Folic acid-mediated fibrosis is driven by C5a receptor 1-mediated activation of kidney myeloid cells

Author:

Sahu Ranjit K.1,Xavier Sandhya1ORCID,Chauss Daniel2,Wang Luopin3,Chew Claude4,Taylor Ronald5,Stallcup William B.6,Ma Jennie Z.7,Kazemian Majid3,Afzali Behdad2,Köhl Jörg89ORCID,Portilla Didier1ORCID

Affiliation:

1. Department of Medicine and Center for Immunity and Regenerative Medicine, University of Virginia, Charlottesville, Virginia

2. Immunoregulation Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland

3. Departments of Biochemistry and Computer Science, Purdue University, West Lafayette, Indiana

4. Flow Cytometry Core, University of Virginia, Charlottesville, Virginia

5. Department of Biochemistry, University of Virginia, Charlottesville, Virginia

6. Sanford Burnham Prebys Medical Discovery Institute, Tumor Microenvironment and Cancer Immunology Program, La Jolla, California

7. Division of Biostatistics, Department of Public Health, University of Virginia, Charlottesville, Virginia

8. Institute for Systemic Inflammation Research, University of Lübeck, Germany

9. Division of Immunobiology, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio

Abstract

This study used novel green fluorescent protein C5a receptor 1 floxed mice and the model of folic acid-mediated kidney fibrosis to demonstrate the pathogenic role of increased expression of this complement receptor on macrophages.

Funder

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

Publisher

American Physiological Society

Subject

Physiology

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