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The immune response of patients with seborrhoeic dermatitis and healthy age- and sex-matched controls was examined to test the hypothesis that an inadequate or inappropriate immune response to Malassezia yeast leads to seborrhoeic dermatitis. Antibody responses were examined using enzyme-linked immunosorbent assays (ELISAs) and Western blots and lymphocyte responses using lymphocyte proliferation assays. The level of IgG and IgM specific for whole yeast cells or extracted proteins of two isolates of M. furfur was tested in ELISA. A wide range of antibody levels was found but the patient and control groups were indistinguishable (n = 19), and the groups could not be distinguished by the pattern of Malassezia proteins recognized by their sera in Western blots. The average affinity of the subjects' antibodies specific for Malassezia cells or proteins was measured using ammonium thiocyanate dissociation. Most of the sera had moderate affinities corresponding to 50% dissociation at thiocyanate concentrations of 0.5-1.0 mol/L. There was no difference between patients and matched controls. The proliferation of the patients' lymphocytes in response to a number of M. furfur cell preparations was measured: whole cells, cytoplasmic proteins, cell walls, soluble molecules extracted from the cell walls using sonication, and a commercial preparation. There was a wide range of responses between individuals, but there was no difference between the three groups: patients with seborrhoeic dermatitis (n = 16), healthy controls (n = 16) and a group suffering from other inflammatory skin conditions (n = 15). The results do not support the hypothesis that an inadequate immune response to Malassezia yeast could lead to seborrhoeic dermatitis. Other possible pathological mechanisms include toxin production or lipase activity.
Parry et al. (Sat,) studied this question.