Increased regulatory T cells and eosinophils characterize atopic dermatitis–like graft-versus-host disease compared with lichen planus–like graft-versus-host disease

Li, Kun; Mu, Zhanglei; Wen, Guangdong; Zhao, Yan; Xu, Cong; Zhang, Jianzhong

doi:10.1016/j.jaad.2019.08.005

Cited by 14 publications

(23 citation statements)

References 28 publications

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“…Figure 3D illustrates the interaction among these signaling pathways (Figure 3C). In addition, Figure 3E confirmed that lnc‐AC145676.2.1‐6‐3 was associated with “Inflammatory pain” and “Dermatitis, Atopic” (Figure 3D), which have also been reported to be associated with aGVHD 18,19 . Next, luciferase reporters were used to verify the lnc‐AC145676.2.1‐6‐3/hsa‐miR‐3064‐5p/IL‐1β relationship (Figure 3E).…”

Section: Resultssupporting

confidence: 56%

“…In addition, Figure 3E confirmed that lnc-AC145676.2.1-6-3 was associated with "Inflammatory pain" and "Dermatitis, Atopic" (Figure which have also been reported to be associated with aGVHD. 18,19 Next, luciferase reporters were used to verify the lnc-AC145676.2.1-6-3/hsa-miR-3064-5p/IL-1β relationship (Figure 3E). Taken together, these bioinformatic enrichment results suggest that lnc-AC145676.2.1-6-3 is a potential regulator of aGVHD.…”

Section: Construction Of the Lncrna-mirna-mrna Interaction Networkmentioning

confidence: 99%

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lnc‐AC145676.2.1‐6‐3 plays an important role in intestinal acute graft‐versus‐host disease through the regulation of interleukin‐1β

Sun

Xia

Liu

et al. 2022

Int J Lab Hematology

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Introduction Acute graft‐versus‐host disease (aGVHD) is one of the major complications of allogeneic hematopoietic stem cell transplantation, and the liver, skin, and gastrointestinal tract are the main target organs. The most common type is intestinal aGVHD. Long noncoding RNAs (lncRNAs) have coregulatory functions and participate in a variety of intracellular regulatory processes. We investigated the expression of lncRNAs and their mechanisms in the development of aGVHD. Methods The participants included 15 patients with aGVHD and 4 healthy controls (HCs). To generate profiles of abnormally expressed lncRNAs, peripheral blood mononuclear cell (PBMC) lncRNAs from four patients and four HCs were validated by high‐throughput sequencing and quantitative real‐time‐PCR (qRT‐PCR). A number of databases, including Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, miRanda, TargetScan, and Metascape, were used for bioinformatics analysis. Bioinformatics analysis indicated that overexpression of lnc‐AC145676.2.1‐6‐3 might induce aGVHD via the interleukin (IL)‐1β axis and a downstream miRNA. After the higher levels of lnc‐AC145676.2.1‐6‐3 in other patients were confirmed by qRT‐PCR, serum IL‐1β, IL‐6, and tumor necrosis factor‐α were measured by enzyme linked immunosorbent assays. Results In our study, a large number of lncRNAs were found in PBMCs of patients with intestinal aGVHD, and bioinformatics analysis showed that the upregulated lncRNA lnc‐AC145676.2.1‐6‐3 probably affected the progression of intestinal aGVHD by regulating the hsa‐miR‐3064‐5p/IL‐1β axis. In addition, the changes in lncRNA expression levels were positively correlated with the clinical characteristics of intestinal aGVHD. Conclusion Our results suggest that lncRNAs in PBMCs may become new biomarkers and therapeutic targets for intestinal aGVHD.

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Section: Resultssupporting

confidence: 56%

Section: Construction Of the Lncrna-mirna-mrna Interaction Networkmentioning

confidence: 99%

lnc‐AC145676.2.1‐6‐3 plays an important role in intestinal acute graft‐versus‐host disease through the regulation of interleukin‐1β

Sun

Xia

Liu

et al. 2022

Int J Lab Hematology

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“…Cutaneous cGVHD is mediated by the activation of alloreactive donor T cells, a defect of CD4 + Foxp3 + CD25 + regulatory T cells (Tregs) 5 , a profound disruption of B cell homeostasis, and pathological tissue repair with fibrosis 3 . Although lichenoid cGVHD has been associated with a mixed Th1/Th17 signature and sclerotic cGVHD with a Th1 signature, other T cell subsets may contribute to its pathogenesis 6,7 . Despite pathogenic and clinical heterogeneity, treatment of cGVHD relies mainly on the severity of the skin involvement.…”

Section: Clinical Trial Registration Information (If Any)mentioning

confidence: 99%

“…In LP cGVHD, "IFN signaling" as well "Th1" and "Th2" pathways were predicted to be activated (Figure 2C). Although lichenoid cGVHD is currently defined by a mixed Th1/Th17 signature, a recent study suggested that the Th2 pathway may also be involved 6,7 . In morphea cGVHD, "IFN signaling" as well as "Th1 and Th2 pathways" were also predicted to be activated (Figure 2D).…”

Section: Common and Specific Molecular Features Of Lp And Morphea Cgvhdmentioning

confidence: 99%

RNA sequencing of chronic GVHD skin lesions defines shared and unique inflammatory pathways characterizing lichen planus and morphea

et al. 2022

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Cutaneous involvement of chronic graft-versus-host disease (cGVHD) has a wide range of manifestations including a lichenoid form with a currently assumed mixed Th1/Th17 signature and a sclerotic form with Th1 signature. Despite substantial heterogeneity of innate and adaptive immune cells recruited to the skin and of the different clinical manifestations, treatment depends mainly on the severity of the skin involvement, and relies on systemic, high-dose glucocorticoids alone or in combination with a calcineurin inhibitor. We performed the first study using RNAseq to profile and compare the transcriptome of lichen planus cGVHD (n=8), morphea cGVHD (n=5), and healthy controls (n=6). Our findings revealed shared and unique inflammatory pathways to each cGVHD subtype that are both pathogenic and targetable. In particular, the deregulation of IFN signaling pathway was strongly associated with cutaneous cGVHD, whereas the triggering receptor expressed on myeloid cells-1 (TREM-1) pathway was found to be specific of lichen planus and likely contributes to its pathogenesis. The results were confirmed at a protein level by performing immunohistochemistry staining and at a transcriptomic level using Real-Time quantitative PCR.

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“…Furthermore, more diversity was lost at the lesional site than the unaffected site in patients with AD-like GVHD, but not in patients with LP-like GVHD. Previous studies have shown that, for AD-like GVHD and LP-like GVHD conditions, both patients had elevated Th2 cells and impaired skin barrier, whereas the counts of eosinophils, Th17 cells, and Treg cells only increased under the former condition (38,39). According to recent work, intestinal microbiota can induce GVHD by influencing the Treg/Th17 balance (37,40).…”

Section: Discussionmentioning

confidence: 93%

Alteration in the Skin Microbiome in Cutaneous Graft Versus Host Disease

Gu¹,

Sun²,

Li³

et al. 2021

Acta Derm Venereol

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Graft-versus-host disease is a severe adverse effect of haematopoietic stem cell transplantation and has a high rate of mortality. The skin is one of the major organs affected. This study represents the first comprehensive analysis of the skin microbiome in patients with graft-versus-host disease. The results indicate that graft-versus-host disease skin exhibits a less diverse skin microbiome compared with healthy skin, with a greater overall abundance of Staphylococcus. The abnormal skin microbiome in graft-versus-host disease dysbiosis may help in our understanding of the pathogenesis of cutaneous graft-versus-host disease. Graft-versus-host disease (GVHD) is a common complication of haematopoietic stem cell transplantation. This study examined the cutaneous microbiome in relation to the pathogenesis of cutaneous GVHD. Bacterial swabs were taken from several sites on 12 patients with cutaneous GVHD. Microbiotas were characterized by sequencing 16S rRNA bacterial genes on the MiSeq platform. Microbiome diversity in patients with cutaneous GVHD was reduced compared with healthy controls. GVHD was related to an increased abundance of Firmicutes and a reduction in Actinobacteria, especially in lesions. Non-parametric multivariate analysis of variance revealed that the skin microbial community disorders in patients with GVHD correlated with several clinical features of cutaneous GVHD. This study indicates that changes in the cutaneous microbiota in lesions could play a key role in the pathogenesis of cutaneous GVHD. Further studies are needed to explore the mechanistic relevance of these microbial dynamics, which may provide new clues to therapeutic interventions.

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Increased regulatory T cells and eosinophils characterize atopic dermatitis–like graft-versus-host disease compared with lichen planus–like graft-versus-host disease

Cited by 14 publications

References 28 publications

lnc‐AC145676.2.1‐6‐3 plays an important role in intestinal acute graft‐versus‐host disease through the regulation of interleukin‐1β

lnc‐AC145676.2.1‐6‐3 plays an important role in intestinal acute graft‐versus‐host disease through the regulation of interleukin‐1β

RNA sequencing of chronic GVHD skin lesions defines shared and unique inflammatory pathways characterizing lichen planus and morphea

Alteration in the Skin Microbiome in Cutaneous Graft Versus Host Disease

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