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One-hundred and two patients from the area of Hamburg, Germany, with vitiligo (photo-skin types II and III, Fitzpatrick classification, 1979), were examined for a possible association of the human lymphocyte antigen (HLA) complex with this disease. Antisera panels for the detection of 75 HLA antigens were utilized for this HLA typing (WHO Bulletin, 1988). The results were compared with 400 unrelated age- and sex-matched controls with photo-skin types II and III from the same geographical area. Nine of 76 vitiligo patients showed a significantly increased expression of the rare antigen HLA DRW 12 (p_c = 0.000708), and 65/102 patients showed a marginally significant increased frequency of HLA A2 (p_c = 0.04850) compared with controls. For HLA BW60 (40), a significant increase in frequency was shown only in the adult vitiligo group (p_c = 0.0126). A ‘preventive’ antigen for the manifestation of vitiligo has not been identified in this study. A comparative analysis of all published data on the possible association of HLA with vitiligo does not support a definitive linkage to the MHC so far.

Objective-Sulfatides are sulfated glycosphingolipids present on the surface of a variety of cells; however, their exact physiological function is not known. Recently, we have shown that the inhibition of sulfatide-P-selectin interactions leads to disaggregation of platelet aggregates. Methods and Results-In this study, we show that sulfatides activated platelets as they increased activation of GPIIb/IIIa (PAC-1 epitope) and expression of P-selectin on the platelet surface. Furthermore, sulfatides aggregated washed platelets in a dose-dependent manner and enhanced platelet aggregation in platelet-rich plasma. Previous activation of platelets was necessary for this effect. Monoclonal anti-P-selectin antibodies inhibited not only sulfatide-induced PAC-1 binding to platelets but also sulfatide-induced platelet aggregation, suggesting that sulfatides activate platelet GPIIb/IIIa via signaling through P-selectin. The proaggegatory effect of sulfatides was also observed in an ex vivo thrombosis model using whole blood and pulsatile flow at 37°C. In this model, sulfatides significantly enhanced platelet aggregation and the formation of platelet-leukocyte aggregates. Conclusions-We show that sulfatide-P-selectin interactions lead to subsequent platelet activation and P-selectin expression, forming a positive feedback loop that can potentiate formation of stable platelet aggregates. In addition, sulfatides enhance the aggregation of platelet-leukocyte aggregates. These mechanisms may play a significant role in hemostasis and thrombosis.

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