Role of TNF-alpha polymorphism in patients with nickel allergy: a marker of susceptibility to contact polysensitization
A. Colagiovanni, L. Di Renzo, F. Sarlo, D. Schiavino, A. De Lorenzo
Allergy Department, Catholic University of the “Sacred Heart”, Agostino Gemelli Hospital, School of Medicine, Rome, Italy. amiracolagiovanni@virgilio.it
OBJECTIVE: Nickel allergy is the most frequent contact allergy in the industrialized country. In allergic contact dermatitis after the presentation of haptenated peptides by resident or newly recruited skin cells, activated CD8+ T cells release IFN-γ and TNF-α, these cytokines are potent activator of keratinocytes. The role of specific cytokines in nickel allergy is not yet fully elucidated. The adenine nucleotide at position -308 in the promoter region of the TNFA gene is associated with an increased production of TNF-α, that is a potent activator of keratinocytes.
PATIENTS AND METHODS: To evaluate the expression of TNF-α polymorphism in patients with allergic contact dermatitis and in healthy people, 41 patients with allergic contact dermatitis to nickel and 40 healthy controls were enrolled. A total of 81 subjects (41 cases and 40 controls) underwent genotyping for the 308 genetic polymorphism in the TNFA gene.
RESULTS: The distribution of TNF genotypes TNF-α 308 G/A polymorphism in cases didn’t differ significantly in the controls group. The genotype GA was present in the 75% of the patients with polysensitization. In one patient was observed the rare genotype A/A.
CONCLUSIONS: The carriage of the TNFA–308 A/A and GA genotype may act as a marker of enhanced susceptibility to contact polysensitization, indicating that TNF-α is a key regulator of the initiation of delayed-type hypersensitivity reactions, the polymorphism seems to be not enough for the development of nickel monosensitization.
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