Th1 and Th2 cytokine production is suppressed at the level of transcriptional regulation in Kawasaki disease

Kimura, Junko; Takada, Hidetoshi; Nomura, Akihiko; Ohno, Takuro; Mizuno, Yumi; Saito, Mitsumasa; Kusuhara, Koichi; Hara, Toshiro

doi:10.1111/j.1365-2249.2004.02506.x

Cited by 39 publications

(35 citation statements)

References 29 publications

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“…The levels of mRNA expression of Th1/Th2 cytokines (interferon-g (IFN-g) and interleukin-4 (IL-4)) have been analyzed, along with Th1/Th2-inducing transcription factors (T-bet and GATA-3) known to play pivotal roles in Th1/Th2 development [15 ]. In the peripheral blood mononuclear cells of patients with Kawasaki disease, a significant decrease in IFN-g mRNA levels was detected when compared with patients with other febrile diseases or healthy controls.…”

Section: Pathologymentioning

confidence: 99%

Kawasaki disease

Falcini

2006

Current Opinion in Rheumatology

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Due to earlier recognition, aggressive medical treatment, and surgical procedures, the quality of life in patients with Kawasaki disease is significantly improved. The identification of children at high risk for coronary artery aneurysms is crucial in order to reduce the occurrence of sudden death in adolescence and early adulthood. High parameters of inflammation, anemia, and low sodium and albumin levels, along with persistent unexplained fever, should alert clinicians to suspect the disease even though all clinical symptoms are lacking.

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Section: Pathologymentioning

confidence: 99%

Kawasaki disease

Falcini

2006

Current Opinion in Rheumatology

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“…A large number of T cells (increased activated CD4 T cells, depressed CD8 T cells and CD4+ CD25+ regulatory T cells), large mononuclear cells, macrophages and plasma cells, with a smaller number of neutrophils, are observed in various organ tissues of fatal cases of acute KD [102–106]. Additionally, various inflammatory cytokines and chemokines [107, 108], matrix metalloproteinases, nitric oxide production [109], autoantibody production [110, 111], and adhesive molecule expression [112, 113] are also overactivated in the acute stage of KD which are considered to facilitate vascular endothelial inflammation and then participate in the pathogenesis of KD and CAL formation. Go processes and DAVID analysis revealed that these genes are significantly enriched in immune responses which have the parallel results with clinical and laboratory findings.…”

Section: Discussionmentioning

confidence: 99%

Understanding the Pathogenesis of Kawasaki Disease by Network and Pathway Analysis

Wang

Sun

et al. 2013

Computational and Mathematical Methods in Medicine

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Kawasaki disease (KD) is a complex disease, leading to the damage of multisystems. The pathogen that triggers this sophisticated disease is still unknown since it was first reported in 1967. To increase our knowledge on the effects of genes in KD, we extracted statistically significant genes so far associated with this mysterious illness from candidate gene studies and genome-wide association studies. These genes contributed to susceptibility to KD, coronary artery lesions, resistance to initial IVIG treatment, incomplete KD, and so on. Gene ontology category and pathways were analyzed for relationships among these statistically significant genes. These genes were represented in a variety of functional categories, including immune response, inflammatory response, and cellular calcium ion homeostasis. They were mainly enriched in the pathway of immune response. We further highlighted the compelling immune pathway of NF-AT signal and leukocyte interactions combined with another transcription factor NF-κB in the pathogenesis of KD. STRING analysis, a network analysis focusing on protein interactions, validated close contact between these genes and implied the importance of this pathway. This data will contribute to understanding pathogenesis of KD.

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“…Pathologic examination of the coronary arteritis in the acute stage of KD indicates that activated T lymphocyte-dependent processes characterized by transmural infiltration of activated T lymphocytes occur with accumulation of CD8 + T cells in vascular lesions [2]. Recently altered T helper and regulatory cell functions are also implicated in dysregulation of the immune response in patients with Kawasaki disease [10,21]. BTNL2 is a member of the butyrophilin family and immunoglobulin superfamily.…”

Section: Discussionmentioning

confidence: 99%

BTNL2 gene polymorphisms may be associated with susceptibility to Kawasaki disease and formation of coronary artery lesions in Taiwanese children

et al. 2009

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The butyrophilin-like 2 (BTNL2) gene is a member of the B7 receptor family that probably functions as a T cell costimulatory molecule. Because altered T cell functions are implicated in dysregulation of the immune response seen in Kawasaki disease (KD), it is reasonable to speculate that BTNL2 gene is involved in the pathophysiology of KD. The purpose of this study was to investigate whether polymorphisms of the BTNL2 gene are associated with KD and the development of coronary artery lesions (CALs) in Taiwanese children. Nine-three patients with KD and 669 ethnically matched healthy controls were genotyped for BTNL2 gene rs1555115 C/G and rs2395158 A/G polymorphisms. The frequency of GG genotype of rs 1555115 was significantly higher in KD patients compared with controls (2.2% vs 0.2%, P = 0.012). The odds ratio for developing KD in individuals with rs 1555115 GG genotype was 14.7 (95% confidence interval, 2.04-105.5, P = 0.003) compared with individuals with rs 1555115 CG and CC genotypes. No significant difference was observed in the genotype and allelic frequencies of rs 2395158 polymorphism between KD patients and controls. However, the frequency of the G allele of rs 2395158 was significantly higher in KD patients with CALs than in those without CALs (P = 0.001). No significant difference was observed in the genotype and allelic frequencies of rs 1555115 polymorphism between KD patients with and without CALs. In conclusion, our results suggest that BTNL2 gene polymorphisms might be genetic markers of KD susceptibility and risk of coronary artery complication in Taiwanese children.

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Th1 and Th2 cytokine production is suppressed at the level of transcriptional regulation in Kawasaki disease

Cited by 39 publications

References 29 publications

Kawasaki disease

Kawasaki disease

Understanding the Pathogenesis of Kawasaki Disease by Network and Pathway Analysis

BTNL2 gene polymorphisms may be associated with susceptibility to Kawasaki disease and formation of coronary artery lesions in Taiwanese children

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