Nickel-induced IL-10 down-regulates Th1- but not Th2-type cytokine responses to the contact allergen nickel

Abstract

SummaryWhereas the involvement of Th1-and Th2-type cytokines in contact allergy to nickel (Ni) is well documented, the role of the regulatory cytokine IL-10 is less clear. We therefore investigated the impact of IL-10 on Ni-induced Th1-(IFN-γ γ γ γ ) and Th2-type (

Clinical immunology Th1 and Th2 cytokine profile of CD4 and CD8 positive peripheral blood lymphocytes in nickel contact dermatitis

“…This cytokine has recently been shown to be capable of downregulating the production of pro-inflammatory cytokines by Th1 and Th2 cells in an antigen-specific fashion [28]. In vitro experiments investigating the role of IL-10 in nickel induced IFN-γ release by CD4+ cells have clearly demonstrated that neutralization of IL-10 enhances IFN-γ production [29]. In addition animal studies involving the induction of nickel tolerance by prolonged oral contact have shown that the key cytokine involved in the nickel tolerance is IL-10.…”

Prevalence of Nickel Allergy and Longitudinal Evaluation of Periodontal Abnormalities in Orthodontic Allergic Patients

“…[1][2][3][4][5] Nickel has often been pointed out as a biological sensitizer capable of causing short-and long-term sensitivity reactions (type IV immune response, cell-mediated by T lymphocytes). 6 Clinical abnormalities, such as gingivitis, gingival hyperplasia, lip desquamation, burning sensation in the mouth, metallic taste, angular cheilitis, and periodontitis, may be associated with the release of nickel from orthodontic appliances.…”

Oral administration of paeoniflorin attenuates allergic contact dermatitis by inhibiting dendritic cell migration and Th1 and Th17 differentiation in a mouse model

“…IL-10, an antiinflammatory cytokine, is secreted by various immunocytes [37,38]. IL-10-deficient mice exhibit enhanced inflammatory response in response to haptens, and exogenous rIL-10 alleviates that response [39]. During the course of ACD, IL-10 reduces inflammation by inhibiting antigen presenting cell migration and down-regulating the secretions of proinflammatory cytokines [39].…”