Background: Demodicosis is a chronic skin disease caused by parasitic mites of the genus Demodex. It usually affects the face area causing major esthetical problems. The pathogenesis of demodicosis is not fully understood; however, it is quite apparent that immunological mechanisms mediate its development. Objective: The goal of this study was to study the correlation between immunological and immunogenetic data obtained from patients with demodicosis in order to clarify the pathogenesis of Demodex infestation. Methods: Twenty-five patients with demodicosis and 13 age- and sex-matched healthy subjects participated in the study. The presence of mites was determined by microscopic inspection of sebum gland secretions. The immune response was evaluated by identifying membrane markers of different immune cells using monoclonal antibodies (anti-CD3+, CD4+, CD8+, CD16+, CD20+ and CD95+) while the concentration of IgA, IgM and IgG was measured by simple radial immunodiffusion. The level of circulating immune complexes and total hemolytic complement as well as the preparatory and digestive function of neutrophils and the functional activity of leukocytes were also studied. Patients were typed for HLA A, B, Bw and Cw using the microlymphocytotoxicity method. Results: The comparison between patients with and without the A2 phenotype showed that the latter have lower numbers of CD8+, lower functional activity of leukocytes, higher concentrations of IgA, larger affected skin areas and are more often affected by deep papular and papulopustular forms of demodicosis than those with the A2 phenotype, showing that this allele has a protective role in demodicosis. Patients exhibiting the Cw2 phenotypes were rather susceptible to demodicosis. They showed decreased numbers of CD3+, increased levels of phagocytic activity, higher mite density and severer skin damage as compared to patients lacking Cw2. Conclusions: The HLA A2 and Cw2 phenotypes have an important diagnostic, prognostic and pathogenetic significance and could play a role in resistance or susceptibility to demodicosis by regulating the end phase of the immune response.

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