Mycosis fungoides, the most common type of
cutaneous T-cell lymphoma (CTCL), is characterized by a helper T-cell 2 (Th2) skewing with a mature CD4(+) memory T-cell phenotype. Using skin samples from patients with
mycosis fungoides (n = 21), healthy volunteers (n = 17), and individuals with
atopic dermatitis (n = 17) and
psoriasis (n = 9), we found IL32
mRNA expression significantly higher in
mycosis fungoides samples than in samples from benign inflammatory
skin diseases, and its expression increases with
disease progression. By IHC and immunofluorescence, we confirmed IL32
protein expression in many CD3(+)CD4(+) T cells and some epidermotropic T cells in
mycosis fungoides lesions. MyLa cells (a
mycosis fungoides cell line) express IL32, which, in turn, could promote cellular proliferation and viability in a dose-dependent fashion. IL32-treated MyLa and CTCL HH cells upregulated cell proliferation and survival genes. Of the major "polarizing" T-cell
cytokines, only IFNγ
mRNA increases with
mycosis fungoides progression and positively correlates with IL32
mRNA expression. Th2
cytokines do not positively correlate with IL32
mRNA expression or
mycosis fungoides progression. Furthermore, by flow cytometry, IL32 production by circulating activated T cells in healthy individuals was found in both IFNγ(+) and IFNγ(-) cells but not in
IL4(+) or
IL13(+) cells. In conclusion, we have identified IL32(+) cells as the likely
tumor cells in
mycosis fungoides, and demonstrated that IL32
mRNA expression increases with
mycosis fungoides progression and is significantly higher than
mRNA expression in other
skin diseases, and that some IL32(+) T cells are independent from the defined Th subsets. Thus, IL32 may play a unique role in
mycosis fungoides progression as an autocrine
cytokine.