The Endogenous Danger Signal Uric Acid Augments Contact Hypersensitivity Responses in Mice

Liu, LanLan; Inoue, Hiroko; Nakayama, Hirofumi; Kanno, Rieko; Kanno, Morio

doi:10.1159/000103377

Cited by 16 publications

(12 citation statements)

References 43 publications

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“…Nickel was able to induce CD69 molecule on both CD4 + and CD8 + T cells after 24 hours in the present study. An study investigating the effect of monosodium urateontrinitrochlorobenzene-induced contact hypersensitivity responses in mice has revealed increased expression of CD69 on both CD4 + and CD8 + T lymphocytes indicating activation of both cell types 22. Interaction between activated T cell subsets particularly in contact dermatitis appears to be complex.…”

Section: Discussionmentioning

confidence: 99%

Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

et al. 2019

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Background Persistent antigenic stimulation due to repeated exposure to nickel may lead to chronic inflammation resulting in allergic contact dermatitis (ACD). Objectives This study was performed to assess nickel induced immune activation among patients sensitized against nickel. Patients and Methods A total of 35 patients (29 females and 6 males; mean age 36±9 years) with nickel contact dermatitis and 20 patch test negative healthy individuals (14 females and 6 males; mean age 29±7 years) were included in this study. Peripheral blood of patients and controls was incubated with nickel sulfate for 24 hours. Immune activation was assessed by CD69 up-regulation on T lymphocyte sub-sets by flow cytometry. Results Base line expression of CD69 on CD8 + lymphocytes was higher among patients compared to controls (4.1±1.3%vs2.8±1.1%;p<0.009). There was no difference in proportions of CD±CD69 + cells between patients and controls (3.2±0.9%vs2.3±0.8%). Exposure to nickel induced expression of CD69 on a significantly higher proportion of CD4 + lymphocytes (22.1±6.2%) of the ACD patients compared to controls (2.8±2.5%;p<0.0001). Similarly nickel induced CD69 expression on a higher proportion of CD8 + lymphocytes (18.2±5.3%) from ACD patients compared to the controls (1.9±1.8%;p<0.0006). Conclusion CD69 molecule appears to be an important regulator of immune response in nickel contact dermatitis.

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Section: Discussionmentioning

confidence: 99%

Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

et al. 2019

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“…Finally we evaluated the expression of CD44 and CD69 on CD4+ T cells after incubation with the supernatant (50 µL) of the eosinophil culture alone or plus anti-HMGB1 antibodies (2 µg/mL). CD44 and CD69 were reported to be T cell activation markers 9. Levels of cytokine and HMGB1 in the culture supernatants were determined by ELISA.…”

Section: Methodsmentioning

confidence: 99%

Eosinophils Modulate CD4⁺T Cell Responses via High Mobility Group Box-1 in the Pathogenesis of Asthma

Shim

Chun

Lee

et al. 2015

Allergy Asthma Immunol Res

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Eosinophils have been reported to modulate T cell responses. Previously, we reported that high-mobility group box 1 protein (HMGB1) played a key role in the pathogenesis of asthma. This study was conducted to test our hypothesis that eosinophils could modulate T cell responses via HMGB1 in the pathogenesis of asthma characterized by eosinophilic airway inflammation. We performed in vitro experiments using eosinophils, dendritic cells (DCs), and CD4+ T cells obtained from a murine model of asthma. The supernatant of the eosinophil culture was found to significantly increase the levels of interleukin (IL)-4 and IL-5 in the supernatant of CD4+ T cells co-cultured with DCs. HMGB1 levels increased in the supernatant of the eosinophil culture stimulated with IL-5. Anti-HMGB1 antibodies significantly attenuated increases of IL-4 and IL-5 levels in the supernatant of CD4+ T cells co-cultured with DCs that were induced by the supernatant of the eosinophil culture. In addition, anti-HMGB1 antibodies significantly attenuated the expressions of activation markers (CD44 and CD69) on CD4+ T cells. Our data suggest that eosinophils modulate CD4+ T cell responses via HMGB1 in the pathogenesis of asthma.

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“…Nevertheless, Liu and colleagues showed that MSU enhances the CHS response in BALB/c mice. Indeed, MSU promoted DC maturation and T cell activation, suggesting that it may act as an endogenous adjuvant to potentiate immune response [ 82 ].…”

Section: Skin Sensitizers and Danger Signalsmentioning

confidence: 99%

NLRP3 Inflammasome and Allergic Contact Dermatitis: A Connection to Demystify

et al. 2020

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Allergic contact dermatitis is a common occupational disease that manifests as a cell-mediated hypersensitivity reaction following skin exposure to small reactive chemicals termed haptens. Haptens penetrate the stratum corneum and covalently modify proteins in the epidermis, inducing intracellular stress, which further leads to the release of damage-associated molecular patterns (DAMPs), such as uric acid, reactive oxygen species, hyaluronic acid fragments and extracellular adenosine triphosphate (ATP). These DAMPs are recognized by pattern recognition receptors (PRRs) in innate immune cells, namely dendritic cells (DCs), leading to their maturation and migration to the draining lymph nodes where they activate naïve T lymphocytes. Among all PRRs, several studies emphasize the role of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome on the allergic contact dermatitis (ACD) sensitization phase. However, skin allergens—danger signals—NLRP3 inflammasome axis is yet to be completely elucidated. Therefore, in this review, we sought to discuss the molecular mechanisms underlying DAMPs release and NLRP3 inflammasome activation triggered by skin allergens. The elucidation of these key events might help to identify novel therapeutic strategies for ACD, as well as the development of nonanimal alternative methods for the identification and potency categorization of skin sensitizers.

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The Endogenous Danger Signal Uric Acid Augments Contact Hypersensitivity Responses in Mice

Cited by 16 publications

References 43 publications

Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

Eosinophils Modulate CD4⁺T Cell Responses via High Mobility Group Box-1 in the Pathogenesis of Asthma

NLRP3 Inflammasome and Allergic Contact Dermatitis: A Connection to Demystify

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The Endogenous Danger Signal Uric Acid Augments Contact Hypersensitivity Responses in Mice

Cited by 16 publications

References 43 publications

Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

Nickel challenge up regulates CD69 expression on T lymphocyte sub-sets from patients with nickel induced contact dermatitis

Eosinophils Modulate CD4+T Cell Responses via High Mobility Group Box-1 in the Pathogenesis of Asthma

NLRP3 Inflammasome and Allergic Contact Dermatitis: A Connection to Demystify

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Eosinophils Modulate CD4⁺T Cell Responses via High Mobility Group Box-1 in the Pathogenesis of Asthma