Differential requirement of MALT1 for BAFF-induced outcomes in B cell subsets
B cell activation factor of the TNF family (BAFF) activates noncanonical nuclear factor kappaB (NF-kappaB) heterodimers that promote B cell survival. We show that although MALT1 is largely dispensable for canonical NF-kappaB signaling downstream of the B cell receptor, the absence of MALT1 results i...
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| Veröffentlicht in: | The Journal of experimental medicine 2009-11, Vol.206 (12), p.2671-2683 |
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| container_title | The Journal of experimental medicine |
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| creator | Tusche, Michael W Ward, Lesley A Vu, Frances McCarthy, Doug Quintela-Fandino, Miguel Ruland, Jurgen Gommerman, Jennifer L Mak, Tak W |
| description | B cell activation factor of the TNF family (BAFF) activates noncanonical nuclear factor kappaB (NF-kappaB) heterodimers that promote B cell survival. We show that although MALT1 is largely dispensable for canonical NF-kappaB signaling downstream of the B cell receptor, the absence of MALT1 results in impaired BAFF-induced phosphorylation of NF-kappaB2 (p100), p100 degradation, and RelB nuclear translocation in B220(+) B cells. This corresponds with impaired survival of MALT1(-/-) marginal zone (MZ) but not follicular B cells in response to BAFF stimulation in vitro. MALT1(-/-) MZ B cells also express higher amounts of TRAF3, a known negative regulator of BAFF receptor-mediated signaling, and TRAF3 was found to interact with MALT1. Furthermore, phenotypes associated with overexpression of BAFF, including increased MZ B cell numbers, elevated serum immunoglobulin titers, and spontaneous germinal center formation, were found to be dependent on B cell-intrinsic MALT1 expression. Our results demonstrate a novel role for MALT1 in biological outcomes induced by BAFF-mediated signal transduction. |
| doi_str_mv | 10.1084/jem.20091802 |
| format | Article |
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We show that although MALT1 is largely dispensable for canonical NF-kappaB signaling downstream of the B cell receptor, the absence of MALT1 results in impaired BAFF-induced phosphorylation of NF-kappaB2 (p100), p100 degradation, and RelB nuclear translocation in B220(+) B cells. This corresponds with impaired survival of MALT1(-/-) marginal zone (MZ) but not follicular B cells in response to BAFF stimulation in vitro. MALT1(-/-) MZ B cells also express higher amounts of TRAF3, a known negative regulator of BAFF receptor-mediated signaling, and TRAF3 was found to interact with MALT1. Furthermore, phenotypes associated with overexpression of BAFF, including increased MZ B cell numbers, elevated serum immunoglobulin titers, and spontaneous germinal center formation, were found to be dependent on B cell-intrinsic MALT1 expression. Our results demonstrate a novel role for MALT1 in biological outcomes induced by BAFF-mediated signal transduction.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>DOI: 10.1084/jem.20091802</identifier><identifier>PMID: 19917778</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; B-Cell Activating Factor - genetics ; B-Cell Activating Factor - immunology ; B-Lymphocyte Subsets - immunology ; Caspases - genetics ; Caspases - immunology ; Mice ; Mice, Knockout ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein ; Neoplasm Proteins - genetics ; Neoplasm Proteins - immunology ; Receptors, Antigen, B-Cell - genetics ; Receptors, Antigen, B-Cell - immunology ; Signal Transduction - genetics ; Signal Transduction - immunology ; TNF Receptor-Associated Factor 3 - genetics ; TNF Receptor-Associated Factor 3 - immunology ; Transcription Factor RelB - genetics ; Transcription Factor RelB - immunology</subject><ispartof>The Journal of experimental medicine, 2009-11, Vol.206 (12), p.2671-2683</ispartof><rights>2009 Tusche et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-f421ea57d8396424f4681f25fa3c96ef70f5cb04950acd0b8d5df280b466f233</citedby><cites>FETCH-LOGICAL-c449t-f421ea57d8396424f4681f25fa3c96ef70f5cb04950acd0b8d5df280b466f233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19917778$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tusche, Michael W</creatorcontrib><creatorcontrib>Ward, Lesley A</creatorcontrib><creatorcontrib>Vu, Frances</creatorcontrib><creatorcontrib>McCarthy, Doug</creatorcontrib><creatorcontrib>Quintela-Fandino, Miguel</creatorcontrib><creatorcontrib>Ruland, Jurgen</creatorcontrib><creatorcontrib>Gommerman, Jennifer L</creatorcontrib><creatorcontrib>Mak, Tak W</creatorcontrib><title>Differential requirement of MALT1 for BAFF-induced outcomes in B cell subsets</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>B cell activation factor of the TNF family (BAFF) activates noncanonical nuclear factor kappaB (NF-kappaB) heterodimers that promote B cell survival. We show that although MALT1 is largely dispensable for canonical NF-kappaB signaling downstream of the B cell receptor, the absence of MALT1 results in impaired BAFF-induced phosphorylation of NF-kappaB2 (p100), p100 degradation, and RelB nuclear translocation in B220(+) B cells. This corresponds with impaired survival of MALT1(-/-) marginal zone (MZ) but not follicular B cells in response to BAFF stimulation in vitro. MALT1(-/-) MZ B cells also express higher amounts of TRAF3, a known negative regulator of BAFF receptor-mediated signaling, and TRAF3 was found to interact with MALT1. Furthermore, phenotypes associated with overexpression of BAFF, including increased MZ B cell numbers, elevated serum immunoglobulin titers, and spontaneous germinal center formation, were found to be dependent on B cell-intrinsic MALT1 expression. Our results demonstrate a novel role for MALT1 in biological outcomes induced by BAFF-mediated signal transduction.</description><subject>Animals</subject><subject>B-Cell Activating Factor - genetics</subject><subject>B-Cell Activating Factor - immunology</subject><subject>B-Lymphocyte Subsets - immunology</subject><subject>Caspases - genetics</subject><subject>Caspases - immunology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - immunology</subject><subject>Receptors, Antigen, B-Cell - genetics</subject><subject>Receptors, Antigen, B-Cell - immunology</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - immunology</subject><subject>TNF Receptor-Associated Factor 3 - genetics</subject><subject>TNF Receptor-Associated Factor 3 - immunology</subject><subject>Transcription Factor RelB - genetics</subject><subject>Transcription Factor RelB - immunology</subject><issn>0022-1007</issn><issn>1540-9538</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkD1PwzAQhi0EoqWwMSNvLKScHdtJFqRSKCC1YuluOY4NrpK42AkS_55UlK_pdLpH7909CJ0TmBLI2fXGNFMKUJAc6AEaE84gKXiaH6IxAKUJAchG6CTGDQBhjItjNCJFQbIsy8dodeesNcG0nVM1Duatd8E0Q4u9xavZck2w9QHfzhaLxLVVr02Ffd9p35iIXYtvsTZ1jWNfRtPFU3RkVR3N2b5O0Hpxv54_Jsvnh6f5bJloxoousYwSo3hW5WkhGGWWiZxYyq1KdSGMzcByXQIrOChdQZlXvLI0h5IJYWmaTtDNV-y2LxtT6eHcoGq5Da5R4UN65eT_Sete5Yt_l0OGEASGgMt9QPBvvYmdbFzcPaJa4_sos5QBzVLCB_Lqi9TBxxiM_dlCQO78y8G__PY_4Bd_L_uF98LTT9rIgOo</recordid><startdate>20091123</startdate><enddate>20091123</enddate><creator>Tusche, Michael W</creator><creator>Ward, Lesley A</creator><creator>Vu, Frances</creator><creator>McCarthy, Doug</creator><creator>Quintela-Fandino, Miguel</creator><creator>Ruland, Jurgen</creator><creator>Gommerman, Jennifer L</creator><creator>Mak, Tak W</creator><general>The Rockefeller University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20091123</creationdate><title>Differential requirement of MALT1 for BAFF-induced outcomes in B cell subsets</title><author>Tusche, Michael W ; Ward, Lesley A ; Vu, Frances ; McCarthy, Doug ; Quintela-Fandino, Miguel ; Ruland, Jurgen ; Gommerman, Jennifer L ; Mak, Tak W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-f421ea57d8396424f4681f25fa3c96ef70f5cb04950acd0b8d5df280b466f233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>B-Cell Activating Factor - genetics</topic><topic>B-Cell Activating Factor - immunology</topic><topic>B-Lymphocyte Subsets - immunology</topic><topic>Caspases - genetics</topic><topic>Caspases - immunology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - immunology</topic><topic>Receptors, Antigen, B-Cell - genetics</topic><topic>Receptors, Antigen, B-Cell - immunology</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - immunology</topic><topic>TNF Receptor-Associated Factor 3 - genetics</topic><topic>TNF Receptor-Associated Factor 3 - immunology</topic><topic>Transcription Factor RelB - genetics</topic><topic>Transcription Factor RelB - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tusche, Michael W</creatorcontrib><creatorcontrib>Ward, Lesley A</creatorcontrib><creatorcontrib>Vu, Frances</creatorcontrib><creatorcontrib>McCarthy, Doug</creatorcontrib><creatorcontrib>Quintela-Fandino, Miguel</creatorcontrib><creatorcontrib>Ruland, Jurgen</creatorcontrib><creatorcontrib>Gommerman, Jennifer L</creatorcontrib><creatorcontrib>Mak, Tak W</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tusche, Michael W</au><au>Ward, Lesley A</au><au>Vu, Frances</au><au>McCarthy, Doug</au><au>Quintela-Fandino, Miguel</au><au>Ruland, Jurgen</au><au>Gommerman, Jennifer L</au><au>Mak, Tak W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential requirement of MALT1 for BAFF-induced outcomes in B cell subsets</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2009-11-23</date><risdate>2009</risdate><volume>206</volume><issue>12</issue><spage>2671</spage><epage>2683</epage><pages>2671-2683</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><abstract>B cell activation factor of the TNF family (BAFF) activates noncanonical nuclear factor kappaB (NF-kappaB) heterodimers that promote B cell survival. We show that although MALT1 is largely dispensable for canonical NF-kappaB signaling downstream of the B cell receptor, the absence of MALT1 results in impaired BAFF-induced phosphorylation of NF-kappaB2 (p100), p100 degradation, and RelB nuclear translocation in B220(+) B cells. This corresponds with impaired survival of MALT1(-/-) marginal zone (MZ) but not follicular B cells in response to BAFF stimulation in vitro. MALT1(-/-) MZ B cells also express higher amounts of TRAF3, a known negative regulator of BAFF receptor-mediated signaling, and TRAF3 was found to interact with MALT1. Furthermore, phenotypes associated with overexpression of BAFF, including increased MZ B cell numbers, elevated serum immunoglobulin titers, and spontaneous germinal center formation, were found to be dependent on B cell-intrinsic MALT1 expression. Our results demonstrate a novel role for MALT1 in biological outcomes induced by BAFF-mediated signal transduction.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>19917778</pmid><doi>10.1084/jem.20091802</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals B-Cell Activating Factor - genetics B-Cell Activating Factor - immunology B-Lymphocyte Subsets - immunology Caspases - genetics Caspases - immunology Mice Mice, Knockout Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein Neoplasm Proteins - genetics Neoplasm Proteins - immunology Receptors, Antigen, B-Cell - genetics Receptors, Antigen, B-Cell - immunology Signal Transduction - genetics Signal Transduction - immunology TNF Receptor-Associated Factor 3 - genetics TNF Receptor-Associated Factor 3 - immunology Transcription Factor RelB - genetics Transcription Factor RelB - immunology |
| title | Differential requirement of MALT1 for BAFF-induced outcomes in B cell subsets |
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