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Here, we investigated the mechanism by which TET2-mutant immune cells enable AITL development using mouse models and human samples. Among the 2 mouse models, mice lacking Tet2 in all the blood cells (Mx-Cre\u00a0\u00d7 Tet2flox\/flox\u00a0\u00d7 G17V RHOA transgenic mice) spontaneously developed AITL for approximately up to a year, while mice lacking Tet2 only in the T cells (Cd4-Cre\u00a0\u00d7 Tet2flox\/flox\u00a0\u00d7 G17V RHOA transgenic mice) did not. Therefore, Tet2-deficient immune cells function as a niche for AITL development. Single-cell RNA-sequencing (scRNA-seq) of &amp;gt;50\u2009000 cells from mouse and human AITL samples revealed significant expansion of aberrant B cells, exhibiting properties of activating light zone (LZ)-like and proliferative dark zone (DZ)-like germinal center B (GCB) cells. The GCB cells in AITL clonally evolved with recurrent mutations in genes related to core histones. In silico network analysis using scRNA-seq data identified Cd40\u2013Cd40lg as a possible mediator of GCB and tumor cell cluster interactions. Treatment of AITL model mice with anti-Cd40lg inhibitory antibody prolonged survival. The genes expressed in aberrantly expanded GCB cells in murine tumors were also broadly expressed in the B-lineage cells of TET2-mutant human AITL. Therefore, ACH-derived GCB cells could undergo independent clonal evolution and support the tumorigenesis in AITL via the CD40\u2013CD40LG axis.<\/jats:p>","DOI":"10.1182\/blood.2022015451","type":"journal-article","created":{"date-parts":[[2022,8,3]],"date-time":"2022-08-03T14:56:31Z","timestamp":1659538591000},"page":"1937-1950","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":63,"title":["Clonal germinal center B cells function as a niche for\u00a0T-cell lymphoma"],"prefix":"10.1182","volume":"140","author":[{"given":"Manabu","family":"Fujisawa","sequence":"first","affiliation":[{"name":"1Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tran B.","family":"Nguyen","sequence":"additional","affiliation":[{"name":"1Department of Hematology, Faculty of Medicine, University of Tsukuba, Tsukuba, 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