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- W2055442125 abstract "Memory B-cell development is impaired by in vivo blockade of the CD40–CD40 ligand (CD40L) interaction using human Fc immunoglobulin G1 (IgG1)-mouse CD40 fusion protein (CD40-Ig); however, germinal centre (GC) formation is not. We show here that the block in B-cell differentiation in these mice is at the stage of rescue from apoptosis and exit from the GC. Thus, GC from CD40-Ig-treated mice contain a three- to fourfold higher level of apoptotic cells than found in control mice injected with human IgG1 alone. This increase in apoptosis is not caused by a blockade of the CD40L-mediated rescue signal but is the result of an intrinsic defect of GC B cells in CD40-Ig-treated mice to receive rescue signals via CD40. While anti-CD40 stimulation maintained the viability in culture of GC B cells from control mice, it did not rescue GC B cells from CD40-Ig-treated mice. This data is consistent with the notion that a ‘rewiring’ of the CD40 molecule is induced by CD40 ligation early in the response and is necessary to allow B-cell rescue from apoptosis when they subsequently enter the GC." @default.
- W2055442125 created "2016-06-24" @default.
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- W2055442125 date "2001-03-01" @default.
- W2055442125 modified "2023-09-26" @default.
- W2055442125 title "Rewiring of CD40 is necessary for delivery of rescue signals to B cells in germinal centres and subsequent entry into the memory pool" @default.
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- W2055442125 doi "https://doi.org/10.1046/j.1365-2567.2001.01162.x" @default.
- W2055442125 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1783186" @default.
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