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Dendritic Cells (DCs) are highly potent Antigen-Presenting Cells (APCs) that have a key role in mediating tolerance or immunity to self and non-self antigens. In their immature stage DCs are highly phagocytic and undergo a maturation process after taking up an antigen. DC maturation is characterized by activation of mechanisms of antigen presentation, increased expression of Major Histocompatibility Complex (MHC) class II and co-stimulatory molecules in the plasma membrane, and secretion of cytokines and chemokines. Despite the fact that the role of calcium (Ca2+) in DC function has been clearly established, regulation of Ca2+ signals in these cells is not well known. However, recently it has been demonstrated that functional capacitative Ca2+ release-activated Ca2+ (CRAC), Transient Receptor Potential (TRP) Melastatin- 2 (TRPM2), and TRP Vanilloid- 1 (TRPV1) channels are critical for mouse DC maturation and migration. Also, Ryanodine Receptor-1 (RyR1) signaling activated by L-type Ca2+ channel CaV1.2 cause rapid MHC- II expression in the plasma membrane of DCs. The understanding of the regulation of Ca2+ signals in DCs is essential to potentially be able to modulate DC functions in disease processes. Therefore, in this review, we discuss recent studies on the expression and roles of Ca2+ channels in DC biology and function.

Regulation of Murine Dendritic Cell Functions by Calcium Channels