Epidemiology of nickel allergy

Schubert, H.; Berova, N; Czernielewski, A; Hegyi, E; Jirasek, L; Kohánka, Valéria; Korossy, S; Michailov, P; Nebenführer, L; Prater, E.; Rothe, A; Rudzki, E; Stranski, L.; Süss, E; Tarnick, M; Temesvári, Erzsébet; Zieoler, V.; Zschunke, E

doi:10.1111/j.1600-0536.1987.tb01403.x

Cited by 70 publications

(24 citation statements)

References 15 publications

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“…Clinical experience indicates that allergic contact hypersensitivity to nickel preferentially develops in irritated compared with healthy skin. Consistent with this, ear piercing for the purpose of wearing nickelreleasing costume jewelry results in a high rate of nickel allergy (4). Nickel ions are released from different alloys at varying rates, depending on the alloy, when they are exposed to body fluids, such as sweat.…”

mentioning

confidence: 67%

“…NiCl 2 ⅐6H 2 O (in the following denoted as NiCl 2 ), and 2,4-dinitrofluorobenzene (DNFB) 4 were purchased from Sigma-Aldrich Chemie (Steinheim, Germany), 2,4-dinitrobenzenesulfonic acid (DNBS) was bought from ICN Biomedicals Inc. (Aurora, OH), and H 2 O 2 was from E. Merck (Darmstadt, Germany). Recombinant mouse IL-2 and streptavidin-FITC were obtained from BD PharMingen (Heidelberg, Germany).…”

Section: Reagentsmentioning

confidence: 99%

“…Whereas administration of nickel ions alone failed to sensitize naive mice, sensitization was achieved by the combined administration of NiSO 4 and CFA (8), NiCl 2 plus irritant, or NiCl 2 and H 2 O 2 (9); the latter is produced at high levels by inflammatory phagocytes and can act as an endogenous adjuvant (10). In mice already sensitized to nickel, however, nickel ions alone sufficed to elicit hypersensitivity reactions (8,9,11).…”

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confidence: 99%

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Tolerance to Nickel: Oral Nickel Administration Induces a High Frequency of Anergic T Cells with Persistent Suppressor Activity

Artik

Haarhuis²,

Wu³

et al. 2001

The Journal of Immunology

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We adapted our mouse model of allergic contact hypersensitivity to nickel for the study of tolerance. Sensitization in this model is achieved by the administration of nickel ions with H2O2; nickel ions alone are unable to prime naive T cells, but can restimulate primed ones. A 4-wk course of oral or i.p. administration of 10 mM NiCl2 to naive mice induced tolerance, preventing the induction of hypersensitivity for at least 20 wk; long term desensitization of nickel-sensitized mice, however, required continuous NiCl2 administration. When splenic T cells of orally tolerized donors, even after a treatment-free interval of 20 wk, were transferred to naive recipients, as with lymph node cells (LNC), they specifically prevented sensitization of the recipients. The LNC of such donors were anergic, because upon in vivo sensitization with NiCl2 in H2O2 and in vitro restimulation with NiCl2, they failed to show the enhanced proliferation and IL-2 production as seen with LNC of mice not tolerized before sensitization. As few as 102 bulk T cells, consisting of both CD4+ and CD8+ cells, were able to specifically transfer tolerance to nickel. A hypothesis is provided to account for this extraordinarily high frequency of nickel-reactive, suppressive T cells; it takes into account that nickel ions fail to act as classical haptens, but form versatile, unstable metal-protein and metal-peptide complexes. Furthermore, a powerful amplification mechanism, such as infectious tolerance, must operate which allows but a few donor T cells to tolerize the recipient.

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mentioning

confidence: 67%

Section: Reagentsmentioning

confidence: 99%

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confidence: 99%

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Tolerance to Nickel: Oral Nickel Administration Induces a High Frequency of Anergic T Cells with Persistent Suppressor Activity

Artik

Haarhuis²,

Wu³

et al. 2001

The Journal of Immunology

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“…Nonoccupational exposures arise from handling metallic objects such as jewelry and coins. A high rate of Ni allergy is associated with ear piercing and subsequent wearing of Ni alloy jewelry [13]. Interestingly, comparing the lower incidence of Ni allergy in those who wore Ni-releasing dental braces before ear piercing, with the higher incidence in those who wore them only after or not at all, provided evidence for the development of tolerance to Ni [14,15].…”

Section: Nickelmentioning

confidence: 87%

Mechanisms of immunosensitization to metals (IUPAC Technical Report)

Templeton¹

2004

Pure and Applied Chemistry

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A project is underway within IUPAC to evaluate and harmonize the use of various biomarkers for immunosensitization to metals. This present review summarizes our knowledge of the mechanisms by which certain trace elements evoke allergenicity. Some physiological electrolytes (e.g., Na+, K+) and macronutrients (e.g., Ca2+, Fe3+) are immunologically inactive. However, some trace elements essential for cell function (e.g., Co2+, Cu2+, Cr3+), as well as nonessential elements generally considered toxic (e.g., Hg species) or in use as therapeutic agents (e.g., some species of Pt and Au), can give rise to adverse immune reactions. Specific immunological responses to Ni, Co, Cr, Hg, Be, Cu, Pt, Pd, Ir, In, and Au are discussed. In general, these elements can activate T or B cells by specific receptor interactions, resulting in clonal expansion of a metal-specific lymphocyte and an immune response (typically dermatitis) upon re-exposure. Compelling evidence points to the primary role of the T cell in responding to the metal. T-cell activation occurs when a protein of the major histocompatibility complex (MHC) binds to a T-cell receptor in the presence of an MHC binding peptide. Many antigenic substances result in presentation of MHC bound antigenic peptides to the T-cell receptor; metal ions appear to act as haptens that directly or indirectly cause structural changes in MHC molecule-peptide complexes that result in recognition of these complexes by specific T-cell subsets. Nickel and gold are particularly instructive in understanding mechanisms, and are used to discuss models in which the metal may bind to the antigenic peptide (i) before or (ii) after its association with the MHC/T-cell receptor complex, (iii) may bind to the MHC/receptor complex prior to recruitment of the antigenic peptide, or (iv) may bind to the formed peptide/MHC/receptor complex through ligands contributed by one or more of the components.

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“…The frequency of nickel hypersensitivity in young women has recently been reported to be around 20%, which is almost 10 times higher than that reported for young men. [2][3][4] Nickel materials are used in dentistry largely in prosthesis production and orthodontic appliances. However, few studies have been conducted to determine the real action of this agent in the mouth and the tissue response when in contact with this substance.…”

Section: Introductionmentioning

confidence: 99%

Cellular, Humoral, and Histopathologic Analysis in Rats Implanted with Orthodontic Nickel Brackets

Pereira¹,

Kaminagakura²,

Bonan³

et al. 2008

The Angle Orthodontist

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Objective: To determine the immune response related to nickel and nickel-free orthodontic appliances using cellular (total and differential leukocytes) and humoral (IgA) quantification. Materials and Methods: Thirty-five Wister rats were randomly distributed into three groups (A, B, and C). In the A group, the animals were subdivided into three subgroups (A1: control, without brackets; A2: nickel-free brackets; and A3: nickel brackets) with seven animals in each group; the animals were sacrificed after 14 days. Groups B and C received only nickel brackets and were kept for 14 days. After this period, the implants were removed and the rats were sacrificed. In group B, the animals were sacrificed 2 days after the appliance removal (16 days in total); and in group C, the animals were sacrificed 7 days after the brackets removal (21 days in total). Total and differential leukocyte number, IgA quantification and histopathologic analysis were done. Histopathologic analysis of subcutaneous tissue related to the orthodontic brackets was done as well. Results: There were significant differences between the number of leukocytes for the nickelimplanted animals and the nickel-free and control groups after 14 days of implantation (P Ͻ .05). However, there was no significant difference among groups A1, A2, and A3 for the differential number of leukocytes and for the IgA quantification, except for the number of monocytes, which was three times higher in the nickel group (A3). The histopathologic findings did not show differences between groups. Conclusions: Nickel did not promote significant adverse biological effects.

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Epidemiology of nickel allergy

Cited by 70 publications

References 15 publications

Tolerance to Nickel: Oral Nickel Administration Induces a High Frequency of Anergic T Cells with Persistent Suppressor Activity

Tolerance to Nickel: Oral Nickel Administration Induces a High Frequency of Anergic T Cells with Persistent Suppressor Activity

Mechanisms of immunosensitization to metals (IUPAC Technical Report)

Cellular, Humoral, and Histopathologic Analysis in Rats Implanted with Orthodontic Nickel Brackets

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