Activated macrophages are an adaptive element of the colonic epithelial progenitor niche necessary for regenerative responses to injury.

By S. L. Pull, J. Doherty, J. Mills, Jeffrey I. Gordon, T. Stappenbeck. Proceedings of the National Academy of Sciences of the United States of America, 2005

630 citations recorded by the source corpus.

Subfields: Immunology, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/4f767cb816b43c3bfb03fff4e3c4329959d35082

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In Immunology

1. D. Cua
2. L. Hooper
3. Wenjun Ouyang
4. M. Abreu
5. Markus F. Neurath
6. C. Tato
7. R. Medzhitov
8. T. Mcclanahan

In Oncology

1. M. Abreu
2. Markus F. Neurath
3. Herbert W. Virgin
4. R. Medzhitov
5. D. Cua
6. Jonathan Kipnis
7. Shizuo Akira

Citations in the corpus

• Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis (2007, background): “With the exception of regulation of infl ammation, studies documenting a direct role of MPs on cell behavior are scant and include intestinal progenitor proliferation (65), erythroblast proliferation and maturation (68), and oligodendrocytic diff erentiation and myelination (69).”
• Paneth cells directly sense gut commensals and maintain homeostasis at the intestinal host-microbial interface (2008, background): “Prior studies have established a role for hematopoietic cell MyD88 in relaying bacterial signals to intestinal epithelial cells during intestinal injury (13, 19).”
• Virus-Plus-Susceptibility Gene Interaction Determines Crohn’s Disease Gene Atg16L1 Phenotypes in Intestine (2010, background): “Instead, this treatment induces a reproducible programmed response in immunocompetent mice including decreased epithelial cell proliferation, loss of epithelial integrity, and generation of ulcers in specific colonic regions (Pull et al., 2005).”
• IL-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability (2015, positive): “lymphocytes (IELs) can also stimulate mucosal healing after 6 days of DSS treatment and recruit macrophages to injured areas to prevent commensal penetration after damage (Ismail et al., 2009; Pull et al., 2005).”
• Origin and physiological roles of inflammation (2008, background): “In organs, such as the intestine, that are colonized by commensal microorganisms, the disruption of the epithelial barrier gives commensal microorganisms access to the TLRs on macrophages that reside in the lamina propria, resulting in TLR-mediated induction of tissue-repair responses in the intesti”