Pharmacological targeting of the IL-17/neutrophil axis attenuates calcific deposits in rat models of calciphylaxis
- Bo Tao 1,2,3,4,5,6, Edward Z Cao 1,2,3,4,5,6, James Hyun 1,2,3,4,5,6, Sivakumar Ramadoss 1,2,3,4,5,6, Juan F Alvarez 1,2,3,4,5,6, Lianjiu Su 1,2,3,4,5,6, Qihao Sun 1,2,3,4,5,6, Zhihao Liu 1,2,3,4,5,6, Linlin Zhang 1,2,3,4,5,6, Alejandro Espinoza 7, Yiqian Gu 3,4,5,6, Feiyang Ma 8, Shen Li 1,2,3,4,5,6, Matteo Pellegrini 3,4,5,6, Arjun Deb 1,2,3,4,5,6
- Bo Tao 1,2,3,4,5,6, Edward Z Cao 1,2,3,4,5,6, James Hyun 1,2,3,4,5,6
- 1Division of Cardiology, Department of Medicine, David Geffen School of Medicine.
- 2UCLA Cardiovascular Theme, David Geffen School of Medicine.
- 3Department of Molecular, Cell and Developmental Biology, College of Letters and Sciences.
- 4Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research.
- 5Molecular Biology Institute.
- 6California Nanosystems Institute, and.
- 7Department of Human Genetics, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
- 8Department of Cell and Developmental Biology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA.
- 0Division of Cardiology, Department of Medicine, David Geffen School of Medicine.
Related Experiment Videos
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Calciphylaxis involves skin calcification driven by inflammation and immune cells. Targeting interleukin-17 (IL-17) and neutrophils shows promise in reducing calcific deposits in animal models.
Area Of Science
- Dermatology
- Immunology
- Pathobiology
Background
- Calciphylaxis is a rare, severe condition with poor survival and unclear mechanisms.
- Ectopic calcification in skin and blood vessels characterizes this disorder.
Purpose Of The Study
- To investigate the pathobiology of calciphylaxis using animal models.
- To explore the role of inflammation and the immune system in disease development.
Main Methods
- Developed animal models mimicking human calciphylaxis.
- Assessed the impact of immune cell activation, immunosuppressants, and targeted therapies.
- Analyzed cytokine and enzyme expression in affected tissues.
Main Results
- Cutaneous calcification was preceded by inflammatory cell infiltration.
- Immune cell-deficient rodents were resistant to calcification.
- IL-17 and neutrophils were identified as key mediators.
- Targeting IL-17 or neutrophils reduced calcific deposits.
Conclusions
- Local inflammation, hypercalcemia, and hyperphosphatemia contribute to calciphylaxis.
- The immune system, particularly the IL-17/neutrophil axis, plays a critical role.
- Therapeutic strategies targeting these pathways may be beneficial.
Related Experiment Videos
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.

