A Critical Role for Thymic Stromal Lymphopoietin in Nickel-Induced Allergy in Mice

Ashrin, Meinar Nur; Arakaki, Rieko; Yamada, Akiko; Kondo, Takao; Kurosawa, Mie; Kudo, Yasusei; Watanabe, Megumi; Ichikawa, Tetsuo; Hayashi, Yoshio; Ishimaru, Naozumi

doi:10.4049/jimmunol.1300276

Cited by 21 publications

(17 citation statements)

References 38 publications

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“…Ni2+ penetrates the skin and activates epithelial cells that produce cytokines and chemokines. Afterwards, there are hyper-reactive immune responses that involve the activation of T-cells and antigen-presenting cells (APCs), such as cutaneous dendritic cells (DCs), 7 - 9 whose main role is to recognize and process external antigens and migrate to the draining lymph nodes (dLNs). 3 , 4 Such process gives rise to antigen-specific T-CD8+ and CD4+, differentiating into effectors T helper 1 (Th1), T helper 17 (Th17) and cytotoxic T lymphocytes (CTLs).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the profile of inflammatory cytokines, through immunohistochemistry, in the skin of patients with allergic contact dermatitis to nickel in the acute and chronic phases

Silvestre

Reis

2018

An. Bras. Dermatol.

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BackgroundAllergic contact dermatitis to ion nickel (Ni+2) is an inflammatory dermatosis, common in industrialized countries. It involves the activation of nickel-specific T-cells, followed by proliferation and induction of a mixed profile of both proinflammatory and regulatory cytokines, suggesting that several T-cell subtypes (helper - Th and cytotoxic - Tc) are involved. A broader understanding of the cytokine profile may lead to new therapeutic approaches.ObjectivesThis study aimed to analyze the cytokines TNF-α, INF-γ, IL-2, IL-4, IL-10, IL-13, IL-17 and IL-23 using the immunohistochemistry technique in order to try to identify their prevalence in chronic and acute eczema of patients with allergic contact dermatitis to Ni+2.MethodsWe performed an immunohistochemical study for eight cytokines in 20 patients with Ni+2 allergic contact dermatitis, biopsied at the site of chronic eczema, triggered by the patient's daily contact with Ni+2, and at the site of acute eczema caused by nickel sulfate, 48 hours after applying the contact test.ResultsThe stained samples showed positive results for the eight cytokines studied. TNF-α, IFN-γ, IL-4, IL-13 and IL-17 had a higher prevalence in chronic eczema, IL-2 and IL-23 in acute eczema, and IL-10 presented a similar prevalence in both acute and chronic eczema. However, these prevalences were statistically significant only for IL-4 and IL-13.Study LimitationsSmall sample size.ConclusionsIn chronic and acute eczema, we observed the presence of a mixed cytokine profile of the T cell subtypes (Th/Tc), suggesting that the responses are expressed at the same time.

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Section: Introductionmentioning

confidence: 99%

Evaluation of the profile of inflammatory cytokines, through immunohistochemistry, in the skin of patients with allergic contact dermatitis to nickel in the acute and chronic phases

Silvestre

Reis

2018

An. Bras. Dermatol.

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“…XCR1 -CD11b -DNcDCs are activated by TSLP in contact hypersensitivity 6 . Although TSLP induces Th2 cytokines, it plays a role in Th1-type Ni allergy 15 . DNcDCs with Ni-binding capabilities may contribute to the TSLP-dependent pathway of Ni allergy.…”

Section: Discussionmentioning

confidence: 99%

Migratory dendritic cells in skin-draining lymph nodes have nickel-binding capabilities

Kuroishi

Bando

Bakti

et al. 2020

Sci Rep

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Nickel (Ni) is the most frequent metal allergen and induces Th1-dependent type-IV allergies. In local skin, epidermal Langerhans cells (Lcs) and/or dermal dendritic cells (Dcs) uptake antigens and migrate to draining lymph nodes (LNs). However, the subsets of antigen-presenting cells that contribute to Ni presentation have not yet been identified. In this study, we analyzed the Ni-binding capabilities of murine DCs using fluorescent metal indicator Newport Green. Elicitation of Ni allergy was assessed after intradermal (i.d.) injection of Ni-treated DCs into ear pinnae of Ni-sensitized mice. The Ni-binding capabilities of MHC class II hi CD11c int migratory DCs were significantly stronger than those of MHC class ii int CD11c hi resident DCs and CD11c int PDCA1 + MHC class II int B220 + plasmacytoid DCs. Migratory DCs in skin-draining and mandibular LNs showed significantly stronger Ni-binding capabilities than those in mesenteric and medial iliac LNs. An i.d. injection of IL-1β induced the activation of Lcs and dermal Dcs with strong Ni-binding capabilities. Ni-binding LCs were detected in draining LNs after i.d. challenge with IL-1β and Ni. Moreover, an i.d. injection of Ni-treated DCs purified from skin-draining LNs elicited Ni-allergic inflammation. These results demonstrated that migratory DCs in skin-draining LNs have strong Ni-binding capabilities and elicit Ni allergy. Cutaneous MHC class II + professional APCs are classified into epidermal CD207 (langerin) + Langerhans cells (LCs) and dermal dendritic cells (DCs) 1,2. LCs were originally considered to be skin-resident DCs, but are now recognized as tissue-resident macrophages, the precursors of which originate from the yolk sac and fetal liver. DCs consist of conventional DCs (cDCs) and plasmacytoid DCs (pDCs). Dermal DCs have been classified into at least three subsets: XCR1 + cDC1, XCR1-CD11b + cDC2, and XCR1-CD11b − double negative (DN) cDCs 2. XCR1 + cDC1s express CD207 and CD103. These professional APCs capture and transport local self and non-self Ags to skin-draining lymph nodes (LNs). Two subsets of DCs are detected in skin-draining LNs: MHC class II hi CD11c int migratory DCs and MHC class II int CD11c hi resident DCs. Migratory DCs have been classified into four subsets: LCs, cDC1s, cDC2s, and DNcDCs, similar to local skin. Resident DCs comprise cDC1s and cDC2s. pDCs are detected in skin-draining LNs but not in steady-state local skin. Although there are high levels of redundancy, each APC contributes to specific immune responses. A previous study reported that LCs mainly induce Th17 responses, particularly against Candida albicans 3. cDC1s have been shown to contribute to Th1 responses and cross-presentation 3,4. cDC2s and DNcDCs contribute to Th2 responses 5,6. Regulatory T (Treg) cells are induced by various APC subsets including epidermal LCs 7 , cDC1s in the intestinal mucosa 8 , and cDC2s in the sublingual mucosa 9. These findings indicated that specific APCs are responsible for immune responses against specific Ags. Metal allergies have b...

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“…Our results showed that elevation of IL-18 has an important role in the promotion of CHS sensitization, such as Th1 differentiation, but is not important for the elicitation phase. Enhancement of CHS may be related to other cytokines, such as thymic stromal lymphopoietin (TSLP), and inflammatory cytokines (Ashrin et al, 2014), and further investigation of other triggers of CHS is needed. Lu (2009) reported that NF-κB, a transcription factor that regulates gene expression of inflammatory cytokines including IL-18, is activated in a redox-dependent manner by oxidative stress, and inhibition of NF-κB activation prevents the induction of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

IL-18 and IFN-gamma expression enhances contact hypersensitivity after oral administration of naturally oxidized olive oil to mice

Ogino

Murano

Okuno

et al. 2018

Food and Agricultural Immunology

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The consumption of oxidized cooking oils may exacerbate some allergic diseases. A contact hypersensitivity (CHS) mouse model was used to investigate the effects of naturally oxidized olive oil on the expression of inflammatory cytokines after a sensitization and elicitation phase. The mRNA expressions of IL-12, IL-18, and IFN-γ in the ear increased seven days after sensitization. IL-18 and IFN-γ mRNA expressions after elicitation were significantly enhanced by administration of oxidized olive oil, which exacerbated ear swelling and mononuclear cell infiltration from CHS after elicitation. IL-18 expression in the ear of oxidized oiltreated mice was highest before elicitation and decreased with an increase in IFN-γ expression after elicitation. The acceleration of an immune reaction by administration of naturally oxidized olive oil in the CHS mouse model was caused by increased expression of IL-18 in the ear auricles after sensitization, which was followed by a significant increase in IFN-γ expression after elicitation.

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A Critical Role for Thymic Stromal Lymphopoietin in Nickel-Induced Allergy in Mice

Cited by 21 publications

References 38 publications

Evaluation of the profile of inflammatory cytokines, through immunohistochemistry, in the skin of patients with allergic contact dermatitis to nickel in the acute and chronic phases

Evaluation of the profile of inflammatory cytokines, through immunohistochemistry, in the skin of patients with allergic contact dermatitis to nickel in the acute and chronic phases

Migratory dendritic cells in skin-draining lymph nodes have nickel-binding capabilities

IL-18 and IFN-gamma expression enhances contact hypersensitivity after oral administration of naturally oxidized olive oil to mice

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