Author
Ki-Wook Kim
Other affiliations: University of Illinois at Chicago, University of Washington, Weizmann Institute of Science ...read more
Bio: Ki-Wook Kim is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: CX3CR1 & Monocyte. The author has an hindex of 29, co-authored 49 publications receiving 5783 citations. Previous affiliations of Ki-Wook Kim include University of Illinois at Chicago & University of Washington.
Topics: CX3CR1, Monocyte, Macrophage, Medicine, Microglia
Papers
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TL;DR: A fate-mapping study of the murine monocyte and macrophage compartment taking advantage of constitutive and conditional CX(3)CR1 promoter-driven Cre recombinase expression is reported, establishing that short-lived Ly6C(+) monocytes constitute obligatory steady-state precursors of blood-resident Ly 6C(-) cells and that the abundance of Ly6 C(+) blood monocytes dynamically controls the circulation lifespan of their progeny.
2,302 citations
TL;DR: It is demonstrated that the route of monocyte entry to central nervous system provides an instructional environment to shape their function, and the homing of proinflammatory and anti-inflammatory macrophages to traumatized spinal cord was distinctly regulated.
528 citations
TL;DR: Unexpectedly, significant portions of pancreas‐resident macrophages originated from embryonic development and expanded through in situ proliferation during tumor progression and demonstrate a unique pro‐fibrotic transcriptional profile distinct from that of their monocyte‐derived counterparts.
467 citations
TL;DR: IL-10 is highlighted as a critical homeostatic macrophage-conditioning agent in the colon and intestinal CX3CR1(hi) macrophages are defined as a decisive factor that determines gut health or inflammation.
430 citations
TL;DR: It is shown that enforced survival of monocytes and plaque-resident phagocytes, including foam cells, restored atherogenesis in CX(3)CR1-deficent mice and introduced a Bcl2 transgene, suggesting that the CX (3)C axis provides an essential survival signal.
425 citations
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01 Feb 2015
TL;DR: In this article, the authors describe the integrative analysis of 111 reference human epigenomes generated as part of the NIH Roadmap Epigenomics Consortium, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression.
Abstract: The reference human genome sequence set the stage for studies of genetic variation and its association with human disease, but epigenomic studies lack a similar reference. To address this need, the NIH Roadmap Epigenomics Consortium generated the largest collection so far of human epigenomes for primary cells and tissues. Here we describe the integrative analysis of 111 reference human epigenomes generated as part of the programme, profiled for histone modification patterns, DNA accessibility, DNA methylation and RNA expression. We establish global maps of regulatory elements, define regulatory modules of coordinated activity, and their likely activators and repressors. We show that disease- and trait-associated genetic variants are enriched in tissue-specific epigenomic marks, revealing biologically relevant cell types for diverse human traits, and providing a resource for interpreting the molecular basis of human disease. Our results demonstrate the central role of epigenomic information for understanding gene regulation, cellular differentiation and human disease.
4,409 citations
TL;DR: How cytokines and pathogen signals influence macrophages' functional phenotypes and the evidence for M1 and M2 functions is assessed and a paradigm initially based on the role of a restricted set of selected ligands in the immune response is revisited.
Abstract: Macrophages are endowed with a variety of receptors for lineage-determining growth factors, T helper (Th) cell cytokines, and B cell, host, and microbial products. In tissues, macrophages mature and are activated in a dynamic response to combinations of these stimuli to acquire specialized functional phenotypes. As for the lymphocyte system, a dichotomy has been proposed for macrophage activation: classic vs. alternative, also M1 and M2, respectively. In view of recent research about macrophage functions and the increasing number of immune-relevant ligands, a revision of the model is needed. Here, we assess how cytokines and pathogen signals influence their functional phenotypes and the evidence for M1 and M2 functions and revisit a paradigm initially based on the role of a restricted set of selected ligands in the immune response.
3,674 citations
TL;DR: It is proposed that reduced innate antiviral defenses coupled with exuberant inflammatory cytokine production are the defining and driving features of COVID-19.
3,286 citations
University of California, San Francisco1, Cold Spring Harbor Laboratory2, Icahn School of Medicine at Mount Sinai3, Oregon Health & Science University4, Wistar Institute5, Huntsman Cancer Institute6, University of Maryland, Baltimore County7, La Jolla Institute for Allergy and Immunology8, University of Pennsylvania9, Harvard University10, University of Michigan11, Massachusetts Institute of Technology12
TL;DR: By parsing the unique classes and subclasses of tumor immune microenvironment (TIME) that exist within a patient’s tumor, the ability to predict and guide immunotherapeutic responsiveness will improve, and new therapeutic targets will be revealed.
Abstract: The clinical successes in immunotherapy have been both astounding and at the same time unsatisfactory. Countless patients with varied tumor types have seen pronounced clinical response with immunotherapeutic intervention; however, many more patients have experienced minimal or no clinical benefit when provided the same treatment. As technology has advanced, so has the understanding of the complexity and diversity of the immune context of the tumor microenvironment and its influence on response to therapy. It has been possible to identify different subclasses of immune environment that have an influence on tumor initiation and response and therapy; by parsing the unique classes and subclasses of tumor immune microenvironment (TIME) that exist within a patient's tumor, the ability to predict and guide immunotherapeutic responsiveness will improve, and new therapeutic targets will be revealed.
2,920 citations
TL;DR: The mechanisms that control monocyte trafficking under homeostatic, infectious and inflammatory conditions are being unravelled and are the focus of this Review.
Abstract: Monocytes originate from progenitors in the bone marrow and traffic via the bloodstream to peripheral tissues. During both homeostasis and inflammation, circulating monocytes leave the bloodstream and migrate into tissues where, following conditioning by local growth factors, pro-inflammatory cytokines and microbial products, they differentiate into macrophage or dendritic cell populations. Recruitment of monocytes is essential for effective control and clearance of viral, bacterial, fungal and protozoal infections, but recruited monocytes also contribute to the pathogenesis of inflammatory and degenerative diseases. The mechanisms that control monocyte trafficking under homeostatic, infectious and inflammatory conditions are being unravelled and are the focus of this Review.
2,309 citations