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This study examined the role of B cell\u2013activating factor (BAFF), a major driver of B cell proliferation and many B cell disorders, in this malignancy using a model in which conditional knockout mice for NOD\u2010like receptor family CARD domain\u2010containing 5 (\n                    <jats:italic>Nlrc5<\/jats:italic>\n                    ) are infected with\n                    <jats:italic>Helicobacter felis<\/jats:italic>\n                    . Gastric BAFF production was significantly increased in\n                    <jats:italic>H. felis<\/jats:italic>\n                    \u2013infected\n                    <jats:italic>Nlrc5<\/jats:italic>\n                    <jats:sup>m\u00f8\u2010KO<\/jats:sup>\n                    mice compared to wild\u2010type. Blocking BAFF signalling, before or after the onset of\n                    <jats:italic>Helicobacter<\/jats:italic>\n                    \u2010induced gastritis, significantly reduced MALT development, with fewer gastric B cell follicles and reduced gland hyperplasia. BAFF blockade also reshaped the immune cell landscape in the stomach, resulting in fewer CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells, Tregs, macrophages and dendritic cells. Using a cell culture model, we identified the protein\u2010coding\n                    <jats:italic>BAFF<\/jats:italic>\n                    transcripts that are upregulated in NLRC5\u2010deficient macrophages stimulated with either\n                    <jats:italic>H. felis<\/jats:italic>\n                    or the NLRC5 agonist, lipopolysaccharide. Among the upregulated variants,\n                    <jats:italic>TNFSF13B (BAFF)\u2010206<\/jats:italic>\n                    acts as a transcription factor and is reported to enhance BAFF production in autoimmune diseases and cancer. Altogether, these findings implicate the NLRC5\u2013BAFF signalling axis in\n                    <jats:italic>Helicobacter<\/jats:italic>\n                    \u2010induced B cell MALT lymphoma, highlighting BAFF inhibition as a potential therapeutic approach.\n                  <\/jats:p>","DOI":"10.1002\/eji.202451355","type":"journal-article","created":{"date-parts":[[2024,12,17]],"date-time":"2024-12-17T03:25:31Z","timestamp":1734405931000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["BAFF Blockade Attenuates B Cell MALT Formation in Conditional\n                    <i>Nlrc5<\/i>\n                    \u2010Deficient Mice With\n                    <i>Helicobacter felis<\/i>\n                    Infection"],"prefix":"10.1002","volume":"55","author":[{"given":"Dongmei","family":"Tong","sequence":"first","affiliation":[{"name":"Centre for Innate Immunity and Infectious Diseases Hudson Institute of Medical Research  Clayton Victoria Australia"},{"name":"Department of Molecular and Translational Science Monash University  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuqi","family":"He","sequence":"additional","affiliation":[{"name":"Centre for Innate Immunity and Infectious Diseases Hudson Institute of Medical Research  Clayton Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shambel Araya","family":"Haile","sequence":"additional","affiliation":[{"name":"Centre for Innate Immunity and Infectious Diseases Hudson Institute of Medical Research  Clayton Victoria Australia"},{"name":"Department of Molecular and Translational Science Monash University  Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zoe","family":"Lee","sequence":"additional","affiliation":[{"name":"Centre for Innate Immunity and Infectious Diseases Hudson Institute of Medical Research  Clayton Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lena H. 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