Phosphatidylserine-dependent ingestion of apoptotic cells promotes TGF-beta1 secretion and the resolution of inflammation.

By Mai-Lan N Huynh, Valerie Fadok, P. Henson. Journal of Clinical Investigation, 2002

1,324 citations recorded by the source corpus.

Subfields: Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/8b8ee169ea187ab2f146bab79e6ae2b7d1bed2b5

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. I. Tabas
2. DM Mosser
3. X. Zhang
4. H. Kono
5. K. Rock
6. D. Gilroy
7. K. Ravichandran
8. I. Azevedo

In Surgery

1. I. Azevedo
2. P. Barnes
3. R. Monteiro
4. Hyon K. Choi
5. Michael A. Matthay
6. D. Gilroy
7. I. Tabas
8. R. Kaufman

Citations in the corpus

• The inflammatory response to cell death. (2008, background): “In contrast, it is often stated that apoptotic cell death doesn’t provoke inflammation (10).”
• The many faces of macrophage activation (2003, background): “The direct removal of inflammatory cells as well as the induction of anti-inflammatory TGF- following apoptotic cell removal [20] contribute to this effect.”
• Macrophage activation by endogenous danger signals (2008, background): “This process not only eliminates inflammatory cells, but the removal process itself can result in the production of TGFβ by macrophages [2].”
• Pathogenesis of Gout (2005, background): “Furthermore, transforming growth factor– (see Glossary) becomes abundant in acute gouty synovial fluid and inhibits IL-1 receptor expression and IL-1– driven cellular inflammatory responses (153, 154).”
• Mediators of Chronic Obstructive Pulmonary Disease (2004, background): “Ingestion of apoptotic granulocytes by macrophages induces the secretion of transforming growth factor (TGF)- 1 (Huynh et al., 2002).”
• Phosphatidylserine is a global immunosuppressive signal in efferocytosis, infectious disease, and cancer (2016, background): “Instead, engulfed apoptotic cells induce the secretion of the anti-inflammatory cytokine interleukin-10 (IL-10) and TGF-β and simultaneously decrease the secretion of the inflammatory cytokines TNF-α, IL-1β, and IL-12.(37,45) Moreover, in vitro experiments have shown that the production of TGF-β, co”
• Chronic Inflammation in Obesity and the Metabolic Syndrome (2010, background): “The apoptosis of inflammatory cells is a nonphlogistic physiological process of removing dead cells and is essential for the resolution of inflammation [16] with the added advantage that after engulfing these apoptotic cells, macrophages acquire a phenotype conductive to resolution, releasing anti-i”
• Anti-inflammatory lipid mediators and insights into the resolution of inflammation (2002, background): “The transfer of apoptotic cells to LPS-stimulated lungs reduced the release of pro-inflammatory mediators and leukocyte recruitment; this effect could be reversed by the administration of TGF-β1-neutralizing antiseru”