ICAP‐1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice
ICAP‐1 regulates β1‐integrin activation and cell adhesion. Here, we used ICAP‐1‐null mice to study ICAP‐1 potential involvement during immune cell development and function. Integrin α4β1‐dependent adhesion was comparable between ICAP‐1‐null and control thymocytes, but lack of ICAP‐1 caused a defecti...
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| Veröffentlicht in: | European journal of immunology 2022-08, Vol.52 (8), p.1228-1242 |
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| creator | Sevilla‐Movilla, Silvia Fuentes, Patricia Rodríguez‐García, Yaiza Arellano‐Sánchez, Nohemi Krenn, Peter W. Val, Soledad Isern Montero‐Herradón, Sara García‐Ceca, Javier Burdiel‐Herencia, Valeria Gardeta, Sofía R. Aguilera‐Montilla, Noemí Barrio‐Alonso, Celia Crainiciuc, Georgiana Bouvard, Daniel García‐Pardo, Angeles Zapata, Agustin G. Hidalgo, Andrés Fässler, Reinhard Carrasco, Yolanda R. Toribio, Maria L. Teixidó, Joaquin |
| description | ICAP‐1 regulates β1‐integrin activation and cell adhesion. Here, we used ICAP‐1‐null mice to study ICAP‐1 potential involvement during immune cell development and function. Integrin α4β1‐dependent adhesion was comparable between ICAP‐1‐null and control thymocytes, but lack of ICAP‐1 caused a defective single‐positive (SP) CD8+ cell generation, thus, unveiling an ICAP‐1 involvement in SP thymocyte development. ICAP‐1 bears a nuclear localization signal and we found it displayed a strong nuclear distribution in thymocytes. Interestingly, there was a direct correlation between the lack of ICAP‐1 and reduced levels in SP CD8+ thymocytes of Runx3, a transcription factor required for CD8+ thymocyte generation. In the spleen, ICAP‐1 was found evenly distributed between cytoplasm and nuclear fractions, and ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion, indicating that ICAP‐1 negatively controls their attachment. Furthermore, CD3+‐ and CD19+‐selected spleen cells from ICAP‐1‐null mice showed reduced proliferation in response to T‐ and B‐cell stimuli, respectively. Finally, loss of ICAP‐1 caused a remarkable decrease in marginal zone B‐ cell frequencies and a moderate increase in follicular B cells. Together, these data unravel an ICAP‐1 involvement in the generation of SP CD8+ thymocytes and in the control of marginal zone B‐cell numbers.
Graphical : Lack of ICAP‐1 leads to impaired single‐positive CD8+ thymocyte development without affecting integrin α4β1‐dependent thymocyte adhesion. ICAP‐1 showed a strong nuclear distribution in thymocytes. ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion and reduced proliferation. Loss of ICAP‐1 led to decreased marginal zone B‐cell frequencies. |
| doi_str_mv | 10.1002/eji.202149560 |
| format | Article |
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Graphical : Lack of ICAP‐1 leads to impaired single‐positive CD8+ thymocyte development without affecting integrin α4β1‐dependent thymocyte adhesion. ICAP‐1 showed a strong nuclear distribution in thymocytes. ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion and reduced proliferation. Loss of ICAP‐1 led to decreased marginal zone B‐cell frequencies.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.202149560</identifier><identifier>PMID: 35491946</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>B‐ cell maturation ; CD19 antigen ; CD3 antigen ; CD8 antigen ; Cell activation ; Cell adhesion ; Cell proliferation ; Cytoplasm ; ICAP‐1 ; integrins ; Life Sciences ; Localization ; Lymphocytes B ; Runx3 protein ; Spleen ; thymocyte development ; Thymocytes</subject><ispartof>European journal of immunology, 2022-08, Vol.52 (8), p.1228-1242</ispartof><rights>2022 The Authors. European Journal of Immunology published by Wiley‐VCH GmbH.</rights><rights>2022 The Authors. European Journal of Immunology published by Wiley-VCH GmbH.</rights><rights>2022. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c3938-c72c1d6c1515077b389d12058cbe3b7e1627df4af2a720f7ebeb978677ce24ff3</cites><orcidid>0000-0002-3177-4151 ; 0000-0002-0145-6937</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Feji.202149560$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.202149560$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35491946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03657861$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Sevilla‐Movilla, Silvia</creatorcontrib><creatorcontrib>Fuentes, Patricia</creatorcontrib><creatorcontrib>Rodríguez‐García, Yaiza</creatorcontrib><creatorcontrib>Arellano‐Sánchez, Nohemi</creatorcontrib><creatorcontrib>Krenn, Peter W.</creatorcontrib><creatorcontrib>Val, Soledad Isern</creatorcontrib><creatorcontrib>Montero‐Herradón, Sara</creatorcontrib><creatorcontrib>García‐Ceca, Javier</creatorcontrib><creatorcontrib>Burdiel‐Herencia, Valeria</creatorcontrib><creatorcontrib>Gardeta, Sofía R.</creatorcontrib><creatorcontrib>Aguilera‐Montilla, Noemí</creatorcontrib><creatorcontrib>Barrio‐Alonso, Celia</creatorcontrib><creatorcontrib>Crainiciuc, Georgiana</creatorcontrib><creatorcontrib>Bouvard, Daniel</creatorcontrib><creatorcontrib>García‐Pardo, Angeles</creatorcontrib><creatorcontrib>Zapata, Agustin G.</creatorcontrib><creatorcontrib>Hidalgo, Andrés</creatorcontrib><creatorcontrib>Fässler, Reinhard</creatorcontrib><creatorcontrib>Carrasco, Yolanda R.</creatorcontrib><creatorcontrib>Toribio, Maria L.</creatorcontrib><creatorcontrib>Teixidó, Joaquin</creatorcontrib><title>ICAP‐1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>ICAP‐1 regulates β1‐integrin activation and cell adhesion. Here, we used ICAP‐1‐null mice to study ICAP‐1 potential involvement during immune cell development and function. Integrin α4β1‐dependent adhesion was comparable between ICAP‐1‐null and control thymocytes, but lack of ICAP‐1 caused a defective single‐positive (SP) CD8+ cell generation, thus, unveiling an ICAP‐1 involvement in SP thymocyte development. ICAP‐1 bears a nuclear localization signal and we found it displayed a strong nuclear distribution in thymocytes. Interestingly, there was a direct correlation between the lack of ICAP‐1 and reduced levels in SP CD8+ thymocytes of Runx3, a transcription factor required for CD8+ thymocyte generation. In the spleen, ICAP‐1 was found evenly distributed between cytoplasm and nuclear fractions, and ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion, indicating that ICAP‐1 negatively controls their attachment. Furthermore, CD3+‐ and CD19+‐selected spleen cells from ICAP‐1‐null mice showed reduced proliferation in response to T‐ and B‐cell stimuli, respectively. Finally, loss of ICAP‐1 caused a remarkable decrease in marginal zone B‐ cell frequencies and a moderate increase in follicular B cells. Together, these data unravel an ICAP‐1 involvement in the generation of SP CD8+ thymocytes and in the control of marginal zone B‐cell numbers.
Graphical : Lack of ICAP‐1 leads to impaired single‐positive CD8+ thymocyte development without affecting integrin α4β1‐dependent thymocyte adhesion. ICAP‐1 showed a strong nuclear distribution in thymocytes. ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion and reduced proliferation. Loss of ICAP‐1 led to decreased marginal zone B‐cell frequencies.</description><subject>B‐ cell maturation</subject><subject>CD19 antigen</subject><subject>CD3 antigen</subject><subject>CD8 antigen</subject><subject>Cell activation</subject><subject>Cell adhesion</subject><subject>Cell proliferation</subject><subject>Cytoplasm</subject><subject>ICAP‐1</subject><subject>integrins</subject><subject>Life Sciences</subject><subject>Localization</subject><subject>Lymphocytes B</subject><subject>Runx3 protein</subject><subject>Spleen</subject><subject>thymocyte development</subject><subject>Thymocytes</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><recordid>eNp90ctu1DAUBmALgei0sGSLLLGhQim-X5ZlKLRoJFjA2nKcE-qRkwxxUjSseASekSfB0ZRZsGBlyfr8-9g_Qs8ouaCEsNewjReMMCqsVOQBWlHJaCWooA_RihAqKmYNOUGnOW8JIVZJ-xidcCkstUKtULhZX376_fMXxWnIGcdu5-OY8fqteYWn2303hP0EuIE7SMOug37Cvm9wAt9kPA14hGYO0ODOj19j7xP-MfSA3-AAKZW0HncxwBP0qPUpw9P79Qx9eXf1eX1dbT6-L9dvqsAtN1XQLNBGBSqpJFrX3NiGMiJNqIHXGqhiummFb5nXjLQaaqitNkrrAEy0LT9D54fcW5_cboxlqL0bfHTXlxu37BGuZDlA72ixLw92Nw7fZsiT62JepvY9DHN2TEmjJLFioS_-odthHstjF2UN04YrUlR1UGEsHzlCe5yAErc05UpT7thU8c_vU-e6g-ao_1ZTADuA7zHB_v9p7urDjWTG8D-iTpvM</recordid><startdate>202208</startdate><enddate>202208</enddate><creator>Sevilla‐Movilla, Silvia</creator><creator>Fuentes, Patricia</creator><creator>Rodríguez‐García, Yaiza</creator><creator>Arellano‐Sánchez, Nohemi</creator><creator>Krenn, Peter W.</creator><creator>Val, Soledad Isern</creator><creator>Montero‐Herradón, Sara</creator><creator>García‐Ceca, Javier</creator><creator>Burdiel‐Herencia, Valeria</creator><creator>Gardeta, Sofía R.</creator><creator>Aguilera‐Montilla, Noemí</creator><creator>Barrio‐Alonso, Celia</creator><creator>Crainiciuc, Georgiana</creator><creator>Bouvard, Daniel</creator><creator>García‐Pardo, Angeles</creator><creator>Zapata, Agustin G.</creator><creator>Hidalgo, Andrés</creator><creator>Fässler, Reinhard</creator><creator>Carrasco, Yolanda R.</creator><creator>Toribio, Maria L.</creator><creator>Teixidó, Joaquin</creator><general>Wiley Subscription Services, Inc</general><general>Wiley-VCH Verlag</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-3177-4151</orcidid><orcidid>https://orcid.org/0000-0002-0145-6937</orcidid></search><sort><creationdate>202208</creationdate><title>ICAP‐1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice</title><author>Sevilla‐Movilla, Silvia ; 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Here, we used ICAP‐1‐null mice to study ICAP‐1 potential involvement during immune cell development and function. Integrin α4β1‐dependent adhesion was comparable between ICAP‐1‐null and control thymocytes, but lack of ICAP‐1 caused a defective single‐positive (SP) CD8+ cell generation, thus, unveiling an ICAP‐1 involvement in SP thymocyte development. ICAP‐1 bears a nuclear localization signal and we found it displayed a strong nuclear distribution in thymocytes. Interestingly, there was a direct correlation between the lack of ICAP‐1 and reduced levels in SP CD8+ thymocytes of Runx3, a transcription factor required for CD8+ thymocyte generation. In the spleen, ICAP‐1 was found evenly distributed between cytoplasm and nuclear fractions, and ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion, indicating that ICAP‐1 negatively controls their attachment. Furthermore, CD3+‐ and CD19+‐selected spleen cells from ICAP‐1‐null mice showed reduced proliferation in response to T‐ and B‐cell stimuli, respectively. Finally, loss of ICAP‐1 caused a remarkable decrease in marginal zone B‐ cell frequencies and a moderate increase in follicular B cells. Together, these data unravel an ICAP‐1 involvement in the generation of SP CD8+ thymocytes and in the control of marginal zone B‐cell numbers.
Graphical : Lack of ICAP‐1 leads to impaired single‐positive CD8+ thymocyte development without affecting integrin α4β1‐dependent thymocyte adhesion. ICAP‐1 showed a strong nuclear distribution in thymocytes. ICAP‐1–/– spleen T and B cells displayed upregulation of α4β1‐mediated adhesion and reduced proliferation. Loss of ICAP‐1 led to decreased marginal zone B‐cell frequencies.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>35491946</pmid><doi>10.1002/eji.202149560</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-3177-4151</orcidid><orcidid>https://orcid.org/0000-0002-0145-6937</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via Wiley Online Library; Wiley Online Library (Open Access Collection) |
| subjects | B‐ cell maturation CD19 antigen CD3 antigen CD8 antigen Cell activation Cell adhesion Cell proliferation Cytoplasm ICAP‐1 integrins Life Sciences Localization Lymphocytes B Runx3 protein Spleen thymocyte development Thymocytes |
| title | ICAP‐1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice |
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