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Journal ArticleDOI

Mechanisms and consequences of Jak–STAT signaling in the immune system

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TLDR
Recent advances in Jak–STAT biology are reviewed, focusing on immune cell function, disease etiology and therapeutic intervention, as well as broader principles of gene regulation and signal-dependent TFs.
Abstract
Kinases of the Jak ('Janus kinase') family and transcription factors (TFs) of the STAT ('signal transducer and activator of transcription') family constitute a rapid membrane-to-nucleus signaling module that affects every aspect of the mammalian immune system. Research on this paradigmatic pathway has experienced breakneck growth in the quarter century since its discovery and has yielded a stream of basic and clinical insights that have profoundly influenced modern understanding of human health and disease, exemplified by the bench-to-bedside success of Jak inhibitors ('jakinibs') and pathway-targeting drugs. Here we review recent advances in Jak-STAT biology, focusing on immune cell function, disease etiology and therapeutic intervention, as well as broader principles of gene regulation and signal-dependent TFs.

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Citations
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Journal ArticleDOI

Targeting STAT3 Signaling Pathway in Colorectal Cancer.

TL;DR: Signal transducer and activator of transcription 3 (STAT3) is a critical transcription factor that has been firmly associated with colorectal cancer initiation and development.
Journal ArticleDOI

Atopic dermatitis: pathomechanisms and lessons learned from novel systemic therapeutic options

TL;DR: The diverse cellular and molecular mechanisms involved in AD, including the critical role of T‐cell‐driven inflammation, are described, primarily via T helper (Th) 2‐ and Th17‐derived cytokines, many of which are mediated by the Janus kinase (JAK) signaling pathway.
Journal ArticleDOI

STAT signaling in polycystic kidney disease

TL;DR: The role of signal transducer and activator of transcription (STAT) signaling pathways in various renal cell types in healthy kidneys as compared to polycystic kidneys is focused on and the possibility to target STAT signaling for PKD therapy is considered.
Journal ArticleDOI

Macrophages Infected by a Pathogen and a Non-pathogen Spotted Fever Group Rickettsia Reveal Differential Reprogramming Signatures Early in Infection.

TL;DR: It is demonstrated that infection with R. conorii results in a profound reprogramming of host gene expression profiles, providing new insights into the early molecular processes hijacked by a pathogenic SFG Rickettsia to establish a replicative niche in macrophage-like cells.
Journal ArticleDOI

JAK-STAT-dependent regulation of scavenger receptors in LPS-activated murine macrophages.

TL;DR: Results suggest that JAK-STAT inhibition could be useful in atherosclerosis therapy, at least for atherosclerotic plaques exacerbated by LPS.
References
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Journal ArticleDOI

Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases.

TL;DR: The authors showed that CD4+CD25+ cells contribute to maintaining self-tolerance by downregulating immune response to self and non-self Ags in an Ag-nonspecific manner, presumably at the T cell activation stage.
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Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins

TL;DR: A previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that phosphorylate substrate proteins called STATs (signal transducers and activators of transcription).
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A Gain-of-Function Mutation of JAK2 in Myeloproliferative Disorders

TL;DR: Genetic evidence and in vitro functional studies indicate that V617F gives hematopoietic precursors proliferative and survival advantages and a high proportion of patients with myeloproliferative disorders carry a dominant gain-of-function mutation of JAK2.
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Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders.

TL;DR: A single acquired mutation of JAK2 was noted in more than half of patients with a myeloproliferative disorder and its presence in all erythropoietin-independent erythroid colonies demonstrates a link with growth factor hypersensitivity, a key biological feature of these disorders.
Journal ArticleDOI

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

TL;DR: A clonal and recurrent mutation in the JH2 pseudo-kinase domain of the Janus kinase 2 (JAK2) gene in most (> 80%) polycythaemia vera patients leads to constitutive tyrosine phosphorylation activity that promotes cytokine hypersensitivity and induces erythrocytosis in a mouse model.
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