Th2 and Th17 Induce Dry Skin in a Mouse Model of Arthritis

• Published in: Biological & pharmaceutical bulletin Vol. 42; no. 3; pp. 468 - 474
• Main Authors: Goto, Kenji, Hiramoto, Keiichi, Ooi, Kazuya
• Format: Journal Article
• Language: English; Japanese
• Published: Japan The Pharmaceutical Society of Japan 01.03.2019; Pharmaceutical Society of Japan; Japan Science and Technology Agency
• Subjects: Arthritis; Collagen; dendritic cell; dry skin; Helper cells; Hypersensitivity; Interleukin 17; Interleukin 6; Lymphocytes T; Mice; Plasma levels; Rheumatoid arthritis; Skin; T helper 17 cell; T helper 2 cell; Thymic stromal lymphopoietin; Thymus; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Water loss; T helper 2 cell; thymic stromal lymphopoietin; arthritis; T helper 17 cell; dry skin; dendritic cell
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.b18-00803

Skin dryness is a characteristic of rheumatoid arthritis (RA) model mice. However, the mechanism underlying the induction of dry skin by RA is unclear. We hypothesized that T helper (Th)2 and Th17 cells mediate this process. A mouse model of DBA/1JJmsSlc collagen-induced arthritis was treated with Th2 or Th17 cell inhibitor, and transepidermal water loss (TEWL) and the expression of markers associated with allergic reaction and inflammation were evaluated. TEWL and plasma levels of thymic stromal lymphopoietin, interleukin (IL)-6 and -17, and tumor necrosis factor (TNF)-α were increased in the arthritis mouse model compared to that in control mice. Administration of Th2 cell inhibitor abolished the increase in TEWL, IL-6, and TNF-α levels, whereas Th17 cell inhibitor reversed TEWL and decreased IL-17 level. Th2 and Th17 cells contribute to the induction of dry skin, but via distinct mechanisms.