Identification of IL-27-induced IL-10-producing innate lymphoid cells.

• Project/Area Number: 25891024
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Functional biochemistry
• Research Institution: Tokyo Medical University
• Principal Investigator: FURUSAWA Jun-ichi 東京医科大学, 医学部, ポスト・ドクター (80570796)
• Project Period (FY): 2013-08-30 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000); Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
• Keywords: 潰瘍性大腸炎 / IBD / IL-10 / IL-27 / マクロファージ / DSS / 潰瘍性大腸炎 DSS / WSX-1 / LP(lamina propria) / 腸管免疫 / 自然免疫 / 炎症

Outline of Final Research Achievements

Interleukin (IL)-27 is one of the IL-6/IL-12 family cytokines, and it is known to induce IL-10-producing T cells (Tr1) to suppress inflammatory response in colitis. In this study, we demonstrated that CD11b+CD11c+CD64+ macrophages produce IL-10 by endogenous IL-27 signal at an early phase of dextran sodium sulfate (DSS)-induced colitis model and suppress inflammatory response. In contrast to T cell-mediated adoptive immune response, it was suggested that IL-27-induced IL-10-producing macrophages contribute to anti-inflammatory innate immune response in inflammatory bowel decease (IBD).