CD38 unresponsiveness of xid B cells implicates Bruton's tyrosine kinase (btk) as a regulator of CD38 induced signal transduction

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概要

• 論文の詳細を見る

著者

• Grimaldi J.

  Dnax Research Institute

• HOWARD Maureen

  DNAX Research Institute

• Wu Wei

  Department Of Immunology Dnax Research Institute

• Howard Maureen

  Department Of Immunology Dnax Research Institute

• SANTOS-ARGUMEDO Leopoldo

  DNAX Research Institute

• LUND Frances

  DNAX Research Institute

• HEATH Andrew

  DNAX Research Institute

• SOLVASON Nanette

  DNAX Research Institute

• WU Wei

  DNAX Research Institute

• PARKHOUSE R.M.E.

  Institute for Animal Health, Guildford

• SOLVASON Nanette

  Department of Immunology DNAX Research Institute

• Parkhouse R.m.e.

  Institute For Animal Health Guildford

関連論文

• Mouse germinal center B cells with the xid mutation retain responsiveness to antimouse CD40 antibodies but diminish IL-5 responsiveness
• Antigen receptor-mediated B cell death is blocked by signaling via CD72 or treatment with dextran sulfate and is defective in autoimmunity-prone mice
• CD38 unresponsiveness of xid B cells implicates Bruton's tyrosine kinase (btk) as a regulator of CD38 induced signal transduction
• Cyclin D2 is essential for BCR-mediated proliferation and CD5 B cell development
• CD38 expression on mouse T cells: CD38 defines functionally distinct subsets of αβ TCR^+CD4^-CD8^- thymocytes

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