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

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. -->
Komentáře: Erratum in: Nat Immunol 2001 Apr;2(4):368.
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Grant Information: AR40908 United States AR NIAMS NIH HHS; R01 AR040908 United States AR NIAMS NIH HHS; T32 AI 07621 United States AI NIAID NIH HHS; T32 AI007621 United States AI NIAID NIH HHS; R56 AI045011 United States AI NIAID NIH HHS; AG 13910 United States AG NIA NIH HHS; R01 AI045011 United States AI NIAID NIH HHS; AI 45011 United States AI NIAID NIH HHS
Substance Nomenclature: 0 (CD28 Antigens)
0 (CD30 Ligand)
0 (CD40 Antigens)
0 (CD8 Antigens)
0 (DNA Primers)
0 (Immunoglobulin A)
0 (Immunoglobulin G)
0 (Ki-1 Antigen)
0 (Membrane Glycoproteins)
0 (OX40 Ligand)
0 (Receptors, Tumor Necrosis Factor)
0 (TNFSF4 protein, human)
0 (TNFSF8 protein, human)
207137-56-2 (Interleukin-4)
Entry Date(s): Date Created: 20010329 Date Completed: 20010412 Latest Revision: 20240610
Update Code: 20240610
PubMed Central ID: PMC4621971
DOI: 10.1038/84254
PMID: 11175813
Autor: Cerutti A; Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA. acerutti@med.cornell.edu, Kim EC, Shah S, Schattner EJ, Zan H, Schaffer A, Casali P
Jazyk: angličtina
Zdroj: Nature immunology [Nat Immunol] 2001 Feb; Vol. 2 (2), pp. 150-6.
DOI: 10.1038/84254
Abstrakt: 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.
Databáze: MEDLINE