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PKCθ: a new target for selective immunosuppression

Immune functions of PKCq Members of the PKC enzyme family play a critical role in diverse intracellular signaling pathways leading to cell proliferation, activation, differentiation, survival and death. Among the ten members of this family, which are divided into three subfamilies based on their domain structure and cofactor requirements, PKCq has attracted particular interest, especially among immunologists and T-cell biologists, owing largely to the fact that, unlike other family members, PKCq is expressed preferentially in T lymphocytes [1,2]. Early in vitro characterization of PKCqdeficient (Prkcq) mice and their T cells revealed that the mature peripheral T cells of these mice display a severe defect in T-cell proliferation and IL-2 production [3]. The underlying molecular basis resides in the highly impaired activation of two transcription factors that are critical for productive T-cell activation and which are now known to be targets of PKCq: NF-kB and AP-1 [3]. Later studies demonstrated that the T-cell receptor (TCR)-stimulated Ca signaling pathway, including activation of the transcription factor NFAT, also represents a PKCq target, although it is substantially less affected by Prkcq deletion [4]. Indeed, residual NFAT activity, which is required for the induction of T-cell anergy, may account for the anergic-like phenotype of Prkcq T cells [5]. Interestingly, PKCq is not overtly required for T-cell development in the thymus [3,4], perhaps reflecting some redundancy with another family member, PKCh [6]. The seemingly global requirement of PKCq for T-cell activation, apparent from the early in vitro studies, has raised doubts about its utility as a drug target due to the perceived ability of potential PKCq inhibitors to induce global, potentially hazardous immunosuppression, similar to immunosuppressive drugs such as calcineurin inhibitors (e.g., cyclosporin A), which render treated patients susceptible to infections.