Abstract
Nuclear receptor 4a3 (Nr4a3) is a transcription factor implicated in various settings such as vascular biology and inflammation. We have recently shown that mast cells dramatically upregulate Nuclear receptor 4a3 upon activation, and here we investigated the functional impact of Nuclear receptor 4a3 on mast cell responses. We show that Nuclear receptor 4a3 is involved in the regulation of cytokine/chemokine secretion in mast cells following activation via the high affinity IgE receptor. Moreover, Nuclear receptor 4a3 negatively affects the transcript and protein levels of mast cell tryptase as well as the mast cell’s responsiveness to allergen. Together, these findings identify Nuclear receptor 4a3 as a novel regulator of mast cell function.
Highlights
Mast cells are important components of the innate and adaptive immune system, most notably taking part in the defense against parasites, bacteria and viruses [1,2]
Nuclear receptor 4a3 (Nr4a3) is Required for Optimal FceRI-induced Cytokine/ Chemokine Generation in Mast Cells
To study the influence of Nr4a3 on mast cell function we cultured bone-marrow cells isolated from wild type (WT) and Nr4a3-deficient mice in the presence of IL-3, which results in maturation of precursor cells into mast cells, i.e. bone marrow-derived mast cells (BMMCs)
Summary
Mast cells are important components of the innate and adaptive immune system, most notably taking part in the defense against parasites, bacteria and viruses [1,2]. In a subsequent study we showed that Nr4a members, in particular Nr4a3, were strongly induced by mast cell activation through FceRI crosslinking [20]. We show that Nr4a3 is required for optimal cytokine generation following antigeninduced mast cell activation.
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