Phagocytosis and clearance of apoptotic cells is mediated by MER

By R. Scott, E. McMahon, Shannon M. Pop, E. Reap, R. Caricchio, P. Cohen, H. Earp, G. Matsushima. Nature, 2001

1,245 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/6c49a56f4a3eb69fd53503c50a9ba8deab9f8713

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In Immunology

Citations in the corpus

TIM genes: a family of cell surface phosphatidylserine receptors that regulate innate and adaptive immunity (2010, background): “However, receptors such as milk fat globule-EGFfactor 8 (MFG-E8) and growth arrest-specific gene 6 (GAS6) (113) are widely expressed in somatic cells and do not appear to specify phagocyte behavior following phagocytosis of apoptotic cells (12).”
Efficient clearance of early apoptotic cells by human macrophages requires “M2c” polarization and MerTK induction (2012, background): “In fact, while the great majority of AC clearance receptors preferentially binds to late ACs (10), MerTK specifically clears early membrane-intact ACs (7, 12).”
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation (2002, background): “But apoptotic cells that escape prompt clearance undergo secondary necrosis leading to an increased amount of nuclear autoantibodie”
A role for Mer tyrosine kinase in αvβ5 integrin-mediated phagocytosis of apoptotic cells (2005, background): “This latter phenotype is recapitulated in Mer-kinase-dead (MerKD)expressing transgenic mice, suggesting that intracellular signals from Mer are required to initiate engulfment signals (Scott et al., 2001).”
Dendritic cells: translating innate to adaptive immunity. (2006, background): “, for the Mer family of tyrosine kinases [115], the phosphatidyl serine receptor [116], and MFG-E8 [117].”
From T to B and back again: positive feedback in systemic autoimmune disease (2001, background): “In addition, defects in mechanisms of clearing apoptotic cells or immune complexes, such as complement, Fc receptor or phagocytic defects, serve to elevate the absolute concentration of available auto-antige”
TAM receptors are pleiotropic inhibitors of the innate immune response. (2007, background): “Autoimmunity in the TAM mutants results from both sustained APC hyperactivation (Lu and Lemke, 2001 and this paper) and also from the delayed phagocytic clearance of apoptotic cells, a process in which TAM signaling also plays an important role (Scott et al., 2001; Lemke and Lu, 2003).”
TIM-1 and TIM-4 glycoproteins bind phosphatidylserine and mediate uptake of apoptotic cells. (2007, background): “These are two component systems composed of a soluble PS ‘‘teth- ering’’ molecule such as MFG-E8 or GAS6 and a mem- brane-bound ‘‘tickle’’ molecule, such as aVb3 or aVb5 integrin or Mer, responsible for recognition of the ‘‘tether’’ and internalization and signaling.”
An Apoptotic 'Eat Me' Signal: Phosphatidylserine Exposure. (2015, background): “MerTK-deficient resident peritoneal macrophages cannot engulf apoptotic cells [58,59].”
Immunobiology of the TAM receptors (2008, background): “Bacterial and viral infections generate a large number of apoptotic-cell corpses, which must be cleared by macrophages and DCs, and this form of homeostatic phagocytosis is also impaired in the TAM-deficient mic”
Delayed Apoptotic Cell Clearance and Lupus-like Autoimmunity in Mice Lacking the c-mer Membrane Tyrosine Kinase (2002, background): “The redundancy of the clearance system is illustrated by apparently normal clearance and by the absence of in vivo apoptotic bodies in most receptor knockout models, with the exceptions of the C1q-deleted mouse (4); and mice with a targeted disruption of the cytoplasmic region of the membrane tyrosi”
Chromatin–IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors (2002, background): “Remarkably, these same autoantigens are the targets in several murine autoimmunity models generated by mutations that disrupt lymphocyte homeostasis or autoantigen metabolis”