Ryan M. O’Connell

ORCID: 0000-0003-0860-1401
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About
Contact & Profiles
Research Areas
  • MicroRNA in disease regulation
  • Circular RNAs in diseases
  • Immune Cell Function and Interaction
  • Extracellular vesicles in disease
  • Immune cells in cancer
  • Immune Response and Inflammation
  • Cancer-related molecular mechanisms research
  • Gut microbiota and health
  • interferon and immune responses
  • Cancer Immunotherapy and Biomarkers
  • Immunotherapy and Immune Responses
  • RNA Interference and Gene Delivery
  • T-cell and B-cell Immunology
  • Cytokine Signaling Pathways and Interactions
  • CAR-T cell therapy research
  • Clostridium difficile and Clostridium perfringens research
  • Acute Myeloid Leukemia Research
  • RNA Research and Splicing
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Adipose Tissue and Metabolism
  • NF-κB Signaling Pathways
  • CRISPR and Genetic Engineering
  • Adipokines, Inflammation, and Metabolic Diseases
  • Galectins and Cancer Biology

University of Utah
2016-2025

University of California, Los Angeles
2002-2025

Huntsman Cancer Institute
2019-2024

University of California, Irvine Medical Center
2024

The Wistar Institute
2021-2022

UC Irvine Health
2022

Yale New Haven Health System
2022

Bipar
2012-2019

University of Toledo
2017

University of California, San Diego
2010-2014

The mammalian inflammatory response to infection involves the induction of several hundred genes, a process that must be carefully regulated achieve pathogen clearance and prevent consequences unregulated expression, such as cancer. Recently, microRNAs (miRNAs) have emerged class gene expression regulators has also been linked However, relationship between inflammation, innate immunity, miRNA is just beginning explored. In present study, we use microarray technology identify miRNAs induced...

10.1073/pnas.0610731104 article EN Proceedings of the National Academy of Sciences 2007-01-23

MicroRNA-155 (miR-155) has emerged as a critical regulator of immune cell development, function, and disease. However, the mechanistic basis for its impact on hematopoietic system remains largely unresolved. Because miRNAs function by repressing specific mRNAs through direct 3'UTR interactions, we have searched targets miR-155 implicated in regulation hematopoiesis. In present study, identify Src homology-2 domain-containing inositol 5-phosphatase 1 (SHIP1) target miR-155, and, using gain...

10.1073/pnas.0902636106 article EN Proceedings of the National Academy of Sciences 2009-04-10

Mammalian microRNAs are emerging as key regulators of the development and function immune system. Here, we report a strong but transient induction miR-155 in mouse bone marrow after injection bacterial lipopolysaccharide (LPS) correlated with granulocyte/monocyte (GM) expansion. Demonstrating sufficiency to drive GM expansion, enforced expression cells caused proliferation manner reminiscent LPS treatment. However, miR-155-induced populations displayed pathological features characteristic...

10.1084/jem.20072108 article EN The Journal of Experimental Medicine 2008-02-25

Abstract MicroRNAs regulate gene expression posttranscriptionally and function within the cells in which they are transcribed. However, recent evidence suggests that microRNAs can be transferred between mediate target repression. We find endogenous miR-155 miR-146a, two critical inflammation, released from dendritic exosomes subsequently taken up by recipient cells. Following uptake, exogenous repression reprogramme cellular response to endotoxin, where exosome-delivered enhances while...

10.1038/ncomms8321 article EN cc-by Nature Communications 2015-06-18

Numerous bacterial products such as lipopolysaccharide potently induce type I interferons (IFNs); however, the contribution of this innate response to host defense against infection remains unclear. Although mice deficient in either IFN regulatory factor (IRF)3 or receptor (IFNAR)1 are highly susceptible viral infection, we show that these exhibit a profound resistance caused by Gram-positive intracellular bacterium Listeria monocytogenes compared with wild-type controls. Furthermore,...

10.1084/jem.20040712 article EN The Journal of Experimental Medicine 2004-08-09

Abstract The triggering molecular mechanism of ischemia-reperfusion injury (IRI), which in clinical settings results excessive and detrimental inflammatory responses, remains unclear. This study analyzes the role TLR system an established murine model liver warm ischemia followed by reperfusion. By contrasting parallel knockout mice with their wild-type counterparts, we found that TLR4, but not TLR2, was specifically required initiating IRI cascade, as manifested function (serum alanine...

10.4049/jimmunol.173.12.7115 article EN The Journal of Immunology 2004-12-15

Toll-like receptor (TLR) signaling and phagocytosis are hallmarks of macrophage-mediated innate immune responses to bacterial infection. However, the relationship between these two processes is not well established. Our data indicate that TLR ligands specifically promote phagocytosis, in both murine human cells, through induction a phagocytic gene program. Importantly, TLR-induced bacteria was found be reliant on myeloid differentiation factor 88–dependent interleukin-1 receptor–associated...

10.1084/jem.20031237 article EN The Journal of Experimental Medicine 2003-12-29

MicroRNA miR-146a has been implicated as a negative feedback regulator of NF-κB activation. Knockout the gene in C57BL/6 mice leads to histologically and immunophenotypically defined myeloid sarcomas some lymphomas. The are transplantable immunologically compromised hosts, showing that they true malignancies. animals also exhibit chronic myeloproliferation their bone marrow. Spleen marrow cells show increased transcription NF-κB–regulated genes tumors have higher nuclear p65. Genetic...

10.1073/pnas.1105398108 article EN Proceedings of the National Academy of Sciences 2011-05-16

IL-1R activation is required for neutrophil recruitment in an effective innate immune response against Staphylococcus aureus infection. In this study, we investigated the mechanism of vivo a model S. to cutaneous challenge, mice deficient IL-1beta, IL-1alpha/IL-1beta, but not IL-1alpha, developed larger lesions with higher bacterial counts and had decreased compared wild-type mice. Neutrophil clearance IL-1beta expression by bone marrow (BM)-derived cells non-BM-derived resident cells....

10.4049/jimmunol.179.10.6933 article EN The Journal of Immunology 2007-11-15

The microbiota influences obesity, yet organisms that protect from disease remain unknown. During studies interrogating host-microbiota interactions, we observed the development of age-associated metabolic syndrome (MetS). Expansion Desulfovibrio and loss Clostridia were key features associated with obesity in this model are present humans MetS. T cell-dependent events required to prevent disease, replacement rescued obesity. Inappropriate immunoglobulin A targeting increased antagonized...

10.1126/science.aat9351 article EN Science 2019-07-25

Abstract MicroRNA (miR)-125b expression is modulated in macrophages response to stimulatory cues. In this study, we report a functional role of miR-125b macrophages. We found that enriched compared with lymphoid cells and whole immune tissues. Enforced drives adapt an activated morphology accompanied by increased costimulatory factor elevated responsiveness IFN-γ, whereas anti–miR-125b treatment decreases CD80 surface expression. To determine whether these alterations cell signaling, gene...

10.4049/jimmunol.1102001 article EN The Journal of Immunology 2011-10-15

The production of blood cells depends on a rare hematopoietic stem-cell (HSC) population, but the molecular mechanisms underlying HSC biology remain incompletely understood. Here, we identify subset microRNAs (miRNAs) that is enriched in HSCs compared with other bone-marrow cells. An vivo gain-of-function screen found three these miRNAs conferred competitive advantage to engrafting cells, whereas attenuated Overexpression most advantageous miRNA, miR-125b, caused dose-dependent...

10.1073/pnas.1009798107 article EN Proceedings of the National Academy of Sciences 2010-07-26
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