| Summary: | <p>Abstract</p> <p>Ceramide kinase (CERK) produces the bioactive lipid ceramide-1-phosphate (C1P) and is a key regulator of ceramide and dihydroceramide levels. It is likely that CERK and C1P play a role in inflammatory processes but the cells involved and the mechanisms used remain to be clarified. In particular, the impact of CERK on T-cell biology has not been studied so far. Here, we used <it>Cerk</it><sup>-/- </sup>mice backcrossed with DO11.10/RAG1<sup>-/- </sup>mice to probe the effect of CERK ablation on T-cell activation. Levels of interleukin (IL)-2, IL-4, IL-5, IL-13, of tumor necrosis factor (TNF)-α, and of interferon (INF)-γ were recorded following ovalbumin challenge in vivo and using ovalbumin-treated splenocytes ex- vivo. Absence of CERK led to a significant decrease in the production of IL-4, thus suggesting that CERK may polarize T cells towards the T<sub>H</sub>2 cell subtype. However, the importance of CERK to T<sub>H</sub>2 cell biology will have to be investigated further because in a model of asthma, which is T<sub>H</sub>2-cell driven, <it>Cerk</it><sup>-/- </sup>mice responded like wild-type animals.</p>
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