The elevated serum levels of calcineurin and nuclear factor of activated T-cells 1 in children with Kawasaki disease

Abstract

Background: The calcineurin and nuclear factor of activated T-cells (CaN-NFAT) signaling pathway had been found to be associated with Kawasaki disease (KD) susceptibility and coronary artery aneurysm formation as a contributor. To evaluate serum calcineurin (CaN) and nuclear factor of activated T-cells 1(NFAT1) levels in patients with Kawasaki disease (KD).Methods: Serum levels of CaN and NFAT1 were measured by enzyme-linked immunosorbent assay method in 66 healthy children and 74 KD patients at acute, afebrile and subacute stage.Results: The serum levels of CaN and NFAT1 increased significantly in the acute stage, and decreased progressively in the afebrile and subacute stage, along with the reduction of C-reactive protein, white blood cells and neutrophil counts. And in the acute stage, the afebrile stage and the subacute stage, the expression of CaN and NFAT1 was upregulated significantly in KD patients compared to that in the healthy control. After the IVIG treatment, the serum levels of CaN and NFAT1 declined significantly in IVIG responders. However, the CaN and NTAT1 levels in the IVIG non-responders declined slowly. And in the afebrile stage, the NFAT1 levels were lower in KD patients with coronary artery lesions (CALs) (268.82 ± 11.96 ng/ml) than those without CALs (285.84 ± 25.13 ng/ml). However, the serum levels of CaN in KD patients with CALs had no significant difference with those in KD patients without CALs. Conclusions: The specific regulation of CaN and NFAT1 serum levels in the course of KD was suggested that both of them were related in the development of KD.

Combined Single Nucleotide Variants of ORAI1 and BLK in a Child with Refractory Kawasaki Disease

“…Recent observation confirmed the involvement of this pathway in KD, demonstrating that the serum levels of calcineurin and NFAT increased significantly in the acute stage and decreased progressively in the afebrile and subacute stage, reducing the CRP, white blood cell, and neutrophil counts [ 22 ]. Furthermore, an in vitro study using cultured endothelial cells of the coronary artery also suggested that the activation of the calcineurin/NFAT signaling pathway plays a vital role in causing the inflammation of the endothelial cells; Wang et al demonstrated that the serum of KD patients promoted the proliferation of coronary artery endothelial cells not only morphologically but also by increasing the expression of proteins involved in cell proliferation and proteins constituting the calcineurin/NFAT signaling pathway.…”

Mycoplasma genitalium Protein of Adhesion Suppresses T Cell Activation via CypA-CaN-NFAT Pathway

“…The CaN-NFAT signaling pathway plays a crucial role in promoting the expression of cytokines, such as IL-2 and IFN-γ, leading to the activation of T cells ( 32 ). Downregulation of CaN phosphorylation inhibits NFAT from entering the nucleus, inhibiting T cells activation.…”