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Type D lymphomatoid papulosis associated with chemotherapy/chemoradiotherapy‐induced severe chronic lymphocytopenia

upper back showed bottom-heavy dense nodular infiltrates consistent with large atypical cells and many small inflammatory cells (Fig. 1c,d). Atypical cells were positive for CD20, CD79a, B-cell lymphoma (Bcl)-2 (Fig. 1e–h) and forkhead box (Fox)P1, partially positive for Bcl-6 (Fig. 1i), but negative for multiple myeloma oncogene 1, CD10 and immunoglobulin (Ig) M. Small lymphoid cells were positive for CD3 (Fig. 1j). Monoclonal Ig heavy chain rearrangement was detected by Southern blotting. Epstein–Barr virus-encoded sRNA was not detected in the tumor by in situ hybridization. Positron emission tomography and enhanced computed tomography did not disclose any nodal or visceral involvement. We diagnosed the patient with primary cutaneous diffuse large B-cell lymphoma (DLBCL), not otherwise specified (T2, N0, M0). Most of the lesions, including unbiopsied ones, disappeared after biopsy; however, the plaque on the left flank remained (Fig. 1k). We performed a skin biopsy on the remaining lesion. Its pathology was similar to that of the previously biopsied lesions, except this lesion remained after biopsy and was treated with 30 Gy of radiation therapy. The patient was free from recurrence or distant metastasis for a year. Tumor-infiltrating T lymphocytes play an important role in anticancer immune responses as cytotoxic T lymphocytes (CTL), through directional exocytosis of cytotoxic granules into the specific target leading to tumor cell death. Previously, CD8-positive cells infiltrated a regressing lesion of primary cutaneous B-cell lymphoma treated with an anti-CD20 antibody. While we previously proposed the possibility that CTL promote spontaneous regression of DLBCL, leg type, inflammatory cells (CD4-positive or CD8-positive cells), including CTL (T-cell intracytoplasmic antigen 1-positive cells, Fig. 1l–n), infiltrated both the lesions that had regressed and those that had not regressed to a similar extent in the present case. The numbers of FoxP3-positive cells and programmed cell death 1 (PD-1)-positive cells were significantly higher in the lesion that did not regress than in the regressed lesions (Fig. 1o–v). FoxP3-positive regulatory T cells (Treg) strongly inhibit effector cells that mediate antitumor immunity. CD4CD25 T cells, assumed to be Treg, suppressed CD8 T-cell proliferation and c-interferon production, and a high density of tumor-infiltrating Treg was associated with a poor outcome in various solid tumors. Regarding PD-1-positive cells, the tumor cells of primary cutaneous B-cell lymphoma were reported not to express PD-1. Thus, PD-1-positive cells in this patient should be tumor infiltrating cells, such as CTL. PD-1 engagement switches activated CD8 T cells to an exhausted phenotype, characterized by the inability to mount a CTL response. Thus, we suppose that the Treg and PD-1-positive cells inhibited the regression of the skin lesion in this patient.