Halo nevus rarely occurs in a congenital nevus. The mechanisms leading to the development of halo nevus are still a matter of debate, but the main hypothesis involves a cellular immune response targeting the pigmented cells, and this is perhaps elicited in some cases by the presence of abnormal, probably premalignant melanocytes either within or at some distance from the halo nevus. Some researchers have postulated that the halo nevus is related to the atypical nuclear changes “commonly” found in the scattered, dark brown speckles in the brown patch of nevus spilus. These atypical nuclear changes act as the initiating factor for an immune response. Once the immune response is initiated, it recognizes common antigens in both the atypical cells and the normal cells. It is the immunologic response that causes the halo phenomenon to cross- react with normal nevus; this would explain the occurrence of multiple halo nevi in some patients.

As for the association between halo nevus and vitiligo, both phenomena are often seen in the same patient at the same time or at the different times. There is controversy about the nature of both conditions as to whether ere there were merely parts of the same phenomenon or they are caused by processes that are unrelated to each other. Halo nevus and vitiligo share some histopathologic features and probably some pathophysiologic features, but a common entity has not yet been confirmed. In both conditions, a mononuclear cell infiltration is found in close contact with melanocytes, and these mela¬nocytes show ultrastructural signs of degeneration and cellular damage, resulting in depigmentation. About 80% of the mononuclear infiltrate of halo nevi are T cells with a relatively high percentage of CD8+ suppressor/cytotoxic T-cells compared to CD4+ cells. Autoantibodies directed against mela¬nocytes have been found in the serum of patients with halo nevus and vitiligo. Because of these observations, autoimmune mechanisms are believed to be essential for the destruction of the melano- cytes in vitiligo as well as those in halo nevus. Nevertheless, halo nevus and vitiligo are distinct entities and they exhibit different pathogenic mecha¬nisms, as has been recently shown. The differences of HLA association within the clinical subtypes of vitiligo support that vitiligo and vitiligo-associated halo nevi may have distinct pathogenic mechanisms. Moreover, even though both conditions clinically present with white appearance, there is a distinct difference under a Wood’s light examination: vitiligo demonstrates a characteristic bluish/yellowish fluorescence, whereas the depigmented area of halo nevus does not. We speculate that halo nevus and vilitgo may be the end points of different im- munological processes despite that the immune responses to the pigment cell antigens are shared by normal melanocytes and the nevus cells.
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