Oral Induction of Tolerance to Nickel Sensitization in Mice

Hoogstraten, Ingrid M.W. van; Boos, Colin; Boden, Dagmar; Blomberg, Mary E. von; Scheper, Rik J.; Kraal, Georg

doi:10.1111/1523-1747.ep12358502

Cited by 70 publications

(61 citation statements)

References 34 publications

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“…Clinical examination after allergies. [38][39][40][41][42] Nevertheless when clinical three days of removal of the archwires In both cases the diagnosis of nickel signs or symptoms presumed to be due demonstrated that lip competence had returned. The patient's lips no longer appeared swollen and the clinical 'anaes thetic-like' symptoms did not return.…”

Section: Case Reportmentioning

confidence: 99%

Nickel allergy and orthodontics, a review and report of two cases

Noble¹,

Ahing²,

Karaiskos³

et al. 2008

Br Dent J

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VERIFIABLE CPD PAPER• Readers will develop an understanding of the background of nickel allergy and its epidemiology in orthodontics.• Readers will learn the signs and symptoms of a nickel allergy in orthodontics.• Readers will have an understanding of making a diagnosis and alternative methods to treat orthodontic patients who have developed an intra-oral nickel allergy due to orthodontic appliances.• Two detailed real life cases are presented. I N B R I E F PRACTICENickel is a common component in many orthodontic materials. An allergy to nickel is commonly seen in the population, more frequently in women. This allergy has increased with the more frequent use of nickel containing jewellery and in traoral piercings. As a result, this allergy can be expected to be more readily encountered in dental practice. Possible allergy to nickel should be a question in the initial patient health history questionnaire. The dental practitioner should be mindful of this allergy during the course of orthodontic treatment, and know how to diagnose a nickel allergy if it appears and subsequent action in treatment and referral if it is suspected. This paper provides a summary of nickel allergy, its epide miology, diagnosis and recommendations and alternatives to treatment. A detailed description of two cases where it was discovered in orthodontic patients is also reported.

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Section: Case Reportmentioning

confidence: 99%

Nickel allergy and orthodontics, a review and report of two cases

Noble¹,

Ahing²,

Karaiskos³

et al. 2008

Br Dent J

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“…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). Likewise, when T cells from nickel-sensitized mice (9) or men (12)(13)(14)(15)(16) were exposed to nickel ions on APCs in vitro, this sufficed to restimulate them.…”

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confidence: 99%

“…Two groups of investigators have shown that tolerance to nickel can be induced in naive animals by several weeks of oral exposure to nickel ions, thus preventing subsequent sensitization of the animals (8,11,17). In orally tolerized guinea pigs, nickel tolerance lasted up to 24 mo (17); in mice, the maximal duration of the tolerant state has not yet been determined.…”

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confidence: 99%

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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“…Nickel elicits increases in nitric oxide production (15), activation of nuclear factor-KB (16), and delayed-type hypersensitivity (DTH) reactions in humans (17) and rodents (18). Nickel-induced DTH is characterized by the presence of IFN-y-producing Thl and ThO CD4+ T cells (19).…”

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confidence: 99%

Lupus-Prone Mice as Models to Study Xenobiotic-Induced Acceleration of Systemic Autoimmunity

Pollard¹,

Pearson²,

Hultman³

et al. 1999

Environmental Health Perspectives

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The linkage between xenobiotic exposures and autoimmune diseases remains to be clearly defined. However, recent studies have raised the possibility that both genetic and environmental factors act synergistically at several stages or checkpoints to influence disease pathogenesis in susceptible populations. These observations predict that individuals susceptible to spontaneous autoimmunity should be more susceptible following xenobiotic exposure by virtue of the presence of predisposing background genes. To test this possibility, mouse strains with differing genetic susceptibility to murine lupus were examined for acceleration of autoimmune features characteristic of spontaneous systemic autoimmune disease following exposure to the immunostimulatory metals nickel and mercury. Although NiCI2 exposure did not exacerbate autoimmunity, HgCI2 significantly accelerated systemic disease in a strain-dependent manner. Mercury-exposed (NZB x NZW)F1 mice had accelerated lymphoid hyperplasia, hypergammaglobulinemia, autoantibodies, and immune complex deposits. Mercury also exacerbated immunopathologic manifestations in MRL+/+ and MR -Ipr mice. However, there was less disease acceleration in lpr mice compared with MRL+/+ mice, likely due to the fact that environmental factors are less critical for disease induction when there is strong genetic susceptibility. Non-major histocompatability complex genes also contributed to mercuryexacerbated disease, as the nonautoimmune AKR mice, which are H-2 identical with the MRL, showed less immunopathology than either the MRL//pr or MRL+/+ strains. This study demonstrates that genetic susceptibility to spontaneous systemic autoimmunity can be a predisposing factor for HgCI2-induced exacerbation of autoimmunity. Such genetic predisposition may have to be considered when assessing the immunotoxicity of xenobiotics. Additional comparative studies using autoimmune-prone and nonautoimmune mice strains with different genetic backgrounds will help determine the contribution that xenobiotic exposure makes in rendering sensitive populations susceptible to autoimmune diseases.

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Oral Induction of Tolerance to Nickel Sensitization in Mice

Cited by 70 publications

References 34 publications

Nickel allergy and orthodontics, a review and report of two cases

Nickel allergy and orthodontics, a review and report of two cases

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

Lupus-Prone Mice as Models to Study Xenobiotic-Induced Acceleration of Systemic Autoimmunity

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