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FEBS Lett. 1997 Nov 17;417(3):301-6.

Evidence for a novel function of the CD40 ligand as a signalling molecule in T-lymphocytes.

Author information

1
Department of Physiology, University of Tübingen, Germany.

Abstract

The interaction of the CD40 receptor with its ligand has been shown to be crucial for the activation of B-lymphocytes. Here, we provide evidence that the pg39 molecule/CD40 ligand (gp39/CD40L) also functions as a stimulatory molecule for T-lymphocytes. Activation of T-lymphocytes via gp39/CD40L induced a strong activation of Jun-N-terminal kinase (JNK) and p38-K. Activation of these kinases correlates with a stimulation of Rac1 and inhibition of Rac1 prevents gp39/CD40L triggered JNK/p38-K activation. Further, cellular stimulation via the CD40 ligand results in tyrosine phosphorylation of cellular proteins and the activation of p56(lck). Inhibition of src-like kinases inhibits Rac1 as well as JNK/p38-K stimulation suggesting a signalling cascade from the gp39/CD40L via p56(lck) and Rac1 to JNK/p38-K.

PMID:
9409738
DOI:
10.1016/s0014-5793(97)01306-9
[Indexed for MEDLINE]
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