Presence of activated lymphocytes in the peripheral blood of patients with halo nevi

Baranda, Lourdes; Torres-Álvarez, Bertha; Moncada, Benjamín; Portales-Pérez, Diana Patricia; Fuente, Hortensia de la; Layseca, Esther; González‐Amaro, Roberto

doi:10.1016/s0190-9622(99)80054-1

Cited by 17 publications

(8 citation statements)

References 38 publications

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“…Although no direct demonstration of melanocyte killing has been observed by the immuno effector cells found within the halo, the abundance of antigen presenting cells in the regressing nevus and the presence of T lymphocytes at the site of depigmentation point to the involvement of CD8+ T cells as the potential effectors in the destruction of nevo melanocytes (24). In peripheral blood of patients with halo nevi, lymphocytes demonstrated significant higher activation markers (CD69+, HLA‐DR+, CD98, with a proliferating/CD71 bright) and high adhesive (HUTS‐21 bright) phenotype, compared with healthy subjects (25).…”

Section: Discussionmentioning

confidence: 98%

Difference in Pathogenesis Between Vitiligo Vulgaris and Halo Nevi Associated with Vitiligo is Supported by an HLA Association Study

Vijlder

Westerhof

Schreuder

et al. 2004

Pigment Cell Research

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Human leukocyte antigen (HLA) class II associations with two subtypes of vitiligo: vitiligo vulgaris and halo nevi associated with vitiligo were investigated. In previous studies associations between vitiligo and HLA antigens have been reported but these two subtypes have never been taken into account. However from a clinical and histological point of view, a difference in (auto)-immune pathogenesis can be expected. This difference might be reflected in an association with different HLA alleles. Seventy-six unrelated Dutch Caucasians, 40 with vitiligo vulgaris and 36 with halo nevi associated with vitiligo were included. A panel of randomly chosen HLA typed healthy Dutch blood donors (n = 2400) served as control population. HLA-DR and -DQ typing was carried out on blood samples by amplifying genomic DNA using polymerase chain reaction followed by dot blot hybridization with sequence specific oligonucleotides. The main outcome measures were odds ratio (OR), uncorrected P-value (P(u)) and corrected P-value. There were distinct differences in the clinical manifestations between vitiligo vulgaris and halo nevi associated with vitiligo with respect to precipitating factors, extent and progress of the disease and the association with other auto-immune diseases in the two subtypes and their respective first degree family members. Our stratification reveals differences in HLA class II between both subtypes and between subtypes and controls. A case-control association study showed a significant positive association of HLA-DR4 (OR = 2.787, P(u) = 0.0022) and DR53 (OR = 2.249, P(u) = 0.0153) and a negative association of HLA-DR3 (OR = 0.195, P(u) = 0.0024) with vitiligo vulgaris. The group with halo nevi associated with vitiligo did not show these associations, but had a significant negative association with HLA-DR11 (OR = 0.083, P(u) = 0.0067). In conclusion, the differences in HLA association within clinical subtypes of vitiligo support our suggestion that vitiligo vulgaris and halo nevi associated with vitiligo have distinct pathogenic mechanisms.

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Section: Discussionmentioning

confidence: 98%

Difference in Pathogenesis Between Vitiligo Vulgaris and Halo Nevi Associated with Vitiligo is Supported by an HLA Association Study

Vijlder

Westerhof

Schreuder

et al. 2004

Pigment Cell Research

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“…During the formation and regression of halo nevi, infiltrates composed of T cells, in particular CD8+ cytotoxic suppressor cells, have been observed [16, 17]. In addition, circulating activated lymphocytes were seen in patients with halo nevi and their disappearance was documented following surgical resection [18]. The immunopathogenesis of halo nevi does seem to overlap with that of inflammatory vitiligo.…”

Section: Discussionmentioning

confidence: 99%

Unusual Halo Nevi – Darkening Rather than Lightening of the Central Nevus

Huynh¹,

Lazova

Bolognia³

2001

Dermatology

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Although the classic halo nevus is a brown nevus with a surrounding rim of depigmentation, i.e. a stage I halo nevus, these nevi can have several clinical stages. The central nevus may lose its pigmentation and appear pink with a surrounding halo (stage II), the central papule may disappear leading to a circular area of depigmentation (stage III) or the depigmented area may repigment (stage IV), leaving no trace of its prior existence. Herein we describe an unusual phenomenon – darkening of the central nevus rather than lightening – following the appearance of the halo phenomenon. An 18-year-old boy who had multiple atypical nevi developed multiple halo nevi beginning at the age of 12 years. Following the appearance of the peripheral halos, 2 of his nevi that were originally solid medium brown in color darkened and the hyperpigmentation had a reticulated pattern with perifollicular sparing. One possible explanation is a postinflammatory hyperpigmentation induced by the infiltrating lymphocytes.

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“…Although HN frequently appears at sites close to areas of vitiligo, as well as at remote sites, 2 it is reported to differ in pathogenesis from vitiligo vulgaris 3 . Some studies have indicated that the halo phenomenon in HN is usually associated with an inflammatory cell infiltration in the central nevus and that T cell‐mediated immunity plays an important role 3,4 . In our case, lymphocytic infiltration of the melanocytic nest from the NS lesion was apparent.…”

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confidence: 51%