrophages.…”

Section: Tigit Mechanisms Of Actionmentioning

confidence: 69%

TIGIT as an emerging immune checkpoint

Harjunpää

Guillerey

2019

Clinical and Experimental Immunology

393

311

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T cell immunoglobulin and ITIM domain (TIGIT) is an inhibitory receptor expressed on lymphocytes that was recently propelled under the spotlight as a major emerging target in cancer immunotherapy. TIGIT interacts with CD155 expressed on antigen-presenting cells or tumour cells to downregulate T cell and natural killer (NK) cell functions. TIGIT has emerged as a key inhibitor of anti-tumour responses that can hinder multiple steps of the cancer immunity cycle. Pre-clinical studies indicated that TIGIT blockade may protect against various solid and haematological cancers. Several monoclonal antibodies (mAbs) that block the inhibitory activity of human TIGIT have been developed. Clinical trials are ongoing, investigating TIGIT blockade as a monotherapy or in combination with anti-PD1/PD-L1 mAbs for the treatment of patients with advanced solid malignancies. In this review, we cover our current knowledge on TIGIT, from its discovery in 2009 to its current status as a clinical target.

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“…Other genes, such as Tnfsf15 (Tumor Necrosis Factor member 15), Hbegf (Heparin-Binding EGF-Like Growth Factor), and Cflar (CASP8 And FADD-Like Apoptosis Regulator) mainly located in the plasma membrane are involved in NF-κB and MAPK signaling pathways, known to be active in M1 macrophages. Additionally, Pvr (poliovirus receptor) and Arid5a (AT Rich Interactive Domain 5 A) are known to be induced by LPS4142. Gpd2 (Glycerol-3-Phosphate Dehydrogenase 2) is prevalent in mitochondria and possibly activates NF-κB and MAPK by producing ROS43.…”

Section: Resultsmentioning

confidence: 99%

Time Series miRNA-mRNA integrated analysis reveals critical miRNAs and targets in macrophage polarization

McCurdy

Huang

et al. 2016

Sci Rep

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Polarization of macrophages is regulated through complex signaling networks. Correlating miRNA and mRNA expression over time after macrophage polarization has not yet been investigated. We used paired RNA-Seq and miRNA-Seq experiments to measure the mRNA and miRNA expression in bone marrow-derived macrophages over a time-series of 8 hours. Bioinformatics analysis identified 31 differentially expressed miRNAs between M1 and M2 polarized macrophages. The top 4 M1 miRNAs (miR-155-3p, miR-155-5p, miR-147-3p and miR-9-5p) and top 4 M2 miRNAs (miR-27a-5p, let-7c-1-3p, miR-23a-5p and miR-23b-5p) were validated by qPCR. Interestingly, M1 specific miRNAs could be categorized to early- and late-response groups, in which three new miRNAs miR-1931, miR-3473e and miR-5128 were validated as early-response miRNAs. M1 polarization led to the enrichment of genes involved in immune responses and signal transduction, whereas M2 polarization enriched genes involved in cell cycle and metabolic processes. C2H2 zinc-finger family members are key targets of DE miRNAs. The integrative analysis between miRNAs and mRNAs demonstrates the regulations of miRNAs on nearly four thousand differentially expressed genes and most of the biological pathways enriched in macrophage polarization. In summary, this study elucidates the expression profiles of miRNAs and their potential targetomes during macrophage polarization.

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TIGIT negatively regulates inflammation by altering macrophage phenotype

Cited by 48 publications

References 36 publications

Cellular and Molecular Mechanisms of CD8+ T Cell Differentiation, Dysfunction and Exhaustion

Cellular and Molecular Mechanisms of CD8+ T Cell Differentiation, Dysfunction and Exhaustion

TIGIT as an emerging immune checkpoint

Time Series miRNA-mRNA integrated analysis reveals critical miRNAs and targets in macrophage polarization

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