Author
Yohei Mikami
Other affiliations: National Institutes of Health
Bio: Yohei Mikami is an academic researcher from Keio University. The author has contributed to research in topics: Medicine & Inflammatory bowel disease. The author has an hindex of 25, co-authored 72 publications receiving 2079 citations. Previous affiliations of Yohei Mikami include National Institutes of Health.
Papers
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TL;DR: A refined organoid culture condition for intestinal epithelia is established that allows human intestinal organoids to concurrently undergo multi-differentiation and self-renewal and offers a viable strategy for modeling human intestinal tissues and diseases in an in vivo relevant context.
283 citations
TL;DR: It is found that chromatin in proximity to effector genes is selectively accessible in ILCs prior to high-level transcription upon activation, which indicates extensive sharing of regulatory circuitry across the innate and adaptive compartments of the immune system, in spite of their divergent developing pathways.
264 citations
TL;DR: Collectively, CB promotes IL-10 production by intestinal macrophages in inflamed mucosa, thereby preventing experimental colitis in mice, and the colitis-preventing effect of CB was negated in macrophage-specific IL- 10-deficient mice, suggesting that induction ofIL-10 by intestinal Macrophages is crucial for the probiotic action of CB.
238 citations
TL;DR: Analysis of single-cell analysis points to CGRP as a context-dependent negative regulatory factor that shapes innate lymphocyte responses to alarmins and neuropeptides during type 2 innate immune responses during helminth infection.
167 citations
TL;DR: The results suggest that endogenous MCP-1 contributes to the composition of resident LPMϕ subsets in the intestine, and may play an important role in maintenance of gut homeostasis in the steady state, and in the termination of excess inflammatory responses inThe intestine, by producing IL-10.
Abstract: Lamina propria macrophages (LPMs) spontaneously produce large amounts of anti-inflammatory IL-10 and play a central role in regulation of immune responses against commensal bacteria. MCP-1 is a chemokine that plays an important role in recruitment of monocytes and macrophages to inflamed tissues. We demonstrated that, in addition to IL-10, LPMs produced large amounts of MCP-1, even in a steady state. MCP-1 deficiency caused impaired IL-10 production by LPMs and led to exacerbation of dextran sulfate sodium-induced acute colitis. As an explanation of this impaired IL-10 production by LPMs, we found that LPMs could be separated into two subsets with distinct side-scattered properties, namely LPM1 (CD11b(+)F4/80(+)CD11c(-)SSC(hi)) and LPM2 (CD11b(+)F4/80(+)CD11c(-)SSC(lo)). Unlike LPM1, the LPM2 subset migrated in response to MCP-1 and produced a larger amount of IL-10 in response to commensal bacteria. LPMs isolated from MCP-1-deficient mice produced less IL-10 as a consequence of the lack of the MCP-1-dependent LPM2 population. This imbalanced composition in LPM population may be involved in the susceptibility to DSS-induced colitis in MCP-1-deficient mice. Our results suggest that endogenous MCP-1 contributes to the composition of resident LPM subsets in the intestine. Moreover, MCP-1-dependent LPM2 subset may play an important role in maintenance of gut homeostasis in the steady state, and in the termination of excess inflammatory responses in the intestine, by producing IL-10.
123 citations
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01 Jan 2000
3,536 citations
Journal Article•
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1,978 citations
TL;DR: The role of cytokines produced by innate and adaptive immune cells, as well as their relevance to the future therapy of IBD are discussed.
Abstract: Erroneous communication between the innate and adaptive immune systems through cytokines results in exaggerated or attenuated immune response. It is not known whether the pathologic immune response in inflammatory bowel disease has its origin in a dysbalance of pro- and anti-inflammatory cytokine release or whether it is secondary in subsequence of a defective intestinal barrier or the destructive power of aggressive microbiota in the gut lumen.
1,938 citations
TL;DR: The Omni-ATAC protocol generates chromatin accessibility profiles from archival frozen tissue samples and 50-μm sections, revealing the activities of disease-associated DNA elements in distinct human brain structures.
Abstract: We present Omni-ATAC, an improved ATAC-seq protocol for chromatin accessibility profiling that works across multiple applications with substantial improvement of signal-to-background ratio and information content. The Omni-ATAC protocol generates chromatin accessibility profiles from archival frozen tissue samples and 50-μm sections, revealing the activities of disease-associated DNA elements in distinct human brain structures. The Omni-ATAC protocol enables the interrogation of personal regulomes in tissue context and translational studies.
1,452 citations
Aix-Marseille University1, Cornell University2, Washington University in St. Louis3, Charité4, French Institute of Health and Medical Research5, Pasteur Institute6, Keio University7, University of California, San Francisco8, Laboratory of Molecular Biology9, VU University Amsterdam10, University of Oxford11, University of Amsterdam12
TL;DR: The advances in ILC biology over the past decade are distill the advances to refine the nomenclature of ILCs and highlight the importance of I LCs in tissue homeostasis, morphogenesis, metabolism, repair, and regeneration.
1,252 citations