{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:18:56Z","timestamp":1790745536527,"version":"4.1.0"},"reference-count":57,"publisher":"American Society of Hematology","issue":"5","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2020,3,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive peripheral T-cell lymphoma driven by a pool of neoplastic cells originating from T follicular helper (Tfh) cells and concomitant expansion of B cells. Conventional chemotherapies for AITL have shown limited efficacy, and as such, there is a need for improved therapeutic options. Because AITL originates from Tfh cells, we hypothesized that AITL tumors continue to rely on essential Tfh components and intimate T-cell\u2013B-cell (T-B) interactions. Using a spontaneous AITL mouse model (Roquinsan\/+ mice), we found that acute loss of Bcl6 activity in growing tumors drastically reduced tumor size, demonstrating that AITL-like tumors critically depend on the Tfh lineage\u2013defining transcription factor Bcl6. Because Bcl6 can upregulate expression of signaling lymphocytic activation molecule\u2013associated protein (SAP), which is known to promote T-B conjugation, we next targeted the SAP-encoding Sh2d1a gene. We observed that Sh2d1a deletion from CD4+ T cells in fully developed tumors also led to tumor regression. Further, we provide evidence that tumor progression depends on T-B cross talk facilitated by SAP and high-affinity LFA-1. In our study, AITL-like tumors relied heavily on molecular pathways that support Tfh cell identity and T-B collaboration, revealing potential therapeutic targets for AITL.<\/jats:p>","DOI":"10.1182\/bloodadvances.2019001114","type":"journal-article","created":{"date-parts":[[2020,3,4]],"date-time":"2020-03-04T16:40:10Z","timestamp":1583340010000},"page":"868-879","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":25,"title":["Progression of AITL-like tumors in mice is driven by Tfh signature proteins and T-B cross talk"],"prefix":"10.1182","volume":"4","author":[{"given":"Mariko","family":"Witalis","sequence":"first","affiliation":[{"name":"Institut de Recherches Cliniques de Montr\u00e9al (IRCM), Montr\u00e9al, QC, Canada;"},{"name":"Molecular Biology Department, University of Montr\u00e9al, Montr\u00e9al, QC, Canada;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinsam","family":"Chang","sequence":"first","affiliation":[{"name":"Institut de Recherches Cliniques de Montr\u00e9al (IRCM), Montr\u00e9al, QC, Canada;"},{"name":"Molecular Biology Department, University of Montr\u00e9al, Montr\u00e9al, QC, Canada;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ming-Chao","family":"Zhong","sequence":"first","affiliation":[{"name":"Institut de Recherches Cliniques de Montr\u00e9al (IRCM), Montr\u00e9al, QC, Canada;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasser","family":"Bouklouch","sequence":"first","affiliation":[{"name":"Institut de Recherches Cliniques de Montr\u00e9al (IRCM), Montr\u00e9al, QC, Canada;"},{"name":"Department of Experimental Medicine, McGill University, Montr\u00e9al, QC, 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