Involvement of BAFF and APRIL in the resistance to apoptosis of B-CLL through an autocrine pathway
Tumor necrosis factor (TNF) superfamily members BAFF, or B-cell activation factor of the TNF family, and APRIL, a proliferation-inducing ligand, are involved in normal B-cell survival and differentiation. They interact with 3 receptors: BAFF-R, specific to BAFF; and TACI and BCMA, which are shared b...
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| Veröffentlicht in: | Blood 2004-01, Vol.103 (2), p.679-688 |
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| creator | Kern, Catherine Cornuel, Jean-François Billard, Christian Tang, Ruoping Rouillard, Danielle Stenou, Virginie Defrance, Thierry Ajchenbaum-Cymbalista, Florence Simonin, Pierre-Yves Feldblum, Sophie Kolb, Jean-Pierre |
| description | Tumor necrosis factor (TNF) superfamily members BAFF, or B-cell activation factor of the TNF family, and APRIL, a proliferation-inducing ligand, are involved in normal B-cell survival and differentiation. They interact with 3 receptors: BAFF-R, specific to BAFF; and TACI and BCMA, which are shared by BAFF and APRIL. We tested the potential role of these proteins in B-cell chronic lymphocytic leukemia (B-CLL) resistance to apoptosis. TACI and BAFF-R mRNAs were found in leukemic B cells. BAFF and APRIL mRNAs and proteins were detected in B-CLL leukemic cells and normal blood or tonsil-derived B lymphocytes. Yet, in contrast to normal B lymphocytes, BAFF and APRIL were expressed at the membranes of leukemic cells. Adding soluble BAFF or APRIL protected B-CLL cells against spontaneous and drug-induced apoptosis and stimulated NF-κB activation. Conversely, adding soluble BCMA-Fc or anti-BAFF and anti-APRIL antibodies enhanced B-CLL apoptosis. Moreover, a soluble form of BAFF was detected using surface-enhanced laser desorption/ionization–time-of-flight mass spectrometry (SELDI-TOF MS) in the sera of B-CLL patients but not of healthy donors. Taken together, our results indicate that B-CLL cells can be rescued from apoptosis through an autocrine process involving BAFF, APRIL, and their receptors. Inhibiting BAFF and APRIL pathways may be of therapeutic value for B-CLL treatment. |
| doi_str_mv | 10.1182/blood-2003-02-0540 |
| format | Article |
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They interact with 3 receptors: BAFF-R, specific to BAFF; and TACI and BCMA, which are shared by BAFF and APRIL. We tested the potential role of these proteins in B-cell chronic lymphocytic leukemia (B-CLL) resistance to apoptosis. TACI and BAFF-R mRNAs were found in leukemic B cells. BAFF and APRIL mRNAs and proteins were detected in B-CLL leukemic cells and normal blood or tonsil-derived B lymphocytes. Yet, in contrast to normal B lymphocytes, BAFF and APRIL were expressed at the membranes of leukemic cells. Adding soluble BAFF or APRIL protected B-CLL cells against spontaneous and drug-induced apoptosis and stimulated NF-κB activation. Conversely, adding soluble BCMA-Fc or anti-BAFF and anti-APRIL antibodies enhanced B-CLL apoptosis. Moreover, a soluble form of BAFF was detected using surface-enhanced laser desorption/ionization–time-of-flight mass spectrometry (SELDI-TOF MS) in the sera of B-CLL patients but not of healthy donors. Taken together, our results indicate that B-CLL cells can be rescued from apoptosis through an autocrine process involving BAFF, APRIL, and their receptors. Inhibiting BAFF and APRIL pathways may be of therapeutic value for B-CLL treatment.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2003-02-0540</identifier><identifier>PMID: 14504101</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Aged ; Antibodies ; Apoptosis ; B-Cell Activating Factor ; Base Sequence ; Biological and medical sciences ; DNA Primers ; Female ; Flow Cytometry ; Gene Expression Regulation, Neoplastic - genetics ; Hematologic and hematopoietic diseases ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell - blood ; Leukemia, Lymphocytic, Chronic, B-Cell - genetics ; Leukemia, Lymphocytic, Chronic, B-Cell - pathology ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Mass Spectrometry ; Medical sciences ; Membrane Proteins - blood ; Membrane Proteins - genetics ; Membrane Proteins - immunology ; Middle Aged ; Neoplasm Staging ; Neuropeptides - blood ; Neuropeptides - genetics ; Neuropeptides - immunology ; NF-kappa B - metabolism ; Nuclear Proteins ; Nucleosomes - genetics ; Receptors, Tumor Necrosis Factor - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Tumor Necrosis Factor Ligand Superfamily Member 13 ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>Blood, 2004-01, Vol.103 (2), p.679-688</ispartof><rights>2004 American Society of Hematology</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-14b0a1cf7e118d145767b963fd694e2f49887ab24a85721f1fbcd2ed7a18636c3</citedby><cites>FETCH-LOGICAL-c492t-14b0a1cf7e118d145767b963fd694e2f49887ab24a85721f1fbcd2ed7a18636c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15524408$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14504101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kern, Catherine</creatorcontrib><creatorcontrib>Cornuel, Jean-François</creatorcontrib><creatorcontrib>Billard, Christian</creatorcontrib><creatorcontrib>Tang, Ruoping</creatorcontrib><creatorcontrib>Rouillard, Danielle</creatorcontrib><creatorcontrib>Stenou, Virginie</creatorcontrib><creatorcontrib>Defrance, Thierry</creatorcontrib><creatorcontrib>Ajchenbaum-Cymbalista, Florence</creatorcontrib><creatorcontrib>Simonin, Pierre-Yves</creatorcontrib><creatorcontrib>Feldblum, Sophie</creatorcontrib><creatorcontrib>Kolb, Jean-Pierre</creatorcontrib><title>Involvement of BAFF and APRIL in the resistance to apoptosis of B-CLL through an autocrine pathway</title><title>Blood</title><addtitle>Blood</addtitle><description>Tumor necrosis factor (TNF) superfamily members BAFF, or B-cell activation factor of the TNF family, and APRIL, a proliferation-inducing ligand, are involved in normal B-cell survival and differentiation. They interact with 3 receptors: BAFF-R, specific to BAFF; and TACI and BCMA, which are shared by BAFF and APRIL. We tested the potential role of these proteins in B-cell chronic lymphocytic leukemia (B-CLL) resistance to apoptosis. TACI and BAFF-R mRNAs were found in leukemic B cells. BAFF and APRIL mRNAs and proteins were detected in B-CLL leukemic cells and normal blood or tonsil-derived B lymphocytes. Yet, in contrast to normal B lymphocytes, BAFF and APRIL were expressed at the membranes of leukemic cells. Adding soluble BAFF or APRIL protected B-CLL cells against spontaneous and drug-induced apoptosis and stimulated NF-κB activation. Conversely, adding soluble BCMA-Fc or anti-BAFF and anti-APRIL antibodies enhanced B-CLL apoptosis. Moreover, a soluble form of BAFF was detected using surface-enhanced laser desorption/ionization–time-of-flight mass spectrometry (SELDI-TOF MS) in the sera of B-CLL patients but not of healthy donors. Taken together, our results indicate that B-CLL cells can be rescued from apoptosis through an autocrine process involving BAFF, APRIL, and their receptors. Inhibiting BAFF and APRIL pathways may be of therapeutic value for B-CLL treatment.</description><subject>Aged</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>B-Cell Activating Factor</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>DNA Primers</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - blood</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</subject><subject>Leukemia, Lymphocytic, Chronic, B-Cell - pathology</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Mass Spectrometry</subject><subject>Medical sciences</subject><subject>Membrane Proteins - blood</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - immunology</subject><subject>Middle Aged</subject><subject>Neoplasm Staging</subject><subject>Neuropeptides - blood</subject><subject>Neuropeptides - genetics</subject><subject>Neuropeptides - immunology</subject><subject>NF-kappa B - metabolism</subject><subject>Nuclear Proteins</subject><subject>Nucleosomes - genetics</subject><subject>Receptors, Tumor Necrosis Factor - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Tumor Necrosis Factor Ligand Superfamily Member 13</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2P0zAQhi0EYsvCH-CAfIGb2bHjxInEpVtRqBSJ1QrOluNMqFEaB9sp2n-Pu620tz2NNHre-XgIec_hM-e1uOlG73smAAoGgkEp4QVZ8VLUDEDAS7ICgIrJRvEr8ibGPwBcFqJ8Ta64LEFy4CvS7aajH494wClRP9Db9XZLzdTT9d39rqVuommPNGB0MZnJIk2emtnPyefOY4Bt2jZDwS-_9zlJzZK8DW5COpu0_2ce3pJXgxkjvrvUa_Jr-_Xn5jtrf3zbbdYts7IRiXHZgeF2UJif6_OFqlJdUxVDXzUSxSCbulamE9LUpRJ84ENne4G9MryuisoW1-TTee4c_N8FY9IHFy2Oo5nQL1HXAEo1ZZ1BcQZt8DEGHPQc3MGEB81Bn8zqR7P6ZFaD0CezOfThMn3pDtg_RS4qM_DxAphozTiErMvFJ64shZRw2v7lzGF2cXQYdLQOs9reBbRJ9949d8d_7y6VHw</recordid><startdate>20040115</startdate><enddate>20040115</enddate><creator>Kern, Catherine</creator><creator>Cornuel, Jean-François</creator><creator>Billard, Christian</creator><creator>Tang, Ruoping</creator><creator>Rouillard, Danielle</creator><creator>Stenou, Virginie</creator><creator>Defrance, Thierry</creator><creator>Ajchenbaum-Cymbalista, Florence</creator><creator>Simonin, Pierre-Yves</creator><creator>Feldblum, Sophie</creator><creator>Kolb, Jean-Pierre</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><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></search><sort><creationdate>20040115</creationdate><title>Involvement of BAFF and APRIL in the resistance to apoptosis of B-CLL through an autocrine pathway</title><author>Kern, Catherine ; Cornuel, Jean-François ; Billard, Christian ; Tang, Ruoping ; Rouillard, Danielle ; Stenou, Virginie ; Defrance, Thierry ; Ajchenbaum-Cymbalista, Florence ; Simonin, Pierre-Yves ; Feldblum, Sophie ; Kolb, Jean-Pierre</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c492t-14b0a1cf7e118d145767b963fd694e2f49887ab24a85721f1fbcd2ed7a18636c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Aged</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>B-Cell Activating Factor</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>DNA Primers</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - blood</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - genetics</topic><topic>Leukemia, Lymphocytic, Chronic, B-Cell - pathology</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Mass Spectrometry</topic><topic>Medical sciences</topic><topic>Membrane Proteins - blood</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - immunology</topic><topic>Middle Aged</topic><topic>Neoplasm Staging</topic><topic>Neuropeptides - blood</topic><topic>Neuropeptides - genetics</topic><topic>Neuropeptides - immunology</topic><topic>NF-kappa B - metabolism</topic><topic>Nuclear Proteins</topic><topic>Nucleosomes - genetics</topic><topic>Receptors, Tumor Necrosis Factor - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Tumor Necrosis Factor Ligand Superfamily Member 13</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kern, Catherine</creatorcontrib><creatorcontrib>Cornuel, Jean-François</creatorcontrib><creatorcontrib>Billard, Christian</creatorcontrib><creatorcontrib>Tang, Ruoping</creatorcontrib><creatorcontrib>Rouillard, Danielle</creatorcontrib><creatorcontrib>Stenou, Virginie</creatorcontrib><creatorcontrib>Defrance, Thierry</creatorcontrib><creatorcontrib>Ajchenbaum-Cymbalista, Florence</creatorcontrib><creatorcontrib>Simonin, Pierre-Yves</creatorcontrib><creatorcontrib>Feldblum, Sophie</creatorcontrib><creatorcontrib>Kolb, Jean-Pierre</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><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><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kern, Catherine</au><au>Cornuel, Jean-François</au><au>Billard, Christian</au><au>Tang, Ruoping</au><au>Rouillard, Danielle</au><au>Stenou, Virginie</au><au>Defrance, Thierry</au><au>Ajchenbaum-Cymbalista, Florence</au><au>Simonin, Pierre-Yves</au><au>Feldblum, Sophie</au><au>Kolb, Jean-Pierre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of BAFF and APRIL in the resistance to apoptosis of B-CLL through an autocrine pathway</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2004-01-15</date><risdate>2004</risdate><volume>103</volume><issue>2</issue><spage>679</spage><epage>688</epage><pages>679-688</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>Tumor necrosis factor (TNF) superfamily members BAFF, or B-cell activation factor of the TNF family, and APRIL, a proliferation-inducing ligand, are involved in normal B-cell survival and differentiation. They interact with 3 receptors: BAFF-R, specific to BAFF; and TACI and BCMA, which are shared by BAFF and APRIL. We tested the potential role of these proteins in B-cell chronic lymphocytic leukemia (B-CLL) resistance to apoptosis. TACI and BAFF-R mRNAs were found in leukemic B cells. BAFF and APRIL mRNAs and proteins were detected in B-CLL leukemic cells and normal blood or tonsil-derived B lymphocytes. Yet, in contrast to normal B lymphocytes, BAFF and APRIL were expressed at the membranes of leukemic cells. Adding soluble BAFF or APRIL protected B-CLL cells against spontaneous and drug-induced apoptosis and stimulated NF-κB activation. Conversely, adding soluble BCMA-Fc or anti-BAFF and anti-APRIL antibodies enhanced B-CLL apoptosis. Moreover, a soluble form of BAFF was detected using surface-enhanced laser desorption/ionization–time-of-flight mass spectrometry (SELDI-TOF MS) in the sera of B-CLL patients but not of healthy donors. Taken together, our results indicate that B-CLL cells can be rescued from apoptosis through an autocrine process involving BAFF, APRIL, and their receptors. Inhibiting BAFF and APRIL pathways may be of therapeutic value for B-CLL treatment.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>14504101</pmid><doi>10.1182/blood-2003-02-0540</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Antibodies Apoptosis B-Cell Activating Factor Base Sequence Biological and medical sciences DNA Primers Female Flow Cytometry Gene Expression Regulation, Neoplastic - genetics Hematologic and hematopoietic diseases Humans Leukemia, Lymphocytic, Chronic, B-Cell - blood Leukemia, Lymphocytic, Chronic, B-Cell - genetics Leukemia, Lymphocytic, Chronic, B-Cell - pathology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Mass Spectrometry Medical sciences Membrane Proteins - blood Membrane Proteins - genetics Membrane Proteins - immunology Middle Aged Neoplasm Staging Neuropeptides - blood Neuropeptides - genetics Neuropeptides - immunology NF-kappa B - metabolism Nuclear Proteins Nucleosomes - genetics Receptors, Tumor Necrosis Factor - genetics Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Tumor Necrosis Factor Ligand Superfamily Member 13 Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - immunology |
| title | Involvement of BAFF and APRIL in the resistance to apoptosis of B-CLL through an autocrine pathway |
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