B Lymphocytes Regulate Dendritic Cell (Dc) Function in Vivo

TLDR

Dendritic cells are the primary antigen‑presenting cells, yet evidence suggests B lymphocytes may be required for optimal T‑cell sensitization. The study aimed to determine whether B cells influence the Th1/Th2 balance by modulating dendritic cell function. Researchers compared immune responses in wild‑type and B‑cell‑deficient μMT mice using antigen emulsified in adjuvant or pulsed on splenic dendritic cells, and transferred antigen‑pulsed DCs from each genotype to assess T‑cell priming. B‑cell deficiency altered cytokine profiles: μMT mice produced IL‑12p70 and failed to induce IL‑4 from T cells, whereas wild‑type mice promoted IL‑4, indicating B lymphocytes regulate dendritic cell capacity to favor a balanced Th1/Th2 response.

Abstract

Increasing evidence indicates that dendritic cells (DCs) are the antigen-presenting cells of the primary immune response. However, several reports suggest that B lymphocytes could be required for optimal T cell sensitization. We compared the immune responses of wild-type and B cell-deficient (μMT) mice, induced by antigen emulsified in adjuvant or pulsed on splenic dendritic cells. Our data show that lymph node cells from both control and μMT animals were primed, but each released distinct cytokine profiles. Lymph node T cells from control animals secreted interferon (IFN)-γ, interleukin (IL)-2, and IL-4, whereas those from μMT mice produced IFN-γ and IL-2 but no IL-4. To test whether B cells may influence the T helper cell type 1 (Th1)/Th2 balance by affecting the function of DCs, we immunized mice by transferring antigen-pulsed DCs from wild-type or mutant mice. Injection of control DCs induced the secretion of IL-4, IFN-γ, and IL-2, whereas administration of DCs from μMT animals failed to sensitize cells to produce IL-4. Analysis of IL-12 production revealed that DCs from μMT mice produce higher levels of IL-12p70 than do DCs from wild-type animals. These data suggest that B lymphocytes regulate the capacity of DCs to promote IL-4 secretion, possibly by downregulating their secretion of IL-12, thereby favoring the induction of a nonpolarized immune response.