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Triggering of calcium signals in antigen-specific B-cells on the supported lipid monolayers
H Katayama1, Y Nagao, T Hamano
1Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.
Using supported lipid monolayers we have studied here calcium signals in antigen-specific B-cells (TNP-specific B-cell hybridomas, TP67.21) triggered by lipid hapten (TNP-Cap-DPPE). Stimulation of the B-cell hybridomas (TP67.21) with a supported DPPC monolayers containing 1% TNP-Cap-DPPE increased the intracellular free calcium ion concentration [Ca2+]i in B-cells. None of B-cells responded to a DPPC monolayers without lipid hapten (TNF-Cap-DPPE). Triggering for calcium signals was clearly dependent on the fluidity of the lipid monolayers. Solid DPPC and DSPC monolayers triggered the calcium signals more efficiently than the fluid DMPC monolayers did. These calcium signals became apparently more efficient in the presence of cholesterol. All of these results suggested that the rigidity of cross-linking for antigen receptors (mIgM) may be a crucial role for triggering calcium signals in B-cells.
Using supported lipid monolayers we have studied here calcium signals in antigen-specific B-cells (TNP-specific B-cell hybridomas, TP67.21) triggered by lipid hapten (TNP-Cap-DPPE). Stimulation of the B-cell hybridomas (TP67.21) with a supported DPPC monolayers containing 1% TNP-Cap-DPPE increased the intracellular free calcium ion concentration [Ca2+]i in B-cells. None of B-cells responded to a DPPC monolayers without lipid hapten (TNF-Cap-DPPE). Triggering for calcium signals was clearly dependent on the fluidity of the lipid monolayers. Solid DPPC and DSPC monolayers triggered the calcium signals more efficiently than the fluid DMPC monolayers did. These calcium signals became apparently more efficient in the presence of cholesterol. All of these results suggested that the rigidity of cross-linking for antigen receptors (mIgM) may be a crucial role for triggering calcium signals in B-cells.