Characterization of Nickel‐Specific T Cell Clones

Silvennoinen-Kassinen, Sylvi; Poikonen, Kari; Ikäheimo, Irma

doi:10.1111/j.1365-3083.1991.tb01791.x

Cited by 33 publications

(21 citation statements)

References 38 publications

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“…An established view of the cellular mechanisms involved in ACD to Ni 2þ is that a detrimental, inflammatory reaction is mediated by Th1-type cytokines [9][10][11] and that Th2-type cytokines or IL-10 could have a downregulatory effect [7,14]. However, the link between these distinct types of responses and the degree of the reactivity to Ni 2þ in vivo has not been well established.…”

Section: Discussionmentioning

confidence: 99%

“…Earlier works suggested that the DTH response to Ni 2þ in humans predominantly involved interferon-g (IFN-g)-producing T cells [9][10][11], but additional studies of Ni 2þ -specific T-cell clones have shown a mixed Th1-and Th2-type cytokine profile [12,13]. Also, production of interleukin-10 (IL-10), a downregulatory cytokine, is induced by Ni 2þ and can inhibit Ni 2þ -specific Th1-type responses [14].…”

Section: Introductionmentioning

confidence: 99%

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Nickel Elicits Concomitant and Correlated in vitro Production of Th1‐, Th2‐Type and Regulatory Cytokines in Subjects with Contact Allergy to Nickel

et al. 2005

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Nickel (Ni 2þ ) elicits production of functionally distinct cytokines in vitro, but the relation between the cytokine profile and the degree of the allergic reaction in vivo needs to be better defined in order to improve the understanding of the immunological mechanisms involved in contact allergy and to facilitate development of in vitro diagnostics. The aim of the study was to define Th1-type [interferon-g (IFN-g)], Th2-type [interleukin-4 (IL-4), IL-5 and IL-13] and regulatory (IL-10) cytokine responses to Ni 2þ in peripheral blood mononuclear cells (PBMC) from subjects with varying patch test reactivity to Ni 2þ . The study included subjects with strong (þ3), moderate (þ2), weak (þ1) or negative (controls) patch test reactivity to Ni 2þ (n ¼ 10 per group). All þ3 and þ2 subjects but only three þ1 subjects had a clinical history of contact allergy to Ni 2þ . Cytokine production of PBMC stimulated with Ni 2þ was determined by enzyme-linked immunospot and/or enzyme-linked immunosorbent assay. Ni 2þ elicited significant production of all cytokines in PBMC from patch-test-positive subjects versus controls with a positive correlation between each cytokine and the patch test reactivity as well as with other cytokines. More subjects responded to Ni 2þ above cut-off values with Th2-type cytokines as compared with IFN-g or IL-10; 100% of þ3, 80% of þ2, 50% of þ1 and 0% of control subjects displayed reactivity to Ni 2þ based on IL-4 and IL-13 assays. Despite the prevailing view of Ni 2þ allergy as a type-1-mediated condition, the in vivo reactivity to Ni 2þ correlated with a mixed Th1-type, Th2-type and regulatory cytokine response to Ni 2þ in vitro. The results accentuate the importance of type 2 responses in contact allergy and also demonstrate that IL-4 and IL-13 are reliable markers for Ni 2þ allergy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nickel Elicits Concomitant and Correlated in vitro Production of Th1‐, Th2‐Type and Regulatory Cytokines in Subjects with Contact Allergy to Nickel

et al. 2005

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“…Ni-induced ACD involves the activation of Ni-specific T cells, followed by the proliferation and induction of cytokine production [5]. Earlier studies suggested that the delayed-type hypersensitivity reaction to Ni in humans predominantly involved interferon (IFN)-γ-producing T cells [6,7,8], but subsequent studies of Ni-specific T cell clones have shown the involvement of mixed T helper (Th)1- and Th2-type cytokine responses in this condition [9,10]. Moreover, Yokozeki et al [11] described a murine model of contact sensitization to paraphenylenediamine (PPD) induced by the application of PPD to mouse skin and demonstrated that Th2-like γδT cells played a role in the development of the ACD in response to exposure to PPD.…”

Section: Introductionmentioning

confidence: 99%

Th2 Immune Response Plays a Critical Role in the Development of Nickel-Induced Allergic Contact Dermatitis

Niiyama¹,

Tamauchi

Amoh³

et al. 2010

Int Arch Allergy Immunol

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Background:The precise roles of T helper (Th)1-type and Th2-type cytokine responses in nickel (Ni)-induced allergic contact dermatitis have not yet been clearly defined. We investigated the involvement of Th2 cytokines in Ni-induced contact hypersensitivity reaction using GATA-3 transgenic (Tg) mice. Methods: A Ni-titanium (Ti) alloy was implanted under the skin of GATA-3 Tg mice. A Ni solution was then injected 1 month after sensitization. The ear swelling response was measured at several time points after the injection; the cytokine levels in the skin were measured at 48 h after injection, and the serum levels of IgE were measured 1 month after injection. In addition, purified CD4+ splenic cells obtained from the GATA-3 Tg mice sensitized with the Ni-Ti alloy were infused into Rag-2^–/– mice, and the ear swelling response of these mice after a further challenge with Ni solution was also measured. Results:Marked ear swelling and elevated serum IgE levels and skin tissue levels of IL-4 were observed in Ni-Ti-sensitized GATA-3 Tg mice. The Rag-2^–/– mice transfused with the CD4+ splenic cells from the Ni-Ti alloy sensitized GATA-3 Tg mice showed a significantly more pronounced ear swelling response than the control mice. Conclusion: We confirmed the participation of Th2-type immune reactions in Ni-induced allergy using GATA-3 Tg mice.

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“…The reacting cells can be studied in vivo at the site of the positive patch test and in vitro in nickel-induced lymphocyte cultures [3,4]. The nickel reaction is dominated by CD4+ cells, as shown with nickel-specific T cell clones [5][6][7][8] and in vivo and in vitro [9], but CD8+ cells are also needed functionally for the nickel reaction to occur [10], The phenotypes of nickel-reacting T cell blasts are further characterized by several acti vation markers and a memory cell marker, and use predom inantly the T cell receptor alpha/beta heterodimer [9].…”

Section: Introductionmentioning

confidence: 99%

Adhesion Molecules in the Nickel Allergic Reaction

Silvennoinen-Kassinen

Vainio²,

Karvonen³

et al. 1995

Int Arch Allergy Immunol

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Nickel is the major cause of allergic contact dermatitis, and to increase our understanding of this immune reaction we studied changes in the expression of adhesion molecules on mononuclear cells during nickel stimulation in vivo and in vitro. Nickel-induced lymphocyte cultures were used in vitro, the cells being examined with monoclonal antibodies (Mabs) and by flow cytometry. Mononuclear cells from skin biopsies of in vivo cutaneous nickel reactions were studied with Mabs and immunohistochemistry. The expression of adhesion molecules in vitro was differential: the number of cells carrying CD11c, CD29, CDw49b, CDw49d, CDw49e, CDw49f, CD54, CD56 and ELAM-1 being significantly overrepresented among the nickel-induced lymphoblasts whereas the number of blasts carrying CD44 was underrepresented and those of CD11a, CD18, CD58 and LAM-1 remained unchanged. CD4+ cells gained adhesion molecules during nickel-induced blast transformation whereas CD8+ cells lost most of their adhesion molecules. The in vivo results were in agreement with the in vitro ones except that CDw49b, CDw49f, CD56 and ELAM-1 could not be detected in a 96-hour nickel reaction in vivo. In conclusion, the nickel allergic reaction favors the expression of certain adhesion molecules, and this expression is induced on CD4+ cells while CD8+ cells tend to lose such molecules. The changes were more sensitively detected with the in vitro method.

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Characterization of Nickel‐Specific T Cell Clones

Cited by 33 publications

References 38 publications

Nickel Elicits Concomitant and Correlated in vitro Production of Th1‐, Th2‐Type and Regulatory Cytokines in Subjects with Contact Allergy to Nickel

Nickel Elicits Concomitant and Correlated in vitro Production of Th1‐, Th2‐Type and Regulatory Cytokines in Subjects with Contact Allergy to Nickel

Th2 Immune Response Plays a Critical Role in the Development of Nickel-Induced Allergic Contact Dermatitis

Adhesion Molecules in the Nickel Allergic Reaction

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