Increasing CCL5/CCR5 on CD4+ T cells in peripheral blood of oral lichen planus

Hu, Jingyu; Zhang, Jing; Cui, Ji-Li; Liang, Xinyi; Li, Rui; Du, Ge-Fei; Xu, Xueyi; Zhou, Gang

doi:10.1016/j.cyto.2013.01.020

Cited by 58 publications

(51 citation statements)

References 36 publications

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“…Our previous work has that shown miR-125a is downregulated in the peripheral CD3 þ T cells of SLE patients 27 . Interestingly, miR-125a was also downregulated in oral lichen planus, which is a T-cell-mediated autoimmune disease of oral mucosa 28 . In this study, we further identified miR-125a as a commonly downregulated miRNA in peripheral CD4 þ T cells of multiple human autoimmune diseases such as SLE and CDs, as well as ARTICLE their related animal disease models.…”

Section: Discussionmentioning

confidence: 99%

MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis

et al. 2015

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Although different autoimmune diseases show discrete clinical features, there are common molecular pathways intimately involved. Here we show that miR-125a is downregulated in peripheral CD4 þ T cells of human autoimmune diseases including systemic lupus erythematosus and Crohn's disease, and relevant autoimmune mouse models. miR-125a stabilizes both the commitment and immunoregulatory capacity of Treg cells. In miR-125a-deficient mice, the balance appears to shift from immune suppression to inflammation, and results in more severe pathogenesis of colitis and experimental autoimmune encephalomyelitis (EAE). The genome-wide target analysis reveals that miR-125a suppresses several effector T-cell factors including Stat3, Ifng and Il13. Using a chemically synthesized miR-125a analogue, we show potential to re-programme the immune homeostasis in EAE models. These findings point to miR-125a as a critical factor that controls autoimmune diseases by stabilizing Treg-mediated immune homeostasis.

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Section: Discussionmentioning

confidence: 99%

MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis

et al. 2015

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“…CCL5/CCR5 interaction has been reported in a number of Th1-associated diseases, such as rheumatoid arthritis, multiple sclerosis [32], human immunodeficiency virus 1 (HIV-1) infection [33], Crohn’s disease [7], and oral lichen planus [8]. In this study, for mRNA levels of CCL5 in PBMCs, no significant difference was found between any group; however, plasma levels of CCL5 in active ITP patients was lower than in controls, perhaps because platelets are the principal source of CCL5 [34].…”

Section: Discussionmentioning

confidence: 99%

“…For example, chemokine CCL5 is not only required for attracting CCR5 + T cells but is also essential for their activation [5]. CCR5 is specifically expressed on Th1 cells and has been reported as a critical chemokine receptor in several autoimmune diseases with polarization of Th1 cells such as rheumatoid arthritis, multiple sclerosis, Crohn’s disease and oral lichen planus [6–8]. CXCL10 expression is essential for Th1 cell differentiation [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Pulsed high-dose dexamethasone modulates Th1-/Th2-chemokine imbalance in immune thrombocytopenia

et al. 2016

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BackgroundChemokines and chemokine receptors play important roles in autoimmune diseases; however, their role in immune thrombocytopenia (ITP) is unclear. High-dose dexamethasone (HD-DXM) may become a first-line therapy for adult patients with ITP, but the effect of HD-DXM on chemokines in ITP patients is unknown. Our aim was to investigate the mechanism of pulsed HD-DXM for management of ITP, specifically regarding the chemokine pathways.MethodsTh1-/Th2-associated chemokine and chemokine receptor profiles in ITP patients before and after pulsed HD-DXM was studied. Plasma levels of CCL5 and CXCL11 (Th1-associated) and of CCL11 (Th2-associated) were determined by ELISA. Gene expression of these three chemokines and their corresponding receptors CCR5, CXCR3, and CCR3, in peripheral blood mononuclear cells (PBMCs) was determined by quantitative RT-PCR.ResultsThirty-three of the thirty-eight ITP patients responded effectively to HD-DXM (oral, 40 mg/day, 4 days). In ITP patients, plasma CXCL11 levels increased, while CCL11 and CCL5 decreased compared to controls (P < 0.05). Similarly, gene expression of CXCL11 and its receptor CXCR3 increased, while CCL11 and CCR3 decreased (P < 0.05). CCL5 expression did not significantly change; however, expression of its receptor CCR5 increased (P < 0.05). Interestingly, in the patients who responded to pulsed HD-DXM, CXCL11 and CXCR3 expression was down-regulated, while CCL11 and CCR3 expression was up-regulated (P < 0.05). Meanwhile, CCL5 expression was up-regulated and CCR5 was down-regulated by HD-DXM (P < 0.05).ConclusionsThe abnormal profiles of Th1-/Th2-associated chemokines and chemokine receptors may play important roles in the pathogenesis of ITP. Importantly, regulating Th1 polarization by pulsed HD-DXM may represent a novel approach for immunoregulation in ITP.

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“…The etiology of OLP remains unclear, however it has been previously reported to be a T cell-mediated autoimmune reaction (17). Hu et al (18) reported that serum levels of CCL5 and the percentage of CCR5 + CD4 + T cells was increased in patients with OLP. Chemokine (C-C motif) ligand 5 and CCR1 have been additionally observed to be expressed in OLP and are associated with mast cell migration (19).…”

Section: Discussionmentioning

confidence: 99%

Changes of gene expression in T lymphocytes following Golli-MBP gene RNA interference

Zhu

Shan

et al. 2016

Molecular Medicine Reports

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The major cell types expressing Golli in the immune system are the T-lineage cells. The aim of the current study was to investigate the changes of gene expression in T lymphocytes subsequent to downregulation of the Golli-myelin basic protein (MBP) gene. RNA interference technology was used to suppress the expression of Golli-MBP in Jurkat cells and DNA microarray techniques were applied to investigate the alterations of gene expression profiles. The results indicated that there were 387 differentially expressed genes. In the Golli-MBP knockdown Jurkat cells, the expression of 108 genes was enhanced, 279 genes were suppressed. Gene ontology analysis identified differentially expressed genes involved in several biological progresses, including cell adhesion and immune responses. Pathway analysis demonstrated that the majority of the differentially expressed genes (23.3%) were involved in cytokine-cytokine receptor interaction. Subsequent to Golli-MBP knockdown, the mechanisms that changed the biological characteristics of Jurkat cells were complex, involving numerous types of functional proteins, and metabolic and signaling pathways. However, further experiments are required to confirm these results.

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Increasing CCL5/CCR5 on CD4+ T cells in peripheral blood of oral lichen planus

Cited by 58 publications

References 36 publications

MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis

MiR-125a targets effector programs to stabilize Treg-mediated immune homeostasis

Pulsed high-dose dexamethasone modulates Th1-/Th2-chemokine imbalance in immune thrombocytopenia

Changes of gene expression in T lymphocytes following Golli-MBP gene RNA interference

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