Serum Amyloid P Inhibits Fibrosis Through FcγR-Dependent Monocyte-Macrophage Regulation in Vivo
- 4 November 2009
- journal article
- research article
- Published by American Association for the Advancement of Science (AAAS) in Science Translational Medicine
- Vol. 1 (5), 5ra13
- https://doi.org/10.1126/scitranslmed.3000111
Abstract
The fibrosis that occus in kidney after tissue injury can be inhibited by serum amyloid protein, which stimulates the cytokine interleukin 10.Keywords
This publication has 52 references indexed in Scilit:
- Pericytes and Perivascular Fibroblasts Are the Primary Source of Collagen-Producing Cells in Obstructive Fibrosis of the KidneyThe American Journal of Pathology, 2008
- Structural recognition and functional activation of FcγR by innate pentraxinsNature, 2008
- Fc receptor engagement mediates differentiation of cardiac fibroblast precursor cellsProceedings of the National Academy of Sciences of the United States of America, 2008
- Kidney injury molecule–1 is a phosphatidylserine receptor that confers a phagocytic phenotype on epithelial cellsJCI Insight, 2008
- Serum amyloid P inhibits dermal wound healingWound Repair and Regeneration, 2008
- Alternative activation of macrophagesNature Reviews Immunology, 2003
- Pentameric and decameric structures in solution of serum amyloid P component by X-ray and neutron scattering and molecular modelling analysesJournal of Molecular Biology, 1997
- Impaired IgG-Dependent Anaphylaxis and Arthus Reaction in FcγRIII (CD16) Deficient MiceImmunity, 1996
- The major acute phase reactants: C-reactive protein, serum amyloid P component and serum amyloid A proteinImmunology Today, 1994
- Calcium-dependent polymerization of human serum amyloid P component is inhibited by heparin and dextran sulfateBiochimica et Biophysica Acta (BBA) - Protein Structure and Molecular Enzymology, 1989