Contractile activity of human follicular dendritic cells.

Follicular dendritic cells (FDCs) present antigens to B cells in the lymphoid follicle and inhibit B-cell apoptosis. In previous work, we obtained human FDC lines that allowed us to study the antigen phenotype and functions of these cells, finding that they expressed α-smooth muscle (SM) actin (a protein involved in cell contraction) and were able to contract collagen gel matrixes in gel contraction assays. Actin polymerization associated with cell contractility is essential for many cellular functions. We report here that interleukin (IL)-2 and interferon (IFN)-γ increased FDC contractility, and IL-10 reduced contractility, whereas IL-4 had no effect. Tumor necrosis factor (TNF) and lymphotoxin (LT)-α1β2, cytokines involved in FDC differentiation, also increased FDC contractility. In different cell systems, cell contraction is related with the incorporation of α-SM actin into stress fibers. By confocal microscopy, we showed that cytochalasin D, an inhibitor of actin polymerization, inhibited α-SM actin incorporation and relaxed FDCs. Likewise, IL-10 significantly decreased the proportion of FDCs with α-SM actin-positive stress fibers, whereas cytokines that increased FDC contractility also increased this proportion. However, none of the cytokines tested significantly affected α-SM actin expression as determined by flow cytometry. IL-10, in addition to decreasing FDC contractility, increased the inhibitory activity of FDC in spontaneous B-cell apoptosis (P<0.05), but the other cytokines did not affect this activity. We conclude that cytokines related with FDC physiology regulate the contractility of these cells, and IL-10 also regulates the effect of FDC on B-cell apoptosis.