Expression and biological functions of the CCL5‐CCR5 axis in oral lichen planus

Shan, Jing; Li, Shan; Wang, Chen; Liu, Lin; Wang, Xuewei; Zhu, Dong; Yuan, Fan; Xu, Jing

doi:10.1111/exd.13946

Cited by 23 publications

(28 citation statements)

References 32 publications

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“…As reported by previous studies, the abnormal interaction of CCL5/CCR5 has been found in multiple types of inflammation, 61 including hepatitis, atherosclerosis, and microglia inflammation. Some viral infections are also mediated by CCL5/CCR5 axis.…”

Section: Ccl5/ccr5 and Diseasessupporting

confidence: 69%

CCL5/CCR5 axis in human diseases and related treatments

et al. 2022

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To defense harmful stimuli or maintain the immune homeostasis, the body produces and recruits a superfamily of cytokines such as interleukins, interferons, chemokines etc. Among them, chemokines act as crucial regulators in defense systems. CCL5/CCR5 combination is known for facilitating inflammatory responses, as well as inducing the adhesion and migration of different T cell subsets in immune responses. In addition, recent studies have shown that the interaction between CCL5 and CCR5 is involved in various pathological processes including inflammation, chronic diseases, cancers as well as the infection of COVID-19. This review focuses on how CCL5/CCR5 axis participates in the pathological processes of different diseases and their relevant signaling pathways for the regulation of the axis. Moreover, we highlighted the gene therapy and chemotherapy studies for treating CCR5-related diseases, including the ongoing clinical trials. The barriers and perspectives for future application and translational research were also summarized.

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Section: Ccl5/ccr5 and Diseasessupporting

confidence: 69%

CCL5/CCR5 axis in human diseases and related treatments

et al. 2022

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“…To explore whether CCN1 promoted the activation of keratinocytes, we tested the keratinocyte using CCK‐8 assay in HaCaT cells with LPS, mimicked the local inflammatory environment of OLP 13,14 . The CCK‐8 assay showed that keratinocyte proliferation significantly ( P < .05) increased by CCN1 stimulation against control (Figure 3A).…”

Section: Resultsmentioning

confidence: 99%

“…[8][9][10]20 Besides, inflammatory cytokines IL-1β, ICAM1, and CCL5 expression in OLP was reported separately. [12][13][14] However, the data of CCN1 and its related cytokines IL-1β, ICAM1, and CCL5 in OLP are not available so far in the literature. Herein, we showed that altered expression of CCN1 in OLP associated with keratinocyte activation and IL-1β, ICAM1, and CCL5 up-regulation.…”

Section: Discussionmentioning

confidence: 99%

“…Altered expression of CCN1, as a novel inflammation‐regulated mediator, 8,19 has been determined in some immune‐mediated inflammatory diseases such as rheumatoid arthritis and psoriasis and may play a role in the inflammatory regulation associated with these diseases 8‐10,20 . Besides, inflammatory cytokines IL‐1β, ICAM1, and CCL5 expression in OLP was reported separately 12‐14 . However, the data of CCN1 and its related cytokines IL‐1β, ICAM1, and CCL5 in OLP are not available so far in the literature.…”

Section: Discussionmentioning

confidence: 99%

“…10 IL-1β and related cytokines intercellular adhesion molecule (ICAM) 1 and CCL5 (also known as RANTES) are pro-inflammatory mediators that response from neonatal airway epithelial cells. 11 Although IL-1β, ICAM1, and CCL5 expression in OLP was reported separately, [12][13][14] whether aberrant expression of CCN1 and its related cytokines IL-1β, ICAM1, and CCL5 in OLP are still unknown.…”

Section: Introductionmentioning

confidence: 99%

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Altered expression of CCN1 in oral lichen planus associated with keratinocyte activation and IL‐1β, ICAM1, and CCL5 up‐regulation

Wang

Shi

et al. 2020

J Oral Pathology Medicine

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Background: Emerging evidence indicates that CCN1 is a novel inflammation-regulated mediator involved in the pathogenesis of some immune-mediated inflammatory diseases. The objective of this study was to investigate the preliminary roles of CCN1 and its related cytokines IL-1β, CCL5, and ICAM1 in oral lichen planus (OLP). Methods: CCN1 expression levels in biopsies from OLP patients against normal oral mucosa (NOM) using immunohistochemistry (42 OLP vs 9 NOM) and RT-qPCR (20 OLP vs 20 NOM) were compared, respectively. The correlation of CCN1 and IL-1β, CCL5, and ICAM1 expression was examined by RT-qPCR in tissue samples and an in vitro cell culture system using keratinocyte HaCaT cells incubated with lipopolysaccharides. Results: Immunohistochemistry showed that CCN1 protein mainly expressed in the cytoplasm of epithelial keratinocytes of OLP. Consistently, RT-qPCR revealed that mRNA expression of CCN1 was increased in OLP compared with NOM (P < .05) and positively correlated with the high expression of IL-1β, ICAM1, and CCL5 (P < .001), respectively. Importantly, an in vitro study showed that keratinocyte proliferation significantly (P < .05) increased by CCN1 stimulation. Moreover, IL-1β, ICAM1, and CCL5 expression in keratinocytes stimulated by CCN1 was increased (P < .05), respectively. Conclusions: This preliminary study for the first time reported that altered expression of CCN1 was associated with high expression of IL-1β, ICAM1, and CCL5 in OLP. And we demonstrated CCN1 promoted keratinocyte activation, as well as IL-1β, ICAM1, and CCL5 production in keratinocytes. Our data indicated that the potential role of CCN1 and its related cytokines was involved in the pathogenesis of OLP.

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PA28γ induces dendritic cell maturation and activates T‐cell immune responses in oral lichen planus

Wang,

Zhang,

Deng

et al. 2024

MedComm

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Oral lichen planus (OLP) is a common chronic inflammatory disease of the oral mucosa, the mechanism of its inflammatory progression has not yet been fully elucidated. PA28γ plays a significant role in a variety of immune‐related diseases. However, the exact role of PA28γ in the pathogenesis of OLP remains unclear. Here, we demonstrated that PA28γ is overexpressed in epithelial cells and inflammatory cells of OLP tissues but has no significant relationship with OLP subtypes. Functionally, keratinocytes with high PA28γ expression could induce dendritic cell (DC) maturation and promote the T‐cell differentiation into Th1 cells in response to the immune response. In addition, we found that a high level of PA28γ expression is associated with high numbers of infiltrating mature DCs and activated T‐cells in OLP tissues. Mechanistically, keratinocytes with high PA28γ expression could promote the secretion of C–C motif chemokine (CCL)5, blocking CCL5 or/and its receptor CD44 could inhibit the induction of T‐cell differentiation by keratinocytes with high PA28γ expression. In conclusion, we reveal that keratinocytes with high expression of PA28γ in OLP can induce DC maturation and promote T‐cell differentiation through the CCL5‐CD44 pathway, providing previously unidentified mechanistic insights into the mechanism of inflammatory progression in OLP.

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Expression and biological functions of the CCL5‐CCR5 axis in oral lichen planus

Cited by 23 publications

References 32 publications

CCL5/CCR5 axis in human diseases and related treatments

CCL5/CCR5 axis in human diseases and related treatments

Altered expression of CCN1 in oral lichen planus associated with keratinocyte activation and IL‐1β, ICAM1, and CCL5 up‐regulation

PA28γ induces dendritic cell maturation and activates T‐cell immune responses in oral lichen planus

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