The dynamic functions of IRF4 in B cell malignancies
The trajectory of B cell development goes through subsequent steps governed by complex genetic programs, strictly regulated by multiple transcription factors. Interferon regulatory factor 4 (IRF4) regulates key points from pre-B cell development and receptor editing to germinal center formation, cla...
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| Veröffentlicht in: | Clinical and experimental medicine 2023-08, Vol.23 (4), p.1171-1180 |
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| creator | Maffei, Rossana Fiorcari, Stefania Atene, Claudio Giacinto Martinelli, Silvia Mesini, Nicolò Pilato, Flora Lagreca, Ivana Barozzi, Patrizia Riva, Giovanni Nasillo, Vincenzo Paolini, Ambra Forghieri, Fabio Potenza, Leonardo Trenti, Tommaso Tagliafico, Enrico Luppi, Mario Marasca, Roberto |
| description | The trajectory of B cell development goes through subsequent steps governed by complex genetic programs, strictly regulated by multiple transcription factors. Interferon regulatory factor 4 (IRF4) regulates key points from pre-B cell development and receptor editing to germinal center formation, class-switch recombination and plasma cell differentiation. The pleiotropic ability of IRF4 is mediated by its “kinetic control”, allowing different IRF4 expression levels to activate distinct genetic programs due to modulation of IRF4 DNA-binding affinity. IRF4 is implicated in B cell malignancies, acting both as tumor suppressor and as tumor oncogene in different types of precursors and mature B cell neoplasia. Here, we summarize the complexity of IRF4 functions related to different DNA-binding affinity, multiple IRF4-specific target DNA motif, and interactions with transcriptional partners. Moreover, we describe the unique role of IRF4 in acute leukemias and B cell mature neoplasia, focusing on pathogenetic implications and possible therapeutic strategies in multiple myeloma and chronic lymphocytic leukemia. |
| doi_str_mv | 10.1007/s10238-022-00968-0 |
| format | Article |
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Interferon regulatory factor 4 (IRF4) regulates key points from pre-B cell development and receptor editing to germinal center formation, class-switch recombination and plasma cell differentiation. The pleiotropic ability of IRF4 is mediated by its “kinetic control”, allowing different IRF4 expression levels to activate distinct genetic programs due to modulation of IRF4 DNA-binding affinity. IRF4 is implicated in B cell malignancies, acting both as tumor suppressor and as tumor oncogene in different types of precursors and mature B cell neoplasia. Here, we summarize the complexity of IRF4 functions related to different DNA-binding affinity, multiple IRF4-specific target DNA motif, and interactions with transcriptional partners. Moreover, we describe the unique role of IRF4 in acute leukemias and B cell mature neoplasia, focusing on pathogenetic implications and possible therapeutic strategies in multiple myeloma and chronic lymphocytic leukemia.</description><identifier>ISSN: 1591-9528</identifier><identifier>ISSN: 1591-8890</identifier><identifier>EISSN: 1591-9528</identifier><identifier>DOI: 10.1007/s10238-022-00968-0</identifier><identifier>PMID: 36495369</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Affinity ; Cell differentiation ; Chronic lymphocytic leukemia ; Class switching ; Deoxyribonucleic acid ; DNA ; Hematology ; Interferon regulatory factor ; Interferon regulatory factor 4 ; Internal Medicine ; Lymphatic leukemia ; Lymphocytes B ; Malignancy ; Medicine ; Medicine & Public Health ; Multiple myeloma ; Oncology ; Recombination ; Review ; Transcription factors ; Tumor suppressor genes ; Tumors</subject><ispartof>Clinical and experimental medicine, 2023-08, Vol.23 (4), p.1171-1180</ispartof><rights>The Author(s) 2022</rights><rights>2022. The Author(s).</rights><rights>The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Interferon regulatory factor 4 (IRF4) regulates key points from pre-B cell development and receptor editing to germinal center formation, class-switch recombination and plasma cell differentiation. The pleiotropic ability of IRF4 is mediated by its “kinetic control”, allowing different IRF4 expression levels to activate distinct genetic programs due to modulation of IRF4 DNA-binding affinity. IRF4 is implicated in B cell malignancies, acting both as tumor suppressor and as tumor oncogene in different types of precursors and mature B cell neoplasia. Here, we summarize the complexity of IRF4 functions related to different DNA-binding affinity, multiple IRF4-specific target DNA motif, and interactions with transcriptional partners. Moreover, we describe the unique role of IRF4 in acute leukemias and B cell mature neoplasia, focusing on pathogenetic implications and possible therapeutic strategies in multiple myeloma and chronic lymphocytic leukemia.</description><subject>Affinity</subject><subject>Cell differentiation</subject><subject>Chronic lymphocytic leukemia</subject><subject>Class switching</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Hematology</subject><subject>Interferon regulatory factor</subject><subject>Interferon regulatory factor 4</subject><subject>Internal Medicine</subject><subject>Lymphatic leukemia</subject><subject>Lymphocytes B</subject><subject>Malignancy</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Multiple myeloma</subject><subject>Oncology</subject><subject>Recombination</subject><subject>Review</subject><subject>Transcription factors</subject><subject>Tumor suppressor genes</subject><subject>Tumors</subject><issn>1591-9528</issn><issn>1591-8890</issn><issn>1591-9528</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><recordid>eNp9kU1LAzEQhoMotn78AQ-y4MXL6iTZbJKTaPGjUBBEzyHNZtuU3WzddIX-e1PXj-rB0wzMO-_My4PQCYYLDMAvAwZCRQqEpAAyj90OGmImcSoZEbtb_QAdhLAAwExQ2EcDmmeS0VwOUfY8t0mx9rp2Jik7b1au8SFpymT8dJclzic3ibFVldS6cjOvvXE2HKG9UlfBHn_WQ_Ryd_s8ekgnj_fj0fUkNRlnq7TEQnOpRVaALSwzRoIh3BSGTONjxJbCABNYYF1YyriWnHKjp7bQBdMEM3qIrnrfZTetbWGsX7W6UsvW1bpdq0Y79Xvi3VzNmjeFgUrICYkO558ObfPa2bBStQubPNrbpguKcEYpxjnNo_Tsj3TRdK2P-RQRWYY5gNgYkl5l2iaE1pbf32BQGyqqp6IiFfVBRUFcOt3O8b3yhSEKaC8IceRntv25_Y_tO-xBlvc</recordid><startdate>20230801</startdate><enddate>20230801</enddate><creator>Maffei, Rossana</creator><creator>Fiorcari, Stefania</creator><creator>Atene, Claudio Giacinto</creator><creator>Martinelli, Silvia</creator><creator>Mesini, Nicolò</creator><creator>Pilato, Flora</creator><creator>Lagreca, Ivana</creator><creator>Barozzi, Patrizia</creator><creator>Riva, Giovanni</creator><creator>Nasillo, Vincenzo</creator><creator>Paolini, Ambra</creator><creator>Forghieri, Fabio</creator><creator>Potenza, Leonardo</creator><creator>Trenti, Tommaso</creator><creator>Tagliafico, Enrico</creator><creator>Luppi, Mario</creator><creator>Marasca, Roberto</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20230801</creationdate><title>The dynamic functions of IRF4 in B cell malignancies</title><author>Maffei, Rossana ; 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| subjects | Affinity Cell differentiation Chronic lymphocytic leukemia Class switching Deoxyribonucleic acid DNA Hematology Interferon regulatory factor Interferon regulatory factor 4 Internal Medicine Lymphatic leukemia Lymphocytes B Malignancy Medicine Medicine & Public Health Multiple myeloma Oncology Recombination Review Transcription factors Tumor suppressor genes Tumors |
| title | The dynamic functions of IRF4 in B cell malignancies |
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