Human intestinal macrophages display profound inflammatory anergy despite avid phagocytic and bacteriocidal activity.
By L. Smythies, M. Sellers, R. Clements, Meg Mosteller-Barnum, G. Meng, W. Benjamin, J. Orenstein, Phillip D. Smith. Journal of Clinical Investigation, 2005
954 citations recorded by the source corpus.
Subfields: Genetics, Immunology
View Paper: https://www.semanticscholar.org/paper/43a8cbb0fec471528164ea3145b68752fe463664
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Citations in the corpus
- Gut microbiota: Role in pathogen colonization, immune responses, and inflammatory disease (2017, background): “Intestinal macrophages are hyporesponsive to bacterial Toll -like receptor ligands such as lipopolysaccharides, which is critical to prevent inappropriate activation of in flammatory responses in the intestine (80, 81).”
- Understanding the Holobiont: How microbial metabolites affect human health and shape the immune system (2017, background): “This mechanism is quite different from the previously reported general hypo-responsiveness of intestinal macrophages that was based on starkly reduced expression of several innate response receptors (Smythies et al., 2005).”
- The Short Chain Fatty Acid Butyrate Imprints an Antimicrobial Program in Macrophages (2019, background): “Thus, circulating monocytes enter the gut and undergo final differentiation in the lamina propria to become mature, highly phagocytic macrophages capable of bactericidal activity via mechanisms such as NADPH-oxidase-derived reactive oxygen species (ROS) and antimicrobial peptides and proteins (Bain ”
- Monocyte and macrophage heterogeneity (2005, background): “This phenotype can be induced in peripheral-blood-derived macrophages by intestinal stromal-cell products, indicating that the tissue microenvironment can markedly influence the phenotype of tissue-resident macrophage”
- Macrophage Phenotype as a Determinant of Biologic Scaffold Remodeling (2008, neutral): “…progenitor cells (e.g., vascular endothelial progenitor cells), 20–23 circulating fibrocytes, 24–26 blood monocytes, 27 and other cell types 28–30 are virtually indistinguishable upon routine examination of peripheral blood or tissue sections and that all satisfy the morphologic description…”
- Macrophage polarization: An opportunity for improved outcomes in biomaterials and regenerative medicine (2012, background): “It has been shown that this “gut” phenotype can be induced in other macrophage populations through exposure to intestinal stromal cell products, suggesting that the local microenvironment plays a large role in determining the phenotype and activity of various macrophage populations [7].”
- Immune adaptations that maintain homeostasis with the intestinal microbiota (2010, background): “Although macrophages from many tissue sites (such as the bone marrow) secrete pro-inflammatory mediators that recruit neutrophils and activate T cells, intestinal macrophages do not mediate strong pro-inflammatory responses following bacterial recognition, despite retaining efficient phagocytic and ”
- Transforming Grown Factor-β Signaling in Immunity and Cancer (2019, neutral): “This anergic phenotype is partially driven by TGF-β produced by intestinal stromal cells (Smythies et al., 2005).”
- Ly6C hi monocytes in the inflamed colon give rise to proinflammatory effector cells and migratory antigen-presenting cells. (2012, background): “Human lamina propria macrophages isolated from healthy intestine were shown to exhibit profound inflammatory anergy as reflected by their inability to produce proinflammatory cytokines in response to a vast array of stimuli and explained by their lack of expression of innate response receptors, incl”
- Dendritic cells in intestinal immune regulation (2008, background): “Intestinal macrophages also display some distinctive characteristics compared with splenic macrophages or those that derive from blood monocyte”
- The Bile Acid Receptor FXR Is a Modulator of Intestinal Innate Immunity1 (2009, background): “Deciphering the pathways involved in the regulation of intestinal macrophages promises to provide new host targets for treating diseases such as inflammatory bowel disease in which a dysregulation of innate immunity plays a role (2).”
- Epithelial-cell recognition of commensal bacteria and maintenance of immune homeostasis in the gut (2008, background): “and limit the expression of pro-inflammatory cytokines by macrophage”