Abstract
Background Kawasaki disease (KD) is a childhood multisystemic vasculitis resulting in the development of coronary aneurysms. Functional polymorphism in Inositol 1,4,5-triphosphate kinase C (ITPKC) has recently been identified and linked to KD susceptibility and severity. ITPKC acts as a negative regulator of T-cell activation through the inhibition of Ca/Nuclear factor of activated T-cells (NFAT) signalling pathway. Lactobacillus casei cell wall extract induced coronary arteritis is an animal model of KD dependent on superantigenic activity.
Highlights
Kawasaki disease (KD) is a childhood multisystemic vasculitis resulting in the development of coronary aneurysms
ITPKC acts as a negative regulator of T-cell activation through the inhibition of Ca2+/Nuclear factor of activated T-cells (NFAT) signalling pathway
ITPKC and the Ca2+/NFAT signalling pathway were activated in lymphocytes following superantigen stimulation, inhibition of ITPKC was not able to alter lymphocyte activation or Ca2+ flux pointing to overlapping or compensatory pathways
Summary
Kawasaki disease (KD) is a childhood multisystemic vasculitis resulting in the development of coronary aneurysms. Functional polymorphism in Inositol 1,4,5-triphosphate kinase C (ITPKC) has recently been identified and linked to KD susceptibility and severity. ITPKC acts as a negative regulator of T-cell activation through the inhibition of Ca2+/Nuclear factor of activated T-cells (NFAT) signalling pathway. Lactobacillus casei cell wall extract induced coronary arteritis is an animal model of KD dependent on superantigenic activity. Superantigen activated human lymphocyte cell line could not completely inhibit cytokine production or Ca2+ flux
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