The diversity of reaginic immune responses to platinum and palladium metallic salts

Re, Biagini; Il, Bernstein; Js, Gallagher; Wj, Moorman; Brooks, Stuart M.; Gann, PH

doi:10.1016/0091-6749(85)90750-x

Cited by 79 publications

(32 citation statements)

References 18 publications

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“…the response is against either the ligand or against new antigenic determinants with no evidence of hapten specificity. For other agents, such as platinum salts, an antibody-mediated response has also been confirmed [50][51][52][53][54]. High levels of both IgE and cutaneous reactivity may persist as long as 4 yrs after the cessation of exposure, suggesting that platinum salts may cause polyclonal (noncognate) stimulation of IgE-producing B-cells.…”

Section: Immunological Mechanismmentioning

confidence: 91%

“…In subjects with occupational asthma induced both by high and low molecular weight compounds, specific immunoglobulins (IgE, IgG) may be found [41][42][43][44]. However, positive skin tests and/or specific antibodies against occupational allergens are often present in subjects both with and without symptoms of asthma, suggesting that their presence may reflect exposure rather than disease [44,45].…”

Section: Immunological Mechanismmentioning

confidence: 99%

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Mechanisms and pathology of occupational asthma

Mapp

Saetta²,

Maestrelli³

et al. 1994

Eur Respir J

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M Me ec ch ha an ni is sm ms s a an nd d p pa at th ho ol lo og gy y o of f o oc cc cu up pa at ti io on na al l a as st th hm ma a More than one mechanism may be operative in occupational asthma. Among the mechanisms proposed, immunological mechanisms and airway inflammation play an important role. There is evidence to confirm that T-lymphocyte activation and local accumulation in the bronchial wall of activated eosinophils occurs in asthma of diverse aetiology, i.e. immunoglobulin E (IgE)-mediated, occupational and intrinsic.Neurogenic pathways should be further investigated as a potential mechanism of modulation and amplification of airway inflammation in occupational asthma.

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Section: Immunological Mechanismmentioning

confidence: 91%

Section: Immunological Mechanismmentioning

confidence: 99%

Mechanisms and pathology of occupational asthma

Mapp

Saetta²,

Maestrelli³

et al. 1994

Eur Respir J

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“…More than 50% of exposed persons may develop symptoms and signs of immediatetype allergy such as conjunctivitis, rhinitis, asthma bronchiale or urticaria [2][3][4], Characterization and clinical rel evance of other cutaneous complaints including pruritus and dermatitis are uncertain [2,3,8]. The diagnosis of Pt-related occupational disease can be confirmed by skin prick test or bronchoprovocation eliciting immedi ate-type reactions to minute doses (10~2 to 10"8 mol/l) of [Pt(IV)Cl6]2-or [Pt(II)Cl4]2- [5,7,9], In contrast to the highly specific but hazardous in vivo tests, attempts to elu cidate the nature of these reactions by demonstrating Ptspecific serum IgE or IgG antibodies in vitro remained in conclusive [7,10], even though elevated total IgE levels were found in Pt-exposed refinery workers [5][6][7], Further more, it has been shown that Pt salts are able to elicit non specific histamine release from human basophils in vitro [71.…”

Section: Introductionmentioning

confidence: 99%

T-Cell-Dependent Popliteal Lymph Node Reactions to Platinum Compounds in Mice

Schuppe

Haas-Raida

Kulig

et al. 1992

Int Arch Allergy Immunol

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The requirements for sensitization to complex salts of platinum were investigated in a mouse model by means of the popliteal lymph node (PLN) assay. A single subcutaneous injection of dissolved hexachloroplatinates without adjuvant induced a vigorous primary immune reaction in the draining PLN. Dose-dependent lymph node activation was determined by an increase in both PLN weight and cellularity. In C57BL/6 mice, peak reactions were obtained around day 6 after administration of 90–180 nmol Na₂[PtCl₆] or (NH₄)₂[PtCl₆] per animal. Mice primed to [PtCl₆]^2–– mounted an enhanced response upon local restimulation with suboptimal doses of the same but not unrelated compounds, indicating a specific secondary response. T cells were required to elicit PLN reactions to [PtCl₆]^2––, because athymic nude mice completely failed to respond, in contrast to their +/nu littermates. Differences between various inbred strains of mice revealed that Pt-induced PLN responses are genetically controlled. Moreover, the immunogenicity of Pt salts in mice is not confined to hexachloroplatinates, but other compounds, such as the antineoplastic agent cis-dichlorodiamine platinum, are able to induce comparable PLN reactions.

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“…Although elevated IgE levels have been observed in some Pt-exposed refinery workers [74,75], Pt-specific antibodies or T cell activation have not been demonstrated in humans [1]. In mice, subcutaneous injections of chloroplatinates induces a primary immune response in a popliteal lymph node assay, that is mediated by CD4 + T cells [76].…”

Section: Platinummentioning

confidence: 99%

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 diversity of reaginic immune responses to platinum and palladium metallic salts

Cited by 79 publications

References 18 publications

Mechanisms and pathology of occupational asthma

Mechanisms and pathology of occupational asthma

T-Cell-Dependent Popliteal Lymph Node Reactions to Platinum Compounds in Mice

Mechanisms of immunosensitization to metals (IUPAC Technical Report)

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