Infliximab regulates monocytes and regulatory T cells in Kawasaki disease

Koizumi, Keiichi; Hoshiai, Minako; Katsumata, Nobuyuki; Toda, Takako; Kise, Hiroaki; Hasebe, Yohei; Kono, Yoshiaki; Sunaga, Yuto; Yoshizawa, Masashi; Watanabe, Atsushi; Kagami, Keiko; Abe, Masako; Sugita, Kanji

doi:10.1111/ped.13555

Cited by 19 publications

(18 citation statements)

References 26 publications

(80 reference statements)

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“…In seven of 13 patients, the dates before PE treatment overlap with those after IFX treatment, as described in reference . The use of PE for KD and the study design were both approved by the ethics committees of the University of Yamanashi Hospital and conformed to the provisions of the Declaration of Helsinki (as revised in Tokyo 2004).…”

Section: Methodsmentioning

confidence: 99%

“…CD14 + CD16 + monocytes, T reg cells, and Th17 cells were measured using flow cytometry methods developed in our laboratory . Peripheral blood was obtained using ethylenediaminetetraacetic acid 2Na as an anticoagulant.…”

Section: Methodsmentioning

confidence: 99%

“…Notably, IVIG was shown to increase the proportion of T reg cells and expression of forkhead box P3 (FOXP3) in the acute phase of KD . Furthermore, we have previously reported that the TNF‐α blocker infliximab (IFX) downregulates CD14 + CD16 + activated monocytes and upregulates T reg cells, bringing proportions of these cells toward normal levels and thus contributing to the attenuation of inflammation .…”

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confidence: 99%

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Plasma Exchange Downregulates Activated Monocytes and Restores Regulatory T Cells in Kawasaki Disease

et al. 2018

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In Kawasaki disease (KD), the effect of plasma exchange (PE) on immune cells has not been fully elucidated. Therefore, we examined the changes in the number of CD14 + CD16 + activated monocytes, regulatory T (T reg ), and T-helper type 17 (Th17) cells in KD patients treated with PE. The percentage of total monocytes and subclasses of lymphocytes, including CD4 + and CD8 + T cells, and CD19 + B cells, showed no significant difference before and after PE. However, the percentage of CD14 + CD16 + monocytes in total leukocytes decreased significantly after PE (1.1% AE 1.5% vs. 2.1% AE 2.3%, P < 0.05). Furthermore, while the percentage of Th17 cells in CD4 + T cells did not change, the percentage of T reg cells in CD4 + T cells increased significantly after PE (11.1% AE 5.1% vs. 8.0% AE 4.4%, P < 0.05). Therefore, PE downregulates activated monocytes and upregulates T reg cells toward normal levels and thus attenuates inflammation in KD.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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confidence: 99%

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Plasma Exchange Downregulates Activated Monocytes and Restores Regulatory T Cells in Kawasaki Disease

et al. 2018

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“…In this issue of the Journal, Koizumi et al . report that regulatory T cells (Treg; CD4+ CD25+ FOXP3+) and T‐helper 17 cells (CD4 + IL‐17A+) significantly increased after IFX compared with baseline . In contrast, in a subgroup of patients with CD14+ CD16+ monocytes above the normal range before IFX, the CD14+ CD16 + monocytes significantly decreased following IFX treatment.…”

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confidence: 99%

“…In contrast, in a subgroup of patients with CD14+ CD16+ monocytes above the normal range before IFX, the CD14+ CD16 + monocytes significantly decreased following IFX treatment. IFX could downregulate activated monocytes and upregulate Treg towards the normal range . Burns et al .…”

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Infliximab for the treatment of Kawasaki disease

Matsubara

2018

Pediatrics International

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Up-regulation of miR-27a promotes monocyte-mediated inflammatory responses in Kawasaki disease by inhibiting function of B10 cells

Luo

Yang

Zhang

et al. 2019

Journal of Leukocyte Biology

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Kawasaki disease (KD) is an acute systemic vasculitis and activation of monocytes plays a central role in the pathogenesis of it. B10 cells, a B cell subset with negative regulatory properties, are functionally identified by their ability to express cytoplasmic IL-10 after ex vivo stimulation. Here, we aimed to explore the functional role of B10 cells during monocyte-mediated inflammatory responses in KD, as well as elucidate the underlying microRNA (miRNA)-mediated regulatory mechanisms. Expression of IL-10 by each group of B cells (total B cells, transitional B cells, naïve B cells, and memory B cells) and inhibition of monocyte-derived TNF-α by activated B cells were measured by flow cytometry. Expression of miRNAs (miR-21-3p, miR-98-5p/3p, miR-27a-3p, let7b-5p, and miR-1423p/5p) that affect IL-10 levels in B cells was quantitated by real-time PCR. The relationship between IL-10 and these miRNAs was examined by multivariate analysis. MiR-mediated RNA interference in B cells was performed to investigate the role of miR-27a on expression of IL-10. The results showed expression of cytoplasmic IL-10 in B cell subsets from patients with KD was down-regulated. The inhibitory effect of B10 cells on production of TNF-α by monocytes from patients with KD was also compromised. The miR-27a-3p expression was markedly up-regulated during the acute phrase of KD, and it promoted monocyte-mediated TNF-α release by negatively regulating expression of cytoplasmic IL-10 within B cells in vitro. The data suggest up-regulated miR-27a in B cells from patients with KD may promote monocyte-mediated inflammatory responses by inhibiting the regulatory function of B10 cells.

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Infliximab regulates monocytes and regulatory T cells in Kawasaki disease

Abstract: IFX could downregulate activated monocytes and upregulate T cells towards the normal range. IFX treatment thus contributes to the process of attenuating inflammation in KD.

Cited by 19 publications

References 26 publications

Plasma Exchange Downregulates Activated Monocytes and Restores Regulatory T Cells in Kawasaki Disease

Plasma Exchange Downregulates Activated Monocytes and Restores Regulatory T Cells in Kawasaki Disease

Infliximab for the treatment of Kawasaki disease

Up-regulation of miR-27a promotes monocyte-mediated inflammatory responses in Kawasaki disease by inhibiting function of B10 cells

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