Brown adipose tissue ameliorates autoimmune arthritis via inhibition of Th17 cells

  • Jeonghyeon Moon
  • , Dasom Kim
  • , Eun Kyung Kim
  • , Seon yeong Lee
  • , Hyun Sik Na
  • , Gyoung Nyun Kim
  • , Aram Lee
  • , Kyung Ah Jung
  • , Jeong Won Choi
  • , Sung Hwan Park
  • , Sangho Roh
  • , Mi La Cho

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

The functions of adipose tissue are associated with autoimmune diseases, such as rheumatoid arthritis (RA). Some studies have shown that the three compositions of adipose tissue (white, brown, and beige) have different functions. Brown adipose tissue (BAT) is known to secrete several factors that differ from those in white adipose tissue. This suggests that BAT might have potential positive advantages in the physiology of autoimmune diseases. We compared the functions of collagen-induced arthritis mice-derived BAT (CIA BAT) with normal mice-derived BAT. DBA/1J mice (6–7 weeks of age) were immunized by intradermal injection at the base of the tail with 100 μg of bovine type II collagen (CII) emulsified in complete Freund’s adjuvant. Immunized mice then received booster immunizations by intraperitoneal injection with 100 μg of CII in incomplete Freund’s adjuvant. We transplanted CIA BAT and normal BAT into CIA recipient mice. After transplantation, we measured the functions of CIA BAT and normal BAT in mice. Normal BAT-transplanted mice showed significantly lower scores of bone damage, inflammation, and cartilage damage. The proinflammatory cytokines in normal BAT-transplanted mice, such as IL-12, IL-17, IL-6, and tumor necrosis factor-α (TNF-α), tended to decrease. Microarray analysis showed that the PI3K-AKT signaling pathway and IL-17 levels of CIA BAT tissues were significantly higher than those of normal BAT tissues. These results suggest that the transplantation of normal brown fat may have a therapeutic effect in RA patients.

Original languageEnglish
Article number12374
JournalScientific Reports
Volume10
Issue number1
DOIs
StatePublished - 1 Dec 2020

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© 2020, The Author(s).

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