directly inhibit the FcεRI-dependent degranulation of mast cells (Gri et al., [@B14]). This effect was achieved by Treg--mast cell contact leading to OX40--OX40L engagement, respectively (Figure [2](#F2){ref-type="fig"}). Suppression was associated with increased cAMP and decreased Ca^2+^ influx, unrelated to PLC-γ2 or intracellular Ca^2+^ stores. Furthermore, abrogation of cAMP increase essentially reversed the impact of Treg on mast cells. The physiological outcome of mast cell suppression was confirmed *in vivo* by the observation that interference with Treg function resulted in exacerbation of anaphylaxis. An elegant mechanistical insight was provided in a subsequent work, in which time-lapse video microscopy and transmission electron microscopy were used to record interactions on a single-cell level (Frossi et al., [@B11]). Co-cultures of mast cells with wild type, but not OX40-deficient, Treg resulted in morphological changes that indicated defective exocytosis, along with inhibition of degranulation and of Ca^2+^ mobilization. Thus, an "Immunological synapse" between the two cell types was convincingly visualized. Intriguingly, these observations have led to the finding that soluble OX40 is sufficient to mimic the inhibitory effects of Treg (Sibilano et al., [@B30]), providing a potentially novel therapeutic approach in allergic diseases.

In summary, we would like to suggest that mast cells can be utilized by T cells in order to enhance the physiological effects of the latter. Although T cells demonstrate considerable mast cell-independent activity, it seems that mast cells are required to obtain an optimal response. This conclusion is based on data provided by studies on both effector and Treg. Nevertheless, it should be noted, that the role of these cell types may be contradictory, thus leading to effects such as T (regulatory) cell counteracting mast cell function.

Conflict of Interest Statement
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The authors declare that the research was conducted in the absence of any