23, 22 Calling the Microbiota to Control Atherosclerosis

TY - JOUR

T1 - 23, 22 Calling the Microbiota to Control Atherosclerosis

AU - Carreras, Alba

AU - Bäckhed, Fredrik

PY - 2018/11/20

Y1 - 2018/11/20

N2 - While the commensal microbiota is considered an important regulator of immunity and metabolism, the mechanisms controlling the interplay between diet, cytokine signaling, and the microbiota in atherosclerosis remains unknown. In this issue of Immunity, Fatkhullina et al. (2018) demonstrate that interlukin-23-22 axis regulates diet-induced atherosclerosis by repressing pro-atherogenic microbiota. While the commensal microbiota is considered an important regulator of immunity and metabolism, the mechanisms controlling the interplay between diet, cytokine signaling, and the microbiota in atherosclerosis remains unknown. In this issue of Immunity, Fatkhullina et al. (2018) demonstrate that interlukin-23-22 axis regulates diet-induced atherosclerosis by repressing pro-atherogenic microbiota.

AB - While the commensal microbiota is considered an important regulator of immunity and metabolism, the mechanisms controlling the interplay between diet, cytokine signaling, and the microbiota in atherosclerosis remains unknown. In this issue of Immunity, Fatkhullina et al. (2018) demonstrate that interlukin-23-22 axis regulates diet-induced atherosclerosis by repressing pro-atherogenic microbiota. While the commensal microbiota is considered an important regulator of immunity and metabolism, the mechanisms controlling the interplay between diet, cytokine signaling, and the microbiota in atherosclerosis remains unknown. In this issue of Immunity, Fatkhullina et al. (2018) demonstrate that interlukin-23-22 axis regulates diet-induced atherosclerosis by repressing pro-atherogenic microbiota.

U2 - 10.1016/j.immuni.2018.11.006

DO - 10.1016/j.immuni.2018.11.006

M3 - Journal article

C2 - 30462992

SN - 1074-7613

VL - 49

SP - 788

EP - 790

JO - Immunity

JF - Immunity

IS - 5

ER -