CD40 ligand‐independent B cell activation revealed by CD40 ligand‐deficient T cell clones: evidence for distinct activation requirements for antibody formation and B …
P Lane, C Burdet, F McConnell… - European journal of …, 1995 - Wiley Online Library
P Lane, C Burdet, F McConnell, A Lanzavecchia, E Padovan
European journal of immunology, 1995•Wiley Online LibraryWe report the capacity of CD40 ligand (CD40L)‐negative T cell clones to activate human B
cells. CD40L‐negative T cells induce a level of B cell proliferation 10–20% of that seen with
normal T cells. The signal provided by the negative clones is synergistic with that derived
from a CD40L transfectant, and restores B cell proliferation to normal levels, showing that
CD40L‐negative T cell clones are not inherently inhibitory for B cells. Although their capacity
to induce proliferation was much reduced, CD40L‐negative T cell clones were still strong …
cells. CD40L‐negative T cells induce a level of B cell proliferation 10–20% of that seen with
normal T cells. The signal provided by the negative clones is synergistic with that derived
from a CD40L transfectant, and restores B cell proliferation to normal levels, showing that
CD40L‐negative T cell clones are not inherently inhibitory for B cells. Although their capacity
to induce proliferation was much reduced, CD40L‐negative T cell clones were still strong …
Abstract
We report the capacity of CD40 ligand (CD40L)‐negative T cell clones to activate human B cells. CD40L‐negative T cells induce a level of B cell proliferation 10–20% of that seen with normal T cells. The signal provided by the negative clones is synergistic with that derived from a CD40L transfectant, and restores B cell proliferation to normal levels, showing that CD40L‐negative T cell clones are not inherently inhibitory for B cells. Although their capacity to induce proliferation was much reduced, CD40L‐negative T cell clones were still strong inducers of B cell differentiation to plasma cells. This differentiation to plasma cells was inhibited by a CD40L transfectant. The data are discussed with regard to the normal in vivo mechanism for maintaining B cell memory and memory antibody responses to T‐dependent antigens.
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