IL-10-Producing B Cells Regulate T Helper Cell Immune Responses during 1,3-β-Glucan-Induced Lung Inflammation

Liu, Fangwei; Lu, Xiaowei; Dai, Wujing; Lu, Yiping; Li, Chao; Du, Shuyan; Chen, Ying; Wu, Dong; Chen, Jie

doi:10.3389/fimmu.2017.00414

Cited by 8 publications

(8 citation statements)

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“…31 Tregs are generally viewed as a suppressor of Th1 immune responses in various inflammatory diseases. 32,33 However, our finding contradicts the result acquired by Liu et al 20 Differences in the genetic background or the microbiome in the animal may lead to these divergent results; moreover, the discrepant results may also be related to Th1 lymphocyte plasticity. 34,35 Although we observe a decrease in Th1 immune responses following LPS-induced pulmonary damage in Treg-depleted mice, we could not exclude the possibility that the kinetics of their elevation presence in the lungs when the observed time points were prolonged.…”

Section: Discussioncontrasting

confidence: 99%

“…Tregs are generally viewed as a suppressor of Th1 immune responses in various inflammatory diseases . However, our finding contradicts the result acquired by Liu et al . Differences in the genetic background or the microbiome in the animal may lead to these divergent results; moreover, the discrepant results may also be related to Th1 lymphocyte plasticity .…”

Section: Discussioncontrasting

confidence: 94%

“…Previous studies on Treg depletion used Foxp3 DTR mice and intraperitoneal administration of diphtheria toxin or anti‐CD25 neutralization. As CD25 mAb (PC61 mAb) has been confirmed to deplete Foxp3 + Tregs and PC61 has been shown to cause a significant reduction in Foxp3 + Tregs by phagocytes via Ab‐dependent cellular cytotoxicity . In our study, we employed the widely used and easily approachable strategy of PC61 anti‐CD25 mAb treatment to deplete CD4 + FOXP3 + Tregs prior to LPS administration in mice.…”

Section: Discussionmentioning

confidence: 99%

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Regulatory T‐cells promote pulmonary repair by modulating T helper cell immune responses in lipopolysaccharide‐induced acute respiratory distress syndrome

et al. 2019

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Summary Acute respiratory distress syndrome (ARDS) induces a strong local infiltration of regulatory T‐cells (Tregs) in the lungs. However, at present, there remains a lack of adequate evidence showing the direct effect of Tregs on pulmonary repair and the related mechanisms of ARDS. Therefore, in this project, we studied the impact of Tregs on lipopolysaccharide (LPS)‐induced ARDS and pulmonary inflammation. Surprisingly, we found that depletion of Tregs by injection of PC61 anti‐CD25 antibody not only interfered with the inflammation resolution, such as inhibited total cell infiltration into the alveolar space, downregulated neutrophils, upregulated macrophages, but also impaired pulmonary epithelium and endothelial cell proliferation. Consistent with the attenuation of pulmonary repair, we found that the Th1 and Th17 immune responses were also impaired in Treg‐depleted mice, suggesting that the presence of Tregs is vital for tissue repair, as Tregs modulate and promote the Th immune response in LPS‐induced pulmonary inflammation.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

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Regulatory T‐cells promote pulmonary repair by modulating T helper cell immune responses in lipopolysaccharide‐induced acute respiratory distress syndrome

et al. 2019

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“…Th1 is inhibited by B cells [9], and EBF3 is an essential factor for B cell maturation [3]. Nonetheless, the role of B cells in Th1/Th2 imbalance, i.e., the change from Th1 dominance to Th2 dominance, in PBL remains unclear.…”

Section: Xiaohong Yangmentioning

confidence: 99%

Associations of Pulmonary Fibrosis with Peripheral Blood Th1/Th2 Cell Imbalance and EBF3 Gene Methylation in Uygur Pigeon Breeder’s Lung Patients

Wu¹,

Luo²,

Pang³

et al. 2018

Cell Physiol Biochem

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Background/Aims Pigeon breeder’s lung (PBL) results from Th1/Th2 cell imbalance. B cells inhibit the immune activity of Th1, and EBF3 is a key B cell factor. This study explored the relationship between EBF3 and Th1/Th2 imbalance in chronic PBL cases complicated with pulmonary fibrosis (PF). Methods Twenty Uygur PBL+PF patients, 20 pigeon breeders without PBL or PF, and 20 healthy individuals without pigeon breeding history constituted the patient I, negative control, and normal control groups, respectively. Peripheral blood specimens and case backgrounds were collected between June 2016 and March 2017. EBF3 gene methylation was analyzed by matrix assisted laser desorption ionization-time of flight mass spectrometry. To compare different mechanisms of PF progression in PBL, samples from 20 Uygur PBL patients without PF (at acute and sub-acute stages) were collected between October 2017 and February 2018, constituting the patient II group. EBF3 mRNA expression was evaluated by real-time polymerase chain reaction. IFN-γ, IL-4 and IL-10 expression and Th1/Th2 imbalance in PBL were evaluated by enzyme-linked immunosorbent assay and flow cytometry. Results CpG-2 and general methylation rates in the patient I group were lower than those in the control groups (P˂0.017). The level of EBF3 mRNA expression in the patient I group was significantly higher than that in any other group. Compared with the control groups, the patient I group showed a significantly higher level of IL-4, whereas the patient II group showed a significantly lower level. IL-10 was also expressed more highly in the patient I group than in any other group (P< 0.01). Flow cytometry showed INF-γ dominance (Th1 cytokine) in PBL at the acute/sub-acute stage and IL-4 dominance (Th2 cytokine) at the chronic stage after PF occurred. The general methylation rate was negatively correlated with the mRNA level, with the latter being positively correlated with the IL-10 level and number of pigeons bred in the past 3 months. IL-4 expression was negatively correlated with INF-γ but positively correlated with PF area and duration of pigeon breeding history. Conclusions After PF occurs in chronic PBL, the inflammation type changes from Th1 dominance to Th2 dominance. During PBL development, IL-10 increases before IL-4 does, which may be associated with EBF3 hypomethylation and the involvement of B lymphocytes.

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“…In order to clarify the regulative mechanism of 1, 3-β-glucan induced IL-10-producing B cells on Teff and Treg respectively, the comprehensive experiments in vitro were carried out. Anti-CD22 mAb was used to restrict the induction of IL-10-producing B cells as previous [23][24][25]. Teff(CD4 + CD25 -), Treg(CD4 + CD25 + ), macrophages and B cells(CD19 + ) were isolated from different group mice.…”

Section: Introductionmentioning

confidence: 99%

IL-10 producing B cells regulated 1,3-β-glucan induced Th responses in coordinated with Treg

Zhang

Liu

2021

Immunology Letters

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Background: Repeated exposure to fungi contaminated dust can lead to multiple adverse effect on lung, such as hypersensitivity pneumonitis, granuloma even irreversible brosis. 1,3-β-glucan, as the major cell wall component of fungi, was considered as its exposure biomarker. Existing studies showed that series of Th response were involved in 1,3-β-glucan induced hypersensitivity pneumonitis, in which macrophages, regulatory T cells (Treg) and IL-10 producing B cells were reported to participate. The reciprocal interaction among those critical immune cells in 1,3-β-glucan induced in ammation were not investigated yet.Results: To clarify the regulatory mechanism of IL-10 producing B cells on Th and Treg, current study set up a primary cell co-culture system. Anti-CD22 antibody was injected intraperitoneally to generate IL-10 producing B cells de ciency mouse model. Cells were isolated and puri ed from different groups' mice.Flow cytometry was used to check the phenotype of different cell subtypes. CBA assay and realtime PCR were used to examine the levels of multiple cytokines. Our results indicated that IL-10 producing B cells were involved in modulating 1,3-β-glucan induced in ammatory response. The modulation of IL-10 producing B cells on Th response after 1,3-β-glucan treatment was independent on cell-cell contact.What's more, the modulation pattern of IL-10 producing B cells might be impaired without Treg response.Conclusions: IL-10-producing B cells regulated 1,3-β-glucan induced Th responses in coordinated with Treg.

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IL-10-Producing B Cells Regulate T Helper Cell Immune Responses during 1,3-β-Glucan-Induced Lung Inflammation

Cited by 8 publications

References 50 publications

Regulatory T‐cells promote pulmonary repair by modulating T helper cell immune responses in lipopolysaccharide‐induced acute respiratory distress syndrome

Regulatory T‐cells promote pulmonary repair by modulating T helper cell immune responses in lipopolysaccharide‐induced acute respiratory distress syndrome

Associations of Pulmonary Fibrosis with Peripheral Blood Th1/Th2 Cell Imbalance and EBF3 Gene Methylation in Uygur Pigeon Breeder’s Lung Patients

IL-10 producing B cells regulated 1,3-β-glucan induced Th responses in coordinated with Treg

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