Search

We report a case of a 74-year-old man with a cluster of differentiation (CD) 7-positive diffuse large B-cell lymphoma (DLBCL) in the right nasal cavity. Flow cytometry analyses showed CD7 and CD20 positivity in tumor cells. The patient received 6 cycles of R-CHOP plus local radiation therapy because positron emission tomography-computed tomography after R-CHOP revealed an intranasal lesion. The patient achieved complete remission (CR) after radiation therapy. The frequency of CD7-positive DLBCL is rare, and only 11 cases with follow-up of clinical course have been reported thus far. CR or partial response was noted in 8 of 11 cases after receiving rituximab combined with chemotherapy. In total, 9 of 12 cases involved the development of extranodal lesions, which occurred as an intranasal tumor in 3 cases. It is important to examine the clinical features by accumulation of further cases.

Since immune responses simultaneously defend and injure the host, the immune system must be finely regulated to insure the host's survival. Here, we show that when injected with high TLR ligand doses or infected with LCMV clone 13, which has a high viral turnover, inflammatory monocyte-derived dendritic cells (Mo-DCs) are induced to engulf apoptotic erythroid cells. In this process, called hemophagocytosis, extracellular ATP and phosphatidylserine (PS) serve as “find-me” and “eat-me” signals, respectively. Type I IFNs are necessary for both PS exposure on erythroid cells and the expression of PS receptors in the Mo-DCs. Importantly, hemophagocytosis is required for IL-10 production from Mo-DCs. Blocking hemophagocytosis or Mo-DC-derived IL-10 significantly increases CTL activity, tissue damage, and mortality in virus-infected hosts, suggesting that hemophagocytosis moderates immune responses to assure the host’s survival in vivo. This sheds light on the induction mechanisms and physiological relevance of hemophagocytosis in severe inflammatory and infectious diseases.