Absence of MYD88 L265P mutation in blastic plasmacytoid dendritic cell neoplasm

high amount of IL-22 (Fig. 2d). We treated the patient with systemic antibiotics (vancomycin and linezolid) because of sepsis due to methicillin-resistant Staphylococcus aureus (MRSA). The antibiotics improved pyogenic spondylitis causative for sepsis, but did not change the frequency of circulating or skin-infiltrating CD8 tumour cells. Concomitantly with the infection improvement, 5 weeks later, the serum IL-22 level was dramatically decreased (Fig. 2e). Both aggressive and indolent subtypes of CD8 CTCL exist. While the indolent type includes CD8 variants of mycosis fungoides, Sézary syndrome and anaplastic large-cell lymphoma, the aggressive type is represented by primary cutaneous CD8 epidermotropic cytotoxic T-cell lymphoma. In our case, circulating CD8 tumour cells were positive for CD7 (CD8CD7; 47Æ7%), but negative for CD2 (CD8CD2; 38Æ2%), which shares the phenotype with the aggressive type of CD8 CTCL. However, we diagnosed the eruption as CD8 variant of Sézary syndrome because of its clinically indolent course or histologically TIA-1-negative property. The enhanced IL-22 production can be seen in the immunoactivation associated with bacterial infection. Recently, increased serum IL-22 levels were reported in patients with CTCL, suggesting the correlation with bacterial infections in affected skin. The mean serum levels of IL-22 in patients with abdominal septic shock was 111Æ8 pg mL. Our patient showed a higher serum level of IL-22 than those patients, suggesting that CD8 tumour cells produced the high amount of IL-22 possibly responding to bacterial pathogens. We speculate that the malignant CD8 T cells responded to bacterial pathogens and had a capacity to produce IL-22, which contributed to host immune defence.