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Updated: Feb 2, 2026

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
Published on: January 25, 2017
23, 22 Calling the Microbiota to Control Atherosclerosis.
Alba Carreras1, Fredrik Bäckhed2
1Department of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
The interleukin-23/22 axis controls diet-induced atherosclerosis by suppressing harmful gut bacteria. This finding reveals a key mechanism linking diet, immunity, and cardiovascular disease progression.
Area of Science:
- Immunology
- Microbiology
- Cardiovascular Research
Background:
- The gut microbiota influences immunity and metabolism.
- Mechanisms linking diet, cytokines, and atherosclerosis are not fully understood.
Purpose of the Study:
- Investigate the role of the interleukin-23/22 axis in diet-induced atherosclerosis.
- Elucidate how cytokine signaling impacts the gut microbiota in the context of atherosclerosis.
Main Methods:
- Utilized mouse models of diet-induced atherosclerosis.
- Analyzed the gut microbiota composition and cytokine profiles.
- Investigated the function of the interleukin-23/22 signaling pathway.
Main Results:
- The interleukin-23/22 axis was found to regulate atherosclerosis development.
- This axis represses the growth of pro-atherogenic microbiota.
- Dietary interventions impact this axis and subsequent microbiota changes.
Conclusions:
- The interleukin-23/22 axis is a critical regulator of diet-induced atherosclerosis.
- Targeting this axis may offer therapeutic strategies for atherosclerosis by modulating the gut microbiota.
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