Immunophenotyping of the Eczematous Flare-Up Reaction in a Nickel-Sensitive Subject

Gawkrodger, David J.; Mcvittie, E.; Hunter, John

doi:10.1159/000248821

Cited by 12 publications

(6 citation statements)

References 10 publications

(11 reference statements)

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“…After 21 days, the presence of CCR10 + T cells at the site of allergen challenge suggests the retention of these cells as a direct result of increased CCL27 expression. Although this retention is essentially non‐specific in nature, the early preferential infiltration of hapten‐specific T cells at allergic skin reaction sites 16, 17 would explain the marked allergen specificity of persistent, locally increased reactivity at these sites, as reported from clinical and experimental studies 10, 18, 19. It is, therefore, most unlikely that continuous attraction and depletion (rather than retention) of CCR10 + cells occur, resulting in a net increase in CCR10 + cells after the inflammatory response.…”

Section: Discussionmentioning

confidence: 91%

Increased CCL27–CCR10 expression in allergic contact dermatitis: implications for local skin memory

Moed

Boorsma

Tensen

et al. 2004

The Journal of Pathology

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Allergic contact dermatitis (ACD) is a T-cell-mediated disease in which expression of a distinct repertoire of chemokines results in the recruitment of effector T cells into the skin. While it is becoming clear which chemokines and receptors determine the development of ACD, the mechanisms involved in the retention of T cells in the skin after resolution of inflammation are still unknown. Unravelling these mechanisms will help us to understand local skin memory as observed in retest reactivity and flare-up reactions. This study was designed to evaluate the role of chemokine-chemokine receptor interactions in local T-cell retention. The results show that expression of the CCR10 targeting ligand CCL27 is not only increased during inflammation, but also remains increased several weeks after clinical responsiveness to patch testing. In parallel with increased CCL27 expression, an increased number of infiltrating cells could still be detected in skin that, clinically, had returned to normal 21 days after patch testing. These persisting cells were characterized as CD4+ cells expressing CCR10, while no CD8+ CCR10+ cells could be detected. The presence of these cells is most likely an allergen-mediated effect, as increased levels of CCL27 and CCR10 could not be detected 21 days after initiating an irritant contact dermatitis reaction. In contrast to CCL27, increased expression of CXCL9, CXCL10, and CXCL11 could only be observed during the clinically inflammatory phase of ACD. In conclusion, local CCL27-mediated retention of CCR10+ CD4+ T cells in sites previously challenged by ACD could be responsible for phenomena such as local skin memory observed in retest reactions and flare-up reactions in which the presence of persisting T cells results in an accelerated inflammatory response upon renewed allergen challenge.

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Section: Discussionmentioning

confidence: 91%

Increased CCL27–CCR10 expression in allergic contact dermatitis: implications for local skin memory

Moed

Boorsma

Tensen

et al. 2004

The Journal of Pathology

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show abstract

Section: Discussionmentioning

confidence: 99%

“…A number of studies show that, after oral nickel challenge, tissue lymphocyte alterations and cytokine profiles are consistent with a T cell-mediated, delayed type IV hypersensitivity reaction. 38,[52][53][54] However, in all cases of generalized skin response (i.e., excluding some cases of mere reactivation of localized ACD), there are no reports in literature of positive oral nickel challenge later than 12 hours. In the present study, the trigger times after oral intake almost always ranged between three and seven hours.…”

Section: Discussionmentioning

confidence: 99%

Nickel Sensitization and Dietary Nickel are a Substantial Cause of Symptoms Provocation in Patients with Chronic Allergic-Like Dermatitis Syndromes

Antico¹,

Soana²

2015

Allergy�Rhinol (Providence)

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Data in literature seem to show that, in patients with contact allergic dermatitis, dietary nickel might be a cause of systemic dermatitis, but little information exists in literature about the role of nickel sensitization and dietary nickel in patients with allergic-like chronic dermatitis syndromes. The prevalence of nickel sensitization in patients with chronic allergic-like, non-IgE-mediated skin diseases, and the possible impact of dietary nickel on symptom provocation and persistence has been assessed in the present retrospective study on a case series of 1726 patients referred to our allergy unit for chronic allergic-like skin diseases. IgE-mediated pathogenesis and other differential diagnoses excluded, patients were patch tested. Nickel-positive patients underwent an elimination diet and double-blind placebo-controlled nickel challenge (DBPCNC) test. A total of 339 (20%) tested nickel-positive. Fifty-two patients (15%) recovered by avoiding sources of nickel contact and 29 (10%) dropped out. Out of the remaining nickel-sensitized patients, 277 (80%) achieved complete or near complete recovery with low-nickel content diet, and 185 of them (89%) were positive to DBPCNC. We conclude that nickel sensitization and dietary nickel seem to be the chief trigger for provocation and persistence of symptoms in an important part (∼11%) of patients with chronic allergic-like dermatitis syndromes.

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“…Several studies investigated the alterations of lymphocytes in tissues following a SCD reaction: an infiltrate of both CD4+ and CD8+ T lymphocytes was observed in the dermis and epidermis in flare‐up reactions following systemic nickel exposure (28). Evidence for a delayed‐type immune reaction in the gastrointestinal mucosa has also been presented: increased levels of CD4+ CD45RO+ T cells were identified in the gastrointestinal mucosa of patients provoked orally with nickel (29).…”

Section: Pathomechanismsmentioning

confidence: 99%

Drug‐elicited systemic allergic (contact) dermatitis – update and possible pathomechanisms

Thyssen

Maibach

2008

Contact Dermatitis

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An allergic dermatitis reaction may develop after systemic exposure to a hapten that reaches the skin through haematogenous transport. This condition can be observed with and without previous cutaneous sensitization to the hapten but has traditionally been described following topical exposure. A heterogeneous clinical picture, in combination with limited insight to its pathomechanisms, makes such systemic reactions an area in need of further study. This article summarizes knowledge about systemic dermatitis elicited by drugs, with a special emphasis on possible pathomechanisms. A list of putative pathomechanisms is offered for future research. Literature was examined using PubMed-MEDLINE, EMBASE, Biosis, and Science Citation Index. Based on the literature, it is likely that humoral type 3, delayed-type hypersensitivity, and drug-driven (i.e. p-i concept) reactions are involved. As commonly used terms may be misleading because skin contact is not a prerequisite, we suggest that the term 'systemic allergic dermatitis' should be used in the future.

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Immunophenotyping of the Eczematous Flare-Up Reaction in a Nickel-Sensitive Subject

Cited by 12 publications

References 10 publications

Increased CCL27–CCR10 expression in allergic contact dermatitis: implications for local skin memory

Increased CCL27–CCR10 expression in allergic contact dermatitis: implications for local skin memory

Nickel Sensitization and Dietary Nickel are a Substantial Cause of Symptoms Provocation in Patients with Chronic Allergic-Like Dermatitis Syndromes

Drug‐elicited systemic allergic (contact) dermatitis – update and possible pathomechanisms

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