A role of CD22 and CD72 in the immune responses

• Project/Area Number: 24591645
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Kanazawa University
• Principal Investigator: HAMAGUCHI Yasuhito 金沢大学, 医学系, 准教授 (60420329)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000); Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000); Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000); Fiscal Year 2012: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
• Keywords: B細胞 / CD22 / CD72

Outline of Final Research Achievements

In this study, we addressed whether CD22 and CD72 have redundant functions using CD22 and CD72 double-deficient (CD22-/-/CD72-/-) mice. CD22-/-/CD72-/- mice showed significantly decreased number of peripheral B cells compared to wild type mice. Turnover of B cells in CD22-/-/CD72-/- mice was significantly augmented than in wild type mice, but significantly reduced compared to CD22-/- mice. CD22-/- mice showed significantly increased serum IgM levels compared to wild type mice, but CD22-/-/CD72-/- mice did not. IgM responses against DNP-Ficoll were significantly decreased in CD22-/-/CD72-/- mice compared to wild type mice. In pristane-induced murine lupus model, both the incidence of ANAs and urine protein levels were similar between wild type and CD22-/-/CD72-/- mice. These results showed that abnormalities observed in CD22-/-/CD72-/- mice did not exceed the degree of those seen in each-deficient mice. Therefore, we concluded that CD22 and CD72 independently regulated B cell function.