Affiliation:
1. Department of Microbiology and Infection, Kochi Medical School Kochi University Nankoku Japan
2. Division of Chemotherapy Kindai University Faculty of Pharmacy Higashi‐Osaka Japan
3. Science Research Center Kochi University Nankoku Japan
4. Department of Pathology, Kochi Medical School Kochi University Nankoku Japan
Abstract
AbstractEpstein–Barr virus (EBV)‐positive diffuse large B‐cell lymphoma associated with chronic inflammation (DLBCL‐CI) develops in the setting of long‐standing inflammation. This type of lymphoma may have specific expression profiles of chemokines involved in the pathogenesis of DLBCL‐CI. EBV‐positive pyothorax‐associated lymphoma (PAL) is a prototype of DLBCL‐CI and represents a valuable model for the study of this disease category. Using a panel of PAL cell lines, we found that PAL cells expressed and secreted C–X–C motif chemokine ligands 9 and 10 (CXCL9 and CXCL10), the ligands of CXCR3, in contrast to EBV‐negative DLBCL cell lines, which did not. Culture supernatants from PAL cell lines attracted CXCR3‐expressing CD4+ T cells, CD8+ T cells, and CD56+ natural killer cells from human peripheral blood mononuclear cells. PAL cells injected into mice also attracted CXCR3‐positive cytotoxic lymphocytes that expressed interferon‐γ. The expression of CXCL9 and CXCL10 was detected in PAL tumor biopsy samples from patients, and CXCR3‐positive lymphocytes were abundant in the tissue samples. Collectively, these findings suggest that CXCL9 and CXCL10 are produced by PAL cells and can elicit cytotoxic responses via CXCR3. This chemokine system is also likely to contribute to tissue necrosis, which is a signature histological feature of DLBCL‐CI. Further studies are warranted to determine whether the CXCL9–CXCL10/CXCR3 axis exerts antitumor effects in DLBCL‐CI.
Funder
Japan Society for the Promotion of Science
Subject
Cancer Research,Oncology,General Medicine
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献