Cytokine profiles in serum of patients with oral lichen planus

Pekiner, Filiz Namdar; Demirel, Gülderen Yanıkkaya; Borahan, M. Oğuz; Özbayrak, Semih

doi:10.1016/j.cyto.2012.08.007

Cited by 71 publications

(79 citation statements)

References 37 publications

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“…In concordance with other observations, OLP patients showed an expression pattern of low‐level saliva IFN‐γ but high‐level IL‐4, and lower serum IFN‐γ and IL‐2 but elevated serum IL‐10 , indicating a Th2‐predominant immune response. While in other studies, researchers concluded that dominating role of Th2 cell in OLP disease may be a result of DTH reaction .…”

Section: Th1/th2 Imbalance In Olp Pathogenesissupporting

confidence: 91%

Role of distinct CD4⁺T helper subset in pathogenesis of oral lichen planus

Wang

Zhang

Han

et al. 2015

J Oral Pathology Medicine

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Oral lichen planus (OLP) is one of the most common chronic inflammatory oral mucosal diseases with T-cell-mediated immune pathogenesis. In subepithelial and lamina propria of OLP local lesions, the presence of CD4(+) T helper (CD4(+) Th) cells appeared as the major lymphocytes. These CD4(+) T lymphocytes can differentiate into distinct Th cell types such as Th1, Th2, Treg, Th17, Th22, Th9, and Tfh within the context of certain cytokines environment. Growing evidence indicated that Th1/Th2 imbalance may greatly participate into the cytokine network of OLP immunopathology. In addition, Th1/Th2 imbalance can be regulated by the Treg subset and also greatly influenced by the emerging novel CD4(+) Th subset Th17. Furthermore, the presence of novel subsets Th22, Th9 and Tfh in OLP patients is yet to be clarified. All these Th subsets and their specific cytokines may play a critical role in determining the character, extent and duration of immune responses in OLP pathogenesis. Therefore, we review the roles of distinct CD4(+) Th subsets and their signature cytokines in determining disease severity and susceptibility of OLP and also reveal the novel therapeutic strategies based on T lymphocytes subsets in OLP treatment.

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Section: Th1/th2 Imbalance In Olp Pathogenesissupporting

confidence: 91%

Role of distinct CD4⁺T helper subset in pathogenesis of oral lichen planus

Wang

Zhang

Han

et al. 2015

J Oral Pathology Medicine

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“…In addition, Liu et al [20] reported that salivary IFN-g (Th1 cytokine) levels decreased significantly compared with the control group. In a recent study, the authors reported that OLP patients showed a significantly higher level of serum IL-10 and lower IL-2 level compared to normal patients and concluded that a Th2 dominant response might shift the balance of Th1/Th2 in OLP [28]. In our study, IL12RB2 expression of the OLP group was significantly lower than that of the Non-OLP group.…”

Section: Discussioncontrasting

confidence: 77%

The potential of interleukin 12 receptor beta 2 (IL12RB2) and tumor necrosis factor receptor superfamily member 8 (TNFRSF8) gene as diagnostic biomarkers of oral lichen planus (OLP)

Jeon

Eun-Hyoung

Lee

et al. 2015

Acta Odontologica Scandinavica

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“…Serum levels of interleukin 2 (IL‐2) were significantly decreased, and interleukin 10 (IL‐10) levels were significantly increased in all OLP patients when compared to controls . The decrease in IL‐2 and increase in IL‐10 suggest a Th1/Th2 imbalance towards the Th2 response . The authors suggest that the shift towards a Th2 profile could indicate that OLP is the result of a true delayed hypersensitivity …”

Section: Immunopathogenesis Of Olpmentioning

confidence: 97%

“…The Th1/Th2 cytokine profiles were assessed in tissue from 30 OLP and 30 healthy control patients with the OLP patients OLP . Serum levels of interleukin 2 (IL‐2) were significantly decreased, and interleukin 10 (IL‐10) levels were significantly increased in all OLP patients when compared to controls . The decrease in IL‐2 and increase in IL‐10 suggest a Th1/Th2 imbalance towards the Th2 response .…”

Section: Immunopathogenesis Of Olpmentioning

confidence: 99%

The immunopathogenesis of oral lichen planus—Is there a role for mucosal associated invariant T cells?

DeAngelis

Cirillo

McCullough

2019

J Oral Pathology Medicine

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Oral lichen planus (OLP) is a chronic, T‐cell‐mediated, immune condition of unknown cause. OLP may present with painful symptoms requiring treatment, as well as lesions outside the oral cavity. It is likely that what initiates the OLP disease process is a complex interaction of host susceptibility and environmental triggers. While it is possible that OLP represents a true autoimmune condition against an epithelial autoantigen, the mechanisms that lead to this immune dysregulation are still poorly understood. In this review article, we discuss current concepts relating to the immunopathogenesis of OLP, as well as the potential contributory roles the oral microbiota and mucosal‐associated invariant T (MAIT) cells.

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Cytokine profiles in serum of patients with oral lichen planus

Cited by 71 publications

References 37 publications

Role of distinct CD4⁺T helper subset in pathogenesis of oral lichen planus

Role of distinct CD4⁺T helper subset in pathogenesis of oral lichen planus

The potential of interleukin 12 receptor beta 2 (IL12RB2) and tumor necrosis factor receptor superfamily member 8 (TNFRSF8) gene as diagnostic biomarkers of oral lichen planus (OLP)

The immunopathogenesis of oral lichen planus—Is there a role for mucosal associated invariant T cells?

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Cytokine profiles in serum of patients with oral lichen planus

Cited by 71 publications

References 37 publications

Role of distinct CD4+T helper subset in pathogenesis of oral lichen planus

Role of distinct CD4+T helper subset in pathogenesis of oral lichen planus

The potential of interleukin 12 receptor beta 2 (IL12RB2) and tumor necrosis factor receptor superfamily member 8 (TNFRSF8) gene as diagnostic biomarkers of oral lichen planus (OLP)

The immunopathogenesis of oral lichen planus—Is there a role for mucosal associated invariant T cells?

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Role of distinct CD4⁺T helper subset in pathogenesis of oral lichen planus

Role of distinct CD4⁺T helper subset in pathogenesis of oral lichen planus