Halo nevus

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The halo nevus is characterized histologically by a dense lymphocytic infiltrate enveloping the cells of a compound nevus. Clinically the nevus develops a depigmented outer ring in the skin surrounding it (Figure). The nevus itself often disappears spontaneously and the depigmented halo usually repigments. Numerous mechanisms have been postulated for this phenomenon of spontaneous regression of a benign tumor.1 Results of recent studies by Copeman et al2 implicated circulating antibody as the mechanism responsible for regression of the halo nevus. The conclusions are based on the demonstration of antibodies in the sera of some halo nevi patients to the cytoplasm of malignant melanoma cells.

Immune response occurs by two mechanisms, cellular (T-cell) and humoral (B-cell). Cell-mediated immunity is primarily responsible for tumor and transplant rejection, not humoral immunity (antibody).


Studies of tumor immunity were performed by the cell inhibition (CI) (microcytotoxicity) assay described by the Hellströms3 with slight modifications. Target cells were derived from melanoma cell lines grown in vitro in tissue culture starting with tumor tissue. At the time of testing, these cells had gone through 5 to 15 passages. Since it was not possible to grow each patient’s tumor cells in every test, the target cells were allogeneic with respect to the patient’s lymphocytes. Approximately 100 cells were seeded into each well of a Falcon No. 3040 microtest plate, and on the following day the cells were exposed to combinations of blood lymphocytes and sera from patients and controls. The tumor cells were known not to divide. . .



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