Narrowband ultraviolet B phototherapy decreased CCR4+ CD8+ T cells in a patient with palmoplantar pustulosis

Editor Palmoplantar pustulosis (PPP) is characterized by symmetrical erythematous scaly plaques with sterile and numerous non-bacterial pinpoint pustules restricted to the palms and soles. As PPP exhibited inflammatory plaque and sterile accumulation of neutrophils, PPP is sometimes regarded as a localized pustular psoriasis. CC chemokine receptor (CCR) 4 has been used as a cell surface marker for type 2 helper and cytotoxic T (Th2 ⁄ Tc2) cells. Recent studies showed that CCR4 CD8 T cells produced interleukin (IL)-4, interferon-c and tumour necrosis factor-a effectively, and that CCR4 CD8 T cells were increased in peripheral blood mononuclear cells (PBMC) in patients with psoriasis. These reports indicate that CCR4 CD8 T cells may be involved in the pathogenesis of psoriasis, but no such increase has been reported in patients with PPP. Here, we report a case of PPP successfully treated with narrowband ultraviolet B (NB-UVB) phototherapy and subsequently exhibiting a decreased CCR4 CD8 T cells. A 63-year-old woman presented with a 10-year history of erythema with pustules and prominent hyperkeratosis on her soles and palms. She had been treated with topical steroid cream prescribed at another clinic over 5 years. As this treatment was not providing sufficient relief of her symptoms, she was referred to our clinic. Physical examination revealed prominent yellowish hyperkeratosis with pustules and vesicles on her soles and palms. Peripheral blood showed a normal leucocyte count. The patient was otherwise healthy. We diagnosed this patient as PPP and started NBUVB treatment at an initial UVB dose of 0.3 J ⁄ cm three times each week. The dose was increased by 0.1 J ⁄ cm every 2 weeks to a maximum dose of 0.7 J ⁄ cm UVB. The patient’s hyperkeratosis with pustules and vesicles improved remarkably within 2 months. In addition, we evaluated the frequency of CCR4 CD8 T cells by means of flow cytometry. APC conjugated anti-CD3 antibody, PE-Cy7 conjugated anti-CD8 antibody and FITC conjugated anti-CCR4 antibody were purchased from eBioscience (San Diego, CA, USA). CD3 CD8 cells were regarded as CD8 T cells (Fig. 1a). The frequency of CCR4 cells in CD8 T cells of the PPP patient before phototherapy (13%) (Fig. 1b) was considerably higher than that of healthy donors (mean ± SD, 2.5 ± 1.4%) (Fig. 1c). After phototherapy, the proportion of CCR4 CD8 T cells had decreased from 13.0% to 7.3% (Fig. 1d). These results suggest that CCR4 CD8 T cells may be involved in the pathogenesis of not only psoriasis but also PPP. Previous reports showed that NB-UVB reduced CD8 memory-effector T cells in psoriatic lesions, although we did not evaluate the infiltration of CCR4 CD8 T cells in the skin lesion of PPP. One possible explanation of systemic effect by localized NB-UVB phototherapy is that CCR4 CD8 T cells may be mainly derived from the skin. In fact, the skin has a potential to develop, maintain and expand memory T cells. Although it is limited to a single case and we still have much to learn, our observation on CCR4 CD8 T cells in PPP may shed light on the mechanisms underlying PPP.