The Expression of CXCL10/CXCR3 and Effect of the Axis on the Function of T Lymphocyte Involved in Oral Lichen Planus

Fang, Jiaxiang; Wang, Chen; Shen, Chen; Shan, Jing; Wang, Xuewei; Liu, Lin; Yuan, Fan

doi:10.1007/s10753-018-0934-0

Cited by 14 publications

(14 citation statements)

References 34 publications

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“…Several alterations in the expression of cytokines and chemokines in lesions or serum of patients with LP have been described. Serum levels of interleukin (IL)-5, IL-6, IL-8, IL-9, IL-10, IL-12 IL-17, IL-22, tumor necrosis factor-α, transforming growth factor-β, interferon (IFN)-γ, CXCR-3, CXCR-4, CXCL-10, CXCL-12, CCR1, CCR3, CCR4, CCL5-CCR5, and CCL17-CCR4) have been found elevated (80)(81)(82)(83)(84)(85)(86)(87)(88)(89). In addition, an increased expression IFN-γ and IL-17 in the skin of LP lesions has been described (81,90)-albeit some other studies refuted these observations (91).…”

Section: Cellular and Molecular Pathogenesismentioning

confidence: 99%

Lichen Planus

et al. 2021

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Lichen planus (LP) is a T cell-mediated disease affecting the stratified squamous epithelia of the skin and/or mucus membrane. Histologically, the disease is characterized by a lichenoid inflammatory infiltrate and vacuolar degeneration of the basal layer of the epidermis. LP has three major subtypes: Cutaneous, mucosal and appendageal LP. Rarely, it may affect the nails in the absence of skin and/or mucosal changes. LP may also be induced by several drugs, typically anti-hypertensive medication or be associated with infections, particularly viral hepatitis. The diagnosis is based on the clinical presentation and characteristic histological findings. Although the disease is often self-limiting, the intractable pruritus and painful mucosal erosions result in significant morbidity. The current first-line treatment are topical and/or systemic corticosteroids. In addition, immunosuppressants may be used as corticosteroid-sparing agents. These, however are often not sufficient to control disease. Janus kinase inhibitors and biologics (anti-IL-12/23, anti-IL17) have emerged as novel future treatment options. Thus, one may expect a dramatic change of the treatment landscape of LP in the near future.

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Section: Cellular and Molecular Pathogenesismentioning

confidence: 99%

Lichen Planus

et al. 2021

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“…To complement these findings, others have shown that CXCL10 neutralization significantly reduces pulmonary edema, the release of inflammatory mediators (IFN-γ, IL-6, and ICAM-1), and inflammatory cells (neutrophils, macrophages, CD8+ T cells) infiltration into the lung in an LPS-induced ARDS rat model [ 88 •]. CXCL10 neutralization also accompanied reduced neutrophil and macrophage CXCR3 expression [ 88 •] and CXCR3 antagonism significantly reduced CXCL10-CXCR3-mediated T lymphocyte migration in vitro [ 120 ]. These promising findings increase support for direct targeting of the CXCL10-CXCR3 signaling axis to treat COVID-19.…”

Section: Cxcl10-cxcr3-targeted Therapeutics In Covid-19mentioning

confidence: 99%

Chemokine-Based Therapeutics for the Treatment of Inflammatory and Fibrotic Convergent Pathways in COVID-19

et al. 2021

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Coronavirus disease 2019 (COVID-19) is an infectious disease caused by the SARS-CoV-2 betacoronavirus and has taken over 761,426 American lives as of the date of publication and will likely result in long-term, if not permanent, tissue damage for countless patients. COVID-19 presents with diverse and multisystemic pathologic processes, including a hyperinflammatory response, acute respiratory distress syndrome (ARDS), vascular injury, microangiopathy, tissue fibrosis, angiogenesis, and widespread thrombosis across multiple organs, including the lungs, heart, kidney, liver, and brain. C-X-C chemokines contribute to these pathologies by attracting inflammatory mediators, the disruption of endothelial cell integrity and function, and the initiation and propagation of the cytokine storm. Among these, CXCL10 is recognized as a critical contributor to the hyperinflammatory state and poor prognosis in COVID-19. CXCL10 is also known to regulate growth factor-induced fibrosis, and recent evidence suggests the CXCL10-CXCR3 signaling system may be vital in targeting convergent pro-inflammatory and pro-fibrotic pathways. This review will explore the mechanistic role of CXCL10 and related chemokines in fibrotic complications associated with COVID-19 and the potential of CXCL10-targeted therapeutics for early intervention and long-term treatment of COVID-19-induced fibrosis.

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“…Previous studies have demonstrated that immune reactions and cytokines play dominant roles in the pathogenesis of OLP. Many inflammatory factors exist in the local microenvironment of OLP, such as interleukins (IL‐6, IL‐8, IL‐2, IL‐4 and IL‐17), TNF‐α 11,12 and chemokines (CXCL10, CCL17, CCL5 and CXCL12) 7,13–15 . Furthermore, immune cells, endothelial cells, fibroblasts and the extracellular matrix constitute the local pathological microenvironment.…”

Section: Introductionmentioning

confidence: 99%

“…Many inflammatory factors exist in the local microenvironment of OLP, such as interleukins (IL-6, IL-8, IL-2, IL-4 and IL-17), TNFα 11,12 and chemokines (CXCL10, CCL17, CCL5 and CXCL12). 7,[13][14][15] Furthermore, immune cells, endothelial cells, fibroblasts and the extracellular matrix constitute the local pathological microenvironment. All cell component types interact with inflammatory factors and regulate the immune responses in OLP.…”

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confidence: 99%

FAP‐α⁺ immunofibroblasts in oral lichen planus promote CD4⁺ T‐cell infiltration via CCL5 secretion

Zhang

Liu

Cheng

et al. 2022

Experimental Dermatology

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Oral lichen planus (OLP) is a T cell–mediated, chronic inflammatory disease. CD4+ T‐cell infiltration plays a crucial role in the pathogenesis of OLP. Fibroblasts are activated under pathological conditions and perform various functions. This study was designed to explore the immune activation and biological functions of OLP fibroblasts on CD4+ T cells. We detected the expression of fibroblast activation protein‐alpha (FAP‐α) in the oral tissues of patients with OLP and healthy controls using immunohistochemistry. Furthermore, expression of FAP‐α and C‐C motif chemokine ligand 5 (CCL5) in fibroblasts isolated from oral tissues of patients with OLP and healthy controls was assayed by quantitative PCR, Western blotting and enzyme‐linked immunosorbent assay. Moreover, we assessed the effects of fibroblasts on CD4+ T‐cell proliferation, apoptosis and migration using flow cytometry and Transwell assays. We found that FAP‐α expression in the oral tissues of patients with OLP was significantly higher than that in healthy controls. FAP‐α and CCL5 expression levels were significantly upregulated in OLP fibroblasts. Moreover, OLP fibroblasts promoted CD4+ T‐cell proliferation and migration and inhibited CD4+ T cell apoptosis. In summary, our findings indicate that OLP fibroblasts are immunologically activated and induce CD4+ T‐cell infiltration in OLP.

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The Expression of CXCL10/CXCR3 and Effect of the Axis on the Function of T Lymphocyte Involved in Oral Lichen Planus

Cited by 14 publications

References 34 publications

Lichen Planus

Lichen Planus

Chemokine-Based Therapeutics for the Treatment of Inflammatory and Fibrotic Convergent Pathways in COVID-19

FAP‐α⁺ immunofibroblasts in oral lichen planus promote CD4⁺ T‐cell infiltration via CCL5 secretion

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The Expression of CXCL10/CXCR3 and Effect of the Axis on the Function of T Lymphocyte Involved in Oral Lichen Planus

Cited by 14 publications

References 34 publications

Lichen Planus

Lichen Planus

Chemokine-Based Therapeutics for the Treatment of Inflammatory and Fibrotic Convergent Pathways in COVID-19

FAP‐α+ immunofibroblasts in oral lichen planus promote CD4+ T‐cell infiltration via CCL5 secretion

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FAP‐α⁺ immunofibroblasts in oral lichen planus promote CD4⁺ T‐cell infiltration via CCL5 secretion