A role for adhesion molecules in contact‐dependent T help for B cells

摘要

AbstractThe role of cell contact in T‐dependent B cell activation was examined. Small resting B cells from C57BL/6 mice were cultured with CBA‐derived, non‐alloreactive cloned T helper cells in anti‐T cell receptor Vβ8‐coated microwells. This induced polyclonal B cell activation to enter cell cycle (as measured by thymidine incorporation at 2 days) and to secrete immunoglobulin (as measured by an enzyme‐linked immunoassay detecting high‐rate Ig secretion at 5 days). The inclusion of monoclonal antibodies against LFA‐1, ICAM‐1 and CD4 in these cultures strongly inhibited antibody responses, although proliferative responses were only inhibited to about 50. Inhibitory monoclonal antibodies did not significantly affect lipopolysaccharide‐induced responses, T cell activation to interleukin (IL) 3 secretion, nor did they inhibit the formation of multicellular clusters containing T and B cells. There was no correlation between the level of expression of adhesion molecules by T cells and their ability to induce B cell responses. Anti‐LFA‐1 abrogated T‐dependent responses to IL 2 which were inducible after 2 days in culture, but did not inhibit the induction of this IL 2 responsiveness. These results suggest that continued cell contact involving adhesion/accessory molecules induces B cells to proliferate and to respond to T cell lymphokines. A signaling role for cell interaction molecules on B cells is proposed, similar to the role of these and anal