These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Toll-like receptor stimulation as a third signal required for activation of human naive B cells.
    Author: Ruprecht CR, Lanzavecchia A.
    Journal: Eur J Immunol; 2006 Apr; 36(4):810-6. PubMed ID: 16541472.
    Abstract:
    According to the current model, naive B cell activation is dependent on the sequential integration of two signals: B cell receptor (BCR) cross-linking by antigen, followed by cognate interaction with helper T cells through an immunological synapse. Using an improved method to purify human naive B cells we found that BCR stimulation and T cell help induced initial cell division but were not sufficient to promote survival and differentiation thus leading to abortive proliferation of naive B cells. Extensive B cell proliferation, isotypic switch and differentiation to immunoglobulin (Ig)-secreting cells was induced by addition of microbial products that trigger any of the Toll-like receptors (TLR) that are up-regulated in naive B cells upon BCR triggering. TLR agonists acted directly on B cells and were required irrespective of the nature of the T helper cells present. Supernatants of dendritic cells (DC) stimulated by DC-specific TLR agonists were also capable of enhancing B cell responses although to a much lower and variable extent. These results indicate that human naive B cell activation is critically dependent on innate stimuli acting optimally on TLR expressed by B cells. The coupling of BCR stimulation to TLR expression endows the human system with a high degree of specificity since it allows focusing of innate signals only on antigen-stimulated B cells.
    [Abstract] [Full Text] [Related] [New Search]