Send to

Choose Destination
See comment in PubMed Commons below
J Immunol Methods. 2000 Dec 1;246(1-2):51-9.

A method for investigating the role of homotypic adhesion in lymphocyte activation.

Author information

Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, WC1E 7HT, London, UK.


B cells activated via CD40 in vitro form striking homotypic aggregates, especially in the presence of costimuli such as anti-IgM, whereas those stimulated by anti-IgM alone do not. Blocking aggregation with anti-LFA-1alpha also significantly inhibits CD40-stimulated B cell proliferation, suggesting that homotypic adhesion is important for B cell activation via this receptor. To investigate this we have developed a culture system where murine B cells are stimulated in semi-solid agarose, which prevents cell-cell interactions. B cells respond to various mitogenic stimuli, including anti-CD40, in an essentially normal fashion when cultured in agarose. Furthermore, anti-LFA-1 exerts similar inhibitory effects on B cell proliferation regardless of whether the cells are in liquid, or semi-solid medium. These results indicate that homotypic aggregation is not necessary for CD40-stimulated B cell proliferation and the inhibitory effects of anti-LFA-1 could, therefore, be due to the delivery of a negative signal via this integrin, rather than as a result of inhibition of B cell clustering. Furthermore, reaggregation experiments indicated that anti-IgM-stimulated B cells are attracted into anti-CD40-generated clusters, even though they do not form clusters themselves. Taken together these results indicate that clustering is a consequence of B cell activation via CD40, rather than a necessary prelude to B cell proliferation. We postulate that homotypic aggregation may involve an unknown B cell-derived chemokine.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center