{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T00:00:49Z","timestamp":1790035249928,"version":"4.0.1"},"reference-count":31,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,8,22]],"date-time":"2012-08-22T00:00:00Z","timestamp":1345593600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2013,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>BACKGROUND:<\/jats:title><jats:p>Mantle cell lymphoma (MCL) is an incurable B\u2010cell malignancy, and patients with this disease have the poorest prognosis among all patients with B\u2010cell lymphomas. The signaling pathways that trigger MCL escape from immune surveillance are unclear. Because Toll\u2010like receptors (TLRs) initiate innate and adaptive immune responses against invading pathogens, the authors investigated the impact of TLR signaling in MCL cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS:<\/jats:title><jats:p>TLR expression was examined in MCL cell lines and in primary tumors. The examination focused on TLR4 and its ligand lipopolysaccharide (LPS) on MCL cells and their function on MCL proliferation and immune evasion.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS:<\/jats:title><jats:p>MCL cells expressed multiple TLRs, and TLR4 was among the highest expressed molecules. The activation of TLR4 signaling in MCL cells by LPS induced MCL proliferation and up\u2010regulated the secretion of cytokines like interleukin\u20106 (IL\u20106), IL\u201010, and vascular endothelial growth factor (VEGF). LPS\u2010pretreated MCL cells inhibited the proliferation and cytolytic activity of T cells by secreted IL\u201010 and VEGF, and neutralizing antibodies against these cytokines restored their functions. Similar results were observed in TLR4\u2010positive\/myeloid differentiation 88 (MyD88)\u2010positive primary lymphoma cells but not in TLR4\u2010positive\/MyD88\u2010negative primary lymphoma cells from patients with MCL. Knockdown of TLR4 on MCL cells abrogated the effect of LPS on MCL cells in term of cell growth or secretion of the cytokines and evasion of the immune system.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSIONS:<\/jats:title><jats:p>The current results indicated that TLR4 signaling triggers a cascade that leads to MCL growth and evasion from immune surveillance. Thus, TLR4 signaling molecules may be novel therapeutic targets in patients with MCL. Cancer 2013. \u00a9 2012 American Cancer Society.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cncr.27792","type":"journal-article","created":{"date-parts":[[2012,8,22]],"date-time":"2012-08-22T13:37:45Z","timestamp":1345642665000},"page":"782-791","source":"Crossref","is-referenced-by-count":48,"title":["Toll\u2010like receptor\u20104 signaling in mantle cell 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