DISTINCTIVE DENDRITIC CELL SUBSETS EXPRESSING FACTOR XIIIA, CD1A, CD1B AND CD1C IN MYCOSIS-FUNGOIDES AND PSORIASIS

The papillary dermis of psoriasis and mycosis fungoides (MF) lesions is characterized by prominent collections of cells with dendritic morphology. Immunophenotypically distinct populations of cutaneous dendritic cells have been identified as CD1a+, FXIIIa-Langerhans cells (LC) and CD1a-, FXIIIa+ dermal dendritic cells (DDC). In this study, antibodies against the human CD1 cluster of antigens (i.e. CD1a, CD1b and CD1c) and the DDC marker (FXIIIa) were used to further characterize the subsets of dendritic cells in normal skin as compared to neonatal foreskin, psoriasis and MF by both immunoperoxidase and double immunofluorescence techniques. Normal skin and foreskin epidermis and dermis contained few CD1b+ or CD1c+ cells along with normal numbers of CD1a+ LC and FXIIIa+ DDC. Both MF and psoriasis were characterized by CD1a+ cells in the epidermis and dermis. FXIIIa+ cells were greatly expanded in the upper dermis of MF lesions and to a lesser degree in psoriasis as has been previously described by our group. MF contained significantly increased epidermal and dermal CD1b+ (15.7/5 high power fields [HPF] and 59.7/5 HPF respectively) and CD1c+ dendritic cells (33.8/5 HPF and 95.9/5 HPF respectively), while in psoriasis these cells were not statistically different from normal skin. Double immunofluorescence studies revealed that some (<25%) FXIIIa+ cells co-expressed CD1b and CD1c in MF>psoriasis> foreskin, while FXIIIa+ DDC never co-expressed CD1a. Thus, in contrast to normal skin in which epidermal or dermal dendritic cells rarely express CD1b and CD1c antigens, these members of the CD1 family are upregulated on both LC and DDC in benign and malignant inflammatory states. Upregulation of CD1b and CD1c on MF epidermal and dermal dendritic cells, as compared to psoriasis, foreskin and normal skin, may be useful in the immunophenotypic recognition of MF, as well as in helping to understand its immunobiology.