Cell-bound IgE and increased expression of Faɛ-receptors on dendritic cells in cutaneous infiltrates of mycosis fungoides

SUMMARY Skin biopsies of 31 non-atopic patients, 20 with mycosis fungoides, six with psoriasis and five with contact dermatitis, and of five non-atopic healthy controls were compared for the presence of cell-bound IgE and vacant IgE binding sites. IgE+ cells were demonstrated in the cutaneous infiltrate of nine (45%) patients with mycosis fungoides, two (33%) with psoriasis and one (20%) with contact dermatitis. Following pre-incubation of skin sections wilh IgE myeloma protein to saturate vacant IgE-binding sites, 14 out of 16 patients (88%) with stage I mycosis fungoides, five (83%) patients with psoriasis and one (20%) with contact dermatitis showed an increase in the number of IgE+ cells. While cell-bound IgE was positively related to serum IgE levels the expression of IgE-binding sites was not. All IgE+ cells were HLA-DR+ dendritic cells identified as either macrophages (CD68+, CDI4+) or Langerhans cells (CDl+). Skin biopsies of non-atopic healthy controls or clinically uninvolved skin in mycosis fungoides had neither any IgE+ cells nor any vacant binding sites. Inhibition studies with IgGl, IgG4 and IgE myeloma proteins as well as with several enzymatic fragments of igE demonstrated that IgE interacled with Fcɛ-receptors through isotype-specific structures on the Fcɛ-fragment. Four anti-CD23 monoclonal antibodies, however, were unuble to stain vacant Fcɛ-receptors nor could they block IgE-binding. We hypothesize that locally-secreted lymphokines, like IL-4 or interferon-γ, induce Fcɛ-receptors on dendritic cells in the cutaneous infiltrate and that these receptors become occupied in parallel wilh elevated serum IgE levels.