The requirement for surface Ig signaling as a prerequisite for T cell:B cell interactions. A possible role for desialylation.
Models for T cell:B cell collaboration suggest that activated B cells process and present Ag to Th cells which subsequently induce B cell proliferation and differentiation. In contrast to activated B cells, resting B cells have generally been shown to be less efficient APC. If this model of T:B collaboration is physiologically correct, then resting B cells must undergo a phenotypic change that permits effective interaction with T cells. In this report, the requirement for rapid signaling through surface Ig on resting B cells for the induction of T:B interaction was investigated with an in vitro clustering assay. Resting splenic B cells were unable to form specific conjugates with T cell clones, unless the B cells were first treated with neuraminidase to remove sialic acid. In contrast, LPS-activated B cells were able to form conjugates without prior treatment. The ability of antibody against LFA-1 or L3T4 to inhibit cluster formation depended on the state of B cell activation in that anti-LFA-1 and anti-L3T4 mAb inhibited cluster formation by neuraminidase-treated resting B cells, but not by LPS-activated B cells. In addition, Ag-specific B cells which were isolated by their capacity to bind specific Ag were able to form clusters without any additional treatment. Moreover, treatment of resting splenic B cells with anti-mu-antibody induced clustering potential in B cells in as little as 10 min, suggesting that signaling through surface Ig was sufficient to induce this phenotypic change in B cells. Furthermore, activation of protein kinase C and Ca2+ mobilization were shown to be involved in that PMA and ionomycin treatment were also able to induce clustering potential in resting B cells. The rapid induction of clustering potential in resting B cells after signaling through surface Ig may represent a fundamental change in B cell physiology which occurs after recognition of specific Ag and may be required for effective cognate recognition between resting hapten-specific B cells and carrier-specific T cells. The potential role of desialylation for the induction of T:B interaction is discussed.
D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D000938:Antigen-Presenting Cells / Q000276:immunology; D000954:Antigens, Surface / Q000502:physiology; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D002449:Cell Aggregation; D005260:Female; D007148:Immunoglobulin mu-Chains / Q000276:immunology; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D019158:N-Acetylneuraminic Acid; D009439:Neuraminidase / Q000494:pharmacology; D011947:Receptors, Antigen, B-Cell / Q000276:immunology / Q000502:physiology*; D012794:Sialic Acids / Q000502:physiology*; D013601:T-Lymphocytes / Q000276:immunology*
D000888:Antibodies, Anti-Idiotypic; D000954:Antigens, Surface; D007148:Immunoglobulin mu-Chains; D011947:Receptors, Antigen, B-Cell; D012794:Sialic Acids; D009439:Neuraminidase; D019158:N-Acetylneuraminic Acid