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Analysis of RP105 in association with the B cell activation in autoimmune diseases

Research Project

Project/Area Number 13670459
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field 内科学一般
Research InstitutionSaga Medical School

Principal Investigator

NAGASAWA Kohei  Saga Medical School, Internal Medicine, Professor, 医学部, 教授 (00108721)

Co-Investigator(Kenkyū-buntansha) TADA Yoshifumi  Saga Medical School, Internal Medicine, Instructor, 医学部, 講師 (70284627)
KOARADA Syuichi  Saga Medical School, Internal Medicine, Instructor, 医学部, 助手 (50304887)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥2,500,000 (Direct Cost: ¥2,500,000)
KeywordsB cell / RP105 / Autoimmune disease / SLE / Sjogren.s Syndrome / Immunoglobulin / Anti-DNA antibody / Immunohistochemical staining / 皮膚筋炎 / 自己抗体 / ELISA法
Research Abstract

RP105, a novel molecule expressed on B cells, has been described to be associated with B cell proliferation or apoptosis in mice. We have already demonstrated that significant percent of B cells in patients with several autoimmune diseases lack RP105 molecules although virtually all peripheral B cells in normal subjects express them on their surface. We have also suggested that those RP105-negative B cells are highly activated and may be associated with the pathophysiology of those autoimmune diseases. In this study we investigated whether RP105-negative B cells from patients with systemic lupus erythematosus (SLE) could produce immunoglobulins (Ig) and anti-DNA antibodies, critically important autoantibodies in SLE, in vitro. We found that RP105- positive B cells produced neither Ig nor anti-DNA antibodies even with various - stimulations. On the other hand, RP105-negative B cells from all the SLE patients produced significant amount of Ig without any stimulation and anti-DNA antibodi … More es when incubated with T cells. Moreover, these production was augmented with the addition of IL-6.
RP105-negative B cells in the peripheral blood from patients with Sjogren's syndrome, another important disease characteristic of B cell activation, were also found to be increased and we analyzed the expression of RP105 on B cells infiltrating salivary glands by immunohistochemical staining. The results showed that large proportion of B ills that infiltrated and proliferated in the salivary glands were RP105-negative. It was also found that the degree of infiltrating RP105-negative B cells tended to correlate with the serum levels of Ig, indicating that those cells may be responsible for the production of Ig and possibly autoantibodies in Sjogren's syndrome as well.
Taken together, RP105-negative B cells may play an important role in the pathogenesis of certain autoimmune diseases such as SLE and Sjogren's syndrome. We are planning to develop a treatment of those diseases taking advantage of the character of RP105-negative B cells. Less

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (19 results)

All Other

All Publications (19 results)

  • [Publications] Koarada S, et al.: "CD180(RP105) in rheumatic diseases"Rheumatology. 40. 1315-1316 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kikuchi Y, et al.: "Difference in B cell activation between dermatomyositis and polymyositis : analysis of the expression of RP105"Ann Rheum Dis.. 60. 1137-1140 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tada Y, et al.: "Collagen-induced arthritis in TNF receptor-1-deficient mice"Clin Immunol.. 99. 325-333 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kikuchi Y, et al.: "RP105-lacking B cells from lupus patients are responsible for the production of immunoglobulins and autoantibodies"Arthritis Rheum.. 46. 3259-3265 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] 小荒田秀一, 他: "自己免疫疾患におけるToll-likeレセプターファミリーの役割-RP105, TLR-4の臨床的意義-"医学のあゆみ. 205. 103-107 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kikuchi Y, et al.: "Increase of RP105-lacking activated B cells in the peripheral blood and salivary glands in patients with Sjogren's syndrome"Ann Rheum Dis.. (in press).

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Koarada, S., et al: "CD180(RP105) in rheumatic diseases"Rheumatology. 40. 1315-1316 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kikuchi, Y., et al.: "Difference in B cell activation between dermatomyositis and polymyositis: analysis of the expression of RP105 on peripheral blood B cells"Ann. Rheum. Dis.. 60. 1137-1140 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tada, Y., et al.: "Collagen-induced arthritis in TNF receptor-1-deficient mice. TNF receptor-2 can modulate arthritis in the absence of TNF receptor-1"Clin. Immunol.. 99. 325-333 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kikuchi, Y., et al: "RP105-lacking B cells from lupus patients are responsible for the production of immunoglobulins and autoantibodies"Arthritis Rheum. 46. 3259-3265 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Tada, Y., et al.: "Platelet endothelial cell adhesion molecule-1(PCAM-1) deficiency accelerates onset of collage-induced arthritis"Arthritis Rheum.. in press.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kikuchi, Y., et at.: "Increase of RP105-lacking B cells in the peripheral blood and salivary glands in patients with Sjogren's syndrome"Ann. Rheum. Dis.. in press.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Kikuchi Y, Koarada S, Tada Y, et al.: "RP105-lacking B cells from lupus patients are responsible for the production of immunoglobulins and autoantibodies"Arthritis Rheum. 46・12. 3259-3265 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Ushiyama O, Yamada T, Koarada S, et al.: "Retinal findings in systemic sclerosis : a comparison with nailfold capillaroscopic patterns"Ann Rheum Dis.. 62・3. 204-207 (2003)

    • Related Report
      2002 Annual Research Report
  • [Publications] Kikuchi Y, Koarada S, Nakamura S, et al.: "Increase of RP105-lacking activated B cells in the peripheral blood and salivary glands in patients with Sjogren's syndrome"J Lab Invest.. (in press).

    • Related Report
      2002 Annual Research Report
  • [Publications] Koarada, S., et al.: "CD180(RP105) in rheumatic diseases"Rheumatology. 40. 1315-1316 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Tada, Y., et al.: "Collagen-induced arthritis in TNF receptor-1-deficient mice."Clin. Immunol. 99. 325-333 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Kikuchi, Y., et al.: "Difference in B cell activation between dermatomyositis and polymyositis : analysis of the expression of RP105"Ann. Rheum. Dis. 60. 1137-1140 (2001)

    • Related Report
      2001 Annual Research Report
  • [Publications] Morita, C., et al.: "Association of tumor necrosis factor receptor type II polymorphism 196R with systemic lupus erythematosus"Arthritis. Rheum. 44. 2819-2827 (2001)

    • Related Report
      2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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