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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Dysregulation of CD30+ T cells by leukemia impairs isotype switching in normal B cells.

Chronic lymphocytic leukemia (CLL) is associated with impaired immunoglobulin (Ig) class-switching from IgM to IgG and IgA, a defect that leads to recurrent infections. When activated in the presence of leukemic CLL B cells, T cells rapidly up-regulate CD30 through an OX40 ligand and interleukin 4 (IL-4)-dependent mechanism. These leukemia-induced CD30+ T cells inhibit CD40 ligand (CD40L)- mediated S mu-->S gamma and S mu-->S alpha class-switch DNA recombination (CSR) by engaging CD30 ligand (CD30L), a molecule that interferes with the assembly of the CD40-tumor necrosis factor receptor- associated factor (TRAF) complex in nonmalignant IgD+ B cells. In addition, engagement of T cell CD30 by CD30L on neoplastic CLL B cells down-regulates the CD3- induced expression of CD40L. These findings indicate that, in CLL, abnormal CD30-CD30L interaction impairs IgG and IgA production by interfering with the CD40-mediated differentiation of nonmalignant B cells.[1]


  1. Dysregulation of CD30+ T cells by leukemia impairs isotype switching in normal B cells. Cerutti, A., Kim, E.C., Shah, S., Schattner, E.J., Zan, H., Schaffer, A., Casali, P. Nat. Immunol. (2001) [Pubmed]
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