Voltage-dependent calcium channels (Cav1) contribute to T-cell activation. The inventors previously showed that Th2 cells co-express Cav1.2 and Cav1.3 calcium channels acting in a non-redundant and concerted way to initiate early TCR-driven calcium influx required for cytokine production and Th2-cell functions. While they have demonstrated that both channels have to be present on the same T-cell to induce allergic asthma, how these channels are regulated under TCR engagement is yet unknown. They investigated the relationship between PKCα and the Cav1.2/Cav1.3 duo channels in Th2 cells. They showed that PKC activation was sufficient to trigger Cav1-dependent calcium response and Th2 cytokine production. Cav1 channels, and especially Cav1.3, expression increased at the cell membrane of Th2 cells upon TCR stimulation and PKCα selectively associated with Cav1.3 upon activation. They showed that PKCα antisense oligonucleotides (PKCα-AS) decreased Th2-cell functions and were beneficial in active and passive models of Th2-mediated airway inflammation induced by OVA. Altogether these results show that PKCα by interacting selectively with Cav1.3 after TCR engagement regulates Cav1.2/Cav1.3 duo-dependent calcium signaling and probably by this way impairs Th2-cell functions and their potential to mediate inflammation.