Anti-CD69 therapy induces rapid mobilization and high proliferation of HSPCs through S1P and mTOR.
Identifieur interne : 000661 ( Main/Exploration ); précédent : 000660; suivant : 000662Anti-CD69 therapy induces rapid mobilization and high proliferation of HSPCs through S1P and mTOR.
Auteurs : Laura Notario [Espagne] ; Elisenda Alari-Pahissa [Espagne] ; Almudena Albentosa [Espagne] ; Magdalena Leiva [Espagne] ; Guadalupe Sabio [Espagne] ; Pilar Lauzurica [Espagne]Source :
- Leukemia [ 1476-5551 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Anticorps monoclonaux (pharmacologie), Antigènes CD (MeSH), Antigènes de différenciation des lymphocytes T (MeSH), Cellules souches hématopoïétiques (physiologie), Chimiokine CXCL12 (biosynthèse), Chlorhydrate de fingolimod (pharmacologie), Composés hétérocycliques (pharmacologie), Femelle (MeSH), Lectines de type C (antagonistes et inhibiteurs), Mobilisation de cellules souches hématopoïétiques (méthodes), Mouvement cellulaire (effets des médicaments et des substances chimiques), Mâle (MeSH), Phosphoric monoester hydrolases (physiologie), Prolifération cellulaire (effets des médicaments et des substances chimiques), Protéines membranaires (physiologie), Souris (MeSH), Sérine-thréonine kinases TOR (physiologie).
- MESH :
- antagonistes et inhibiteurs : Lectines de type C.
- biosynthèse : Chimiokine CXCL12.
- effets des médicaments et des substances chimiques : Mouvement cellulaire, Prolifération cellulaire.
- méthodes : Mobilisation de cellules souches hématopoïétiques.
- pharmacologie : Anticorps monoclonaux, Chlorhydrate de fingolimod, Composés hétérocycliques.
- physiologie : Cellules souches hématopoïétiques, Phosphoric monoester hydrolases, Protéines membranaires, Sérine-thréonine kinases TOR.
- Animaux, Antigènes CD, Antigènes de différenciation des lymphocytes T, Femelle, Mâle, Souris.
English descriptors
- KwdEn :
- Animals (MeSH), Antibodies, Monoclonal (pharmacology), Antigens, CD (MeSH), Antigens, Differentiation, T-Lymphocyte (MeSH), Cell Movement (drug effects), Cell Proliferation (drug effects), Chemokine CXCL12 (biosynthesis), Female (MeSH), Fingolimod Hydrochloride (pharmacology), Hematopoietic Stem Cell Mobilization (methods), Hematopoietic Stem Cells (physiology), Heterocyclic Compounds (pharmacology), Lectins, C-Type (antagonists & inhibitors), Male (MeSH), Membrane Proteins (physiology), Mice (MeSH), Phosphoric Monoester Hydrolases (physiology), TOR Serine-Threonine Kinases (physiology).
- MESH :
- chemical , antagonists & inhibitors : Lectins, C-Type.
- chemical , biosynthesis : Chemokine CXCL12.
- chemical , pharmacology : Antibodies, Monoclonal, Fingolimod Hydrochloride, Heterocyclic Compounds.
- drug effects : Cell Movement, Cell Proliferation.
- methods : Hematopoietic Stem Cell Mobilization.
- physiology : Hematopoietic Stem Cells, Membrane Proteins, Phosphoric Monoester Hydrolases, TOR Serine-Threonine Kinases.
- Animals, Antigens, CD, Antigens, Differentiation, T-Lymphocyte, Female, Male, Mice.
Abstract
CD69 regulates lymphocyte egress from the thymus and lymph nodes through cis-interactions and the downregulation of surface sphingosine-1-phosphate (S1P) receptor-1 (S1P1). However, its role in the regulation of cell egress from bone marrow has not been extensively studied. We show here that CD69 targeting induced rapid and massive mobilization of BM leukocytes, which was inhibited by desensitization to S1P with FTY720. This mobilization was reproduced with anti-human CD69 mAb treatment of mice expressing human CD69. In this strain, the mobilization occurred to the same extent as that induced by AMD3100. The anti-human CD69 treatment highly increased LSK and CLP cell proliferation and numbers, both in the periphery and in the BM, and also augmented S1P1 and CXCR4 expression. Additionally, increased mTOR, p70S6K, S6, and 4E-BP1 phosphorylation was detected after in vivo anti-CD69 treatment in the bone marrow. Importantly, mTOR inhibition with rapamycin inhibited anti-huCD69-induced mobilization of hematopoietic stem and progenitor cells (HSPCs). Together, our results indicated that CD69 targeting induces not only mobilization but also high proliferation of HSPCs, and thus is crucial for precursor cell replenishment over time. These results suggest that anti-CD69 mAbs are putative novel candidates for mobilization strategies.
DOI: 10.1038/s41375-018-0052-x
PubMed: 29483712
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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sortKey="Sabio, Guadalupe" sort="Sabio, Guadalupe" uniqKey="Sabio G" first="Guadalupe" last="Sabio">Guadalupe Sabio</name><affiliation wicri:level="3"><nlm:affiliation>Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid</wicri:regionArea><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Lauzurica, Pilar" sort="Lauzurica, Pilar" uniqKey="Lauzurica P" first="Pilar" last="Lauzurica">Pilar Lauzurica</name><affiliation wicri:level="3"><nlm:affiliation>Microbiology National Center, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain. lauzurica@isciii.es.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Microbiology National Center, Instituto de Salud Carlos III, Majadahonda, Madrid</wicri:regionArea><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author></analytic><series><title level="j">Leukemia</title><idno type="eISSN">1476-5551</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Antibodies, Monoclonal (pharmacology)</term><term>Antigens, CD (MeSH)</term><term>Antigens, Differentiation, T-Lymphocyte (MeSH)</term><term>Cell Movement (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Chemokine CXCL12 (biosynthesis)</term><term>Female (MeSH)</term><term>Fingolimod Hydrochloride (pharmacology)</term><term>Hematopoietic Stem Cell Mobilization (methods)</term><term>Hematopoietic Stem Cells (physiology)</term><term>Heterocyclic Compounds (pharmacology)</term><term>Lectins, C-Type (antagonists & inhibitors)</term><term>Male (MeSH)</term><term>Membrane Proteins (physiology)</term><term>Mice (MeSH)</term><term>Phosphoric Monoester Hydrolases (physiology)</term><term>TOR Serine-Threonine Kinases (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Anticorps monoclonaux (pharmacologie)</term><term>Antigènes CD (MeSH)</term><term>Antigènes de différenciation des lymphocytes T (MeSH)</term><term>Cellules souches hématopoïétiques (physiologie)</term><term>Chimiokine CXCL12 (biosynthèse)</term><term>Chlorhydrate de fingolimod (pharmacologie)</term><term>Composés hétérocycliques (pharmacologie)</term><term>Femelle (MeSH)</term><term>Lectines de type C (antagonistes et inhibiteurs)</term><term>Mobilisation de cellules souches hématopoïétiques (méthodes)</term><term>Mouvement cellulaire (effets des médicaments et des substances chimiques)</term><term>Mâle (MeSH)</term><term>Phosphoric monoester hydrolases (physiologie)</term><term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term><term>Protéines membranaires (physiologie)</term><term>Souris (MeSH)</term><term>Sérine-thréonine kinases TOR (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Lectins, C-Type</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Chemokine CXCL12</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antibodies, Monoclonal</term><term>Fingolimod Hydrochloride</term><term>Heterocyclic Compounds</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Lectines de type C</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Chimiokine CXCL12</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term><term>Cell Proliferation</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Mouvement cellulaire</term><term>Prolifération cellulaire</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Hematopoietic Stem Cell Mobilization</term></keywords><keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Mobilisation de cellules souches hématopoïétiques</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anticorps monoclonaux</term><term>Chlorhydrate de fingolimod</term><term>Composés hétérocycliques</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Cellules souches hématopoïétiques</term><term>Phosphoric monoester hydrolases</term><term>Protéines membranaires</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Hematopoietic Stem Cells</term><term>Membrane Proteins</term><term>Phosphoric Monoester Hydrolases</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Antigens, CD</term><term>Antigens, Differentiation, T-Lymphocyte</term><term>Female</term><term>Male</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Antigènes CD</term><term>Antigènes de différenciation des lymphocytes T</term><term>Femelle</term><term>Mâle</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">CD69 regulates lymphocyte egress from the thymus and lymph nodes through cis-interactions and the downregulation of surface sphingosine-1-phosphate (S1P) receptor-1 (S1P1). However, its role in the regulation of cell egress from bone marrow has not been extensively studied. We show here that CD69 targeting induced rapid and massive mobilization of BM leukocytes, which was inhibited by desensitization to S1P with FTY720. This mobilization was reproduced with anti-human CD69 mAb treatment of mice expressing human CD69. In this strain, the mobilization occurred to the same extent as that induced by AMD3100. The anti-human CD69 treatment highly increased LSK and CLP cell proliferation and numbers, both in the periphery and in the BM, and also augmented S1P1 and CXCR4 expression. Additionally, increased mTOR, p70S6K, S6, and 4E-BP1 phosphorylation was detected after in vivo anti-CD69 treatment in the bone marrow. Importantly, mTOR inhibition with rapamycin inhibited anti-huCD69-induced mobilization of hematopoietic stem and progenitor cells (HSPCs). Together, our results indicated that CD69 targeting induces not only mobilization but also high proliferation of HSPCs, and thus is crucial for precursor cell replenishment over time. These results suggest that anti-CD69 mAbs are putative novel candidates for mobilization strategies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29483712</PMID><DateCompleted><Year>2019</Year><Month>04</Month><Day>01</Day></DateCompleted><DateRevised><Year>2019</Year><Month>10</Month><Day>08</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-5551</ISSN><JournalIssue CitedMedium="Internet"><Volume>32</Volume><Issue>6</Issue><PubDate><Year>2018</Year><Month>06</Month></PubDate></JournalIssue><Title>Leukemia</Title><ISOAbbreviation>Leukemia</ISOAbbreviation></Journal><ArticleTitle>Anti-CD69 therapy induces rapid mobilization and high proliferation of HSPCs through S1P and mTOR.</ArticleTitle><Pagination><MedlinePgn>1445-1457</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41375-018-0052-x</ELocationID><Abstract><AbstractText>CD69 regulates lymphocyte egress from the thymus and lymph nodes through cis-interactions and the downregulation of surface sphingosine-1-phosphate (S1P) receptor-1 (S1P1). However, its role in the regulation of cell egress from bone marrow has not been extensively studied. We show here that CD69 targeting induced rapid and massive mobilization of BM leukocytes, which was inhibited by desensitization to S1P with FTY720. This mobilization was reproduced with anti-human CD69 mAb treatment of mice expressing human CD69. In this strain, the mobilization occurred to the same extent as that induced by AMD3100. The anti-human CD69 treatment highly increased LSK and CLP cell proliferation and numbers, both in the periphery and in the BM, and also augmented S1P1 and CXCR4 expression. Additionally, increased mTOR, p70S6K, S6, and 4E-BP1 phosphorylation was detected after in vivo anti-CD69 treatment in the bone marrow. Importantly, mTOR inhibition with rapamycin inhibited anti-huCD69-induced mobilization of hematopoietic stem and progenitor cells (HSPCs). Together, our results indicated that CD69 targeting induces not only mobilization but also high proliferation of HSPCs, and thus is crucial for precursor cell replenishment over time. These results suggest that anti-CD69 mAbs are putative novel candidates for mobilization strategies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Notario</LastName><ForeName>Laura</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Microbiology National Center, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alari-Pahissa</LastName><ForeName>Elisenda</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Universitat Pompeu Fabra, Barcelona, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Albentosa</LastName><ForeName>Almudena</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Microbiology National Center, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leiva</LastName><ForeName>Magdalena</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sabio</LastName><ForeName>Guadalupe</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Fundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lauzurica</LastName><ForeName>Pilar</ForeName><Initials>P</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-6579-1948</Identifier><AffiliationInfo><Affiliation>Microbiology National Center, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain. lauzurica@isciii.es.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>260464</GrantID><Agency>European Research Council</Agency><Country>International</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>02</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Leukemia</MedlineTA><NlmUniqueID>8704895</NlmUniqueID><ISSNLinking>0887-6924</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000911">Antibodies, Monoclonal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015703">Antigens, CD</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000945">Antigens, Differentiation, T-Lymphocyte</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C055855">CD69 antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054377">Chemokine CXCL12</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006571">Heterocyclic Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D037181">Lectins, C-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546843">mTOR protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.-</RegistryNumber><NameOfSubstance UI="C401298">sphingosine-1-phosphate phosphatase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.2</RegistryNumber><NameOfSubstance UI="D010744">Phosphoric Monoester Hydrolases</NameOfSubstance></Chemical><Chemical><RegistryNumber>G926EC510T</RegistryNumber><NameOfSubstance UI="D000068876">Fingolimod Hydrochloride</NameOfSubstance></Chemical><Chemical><RegistryNumber>OD49913540</RegistryNumber><NameOfSubstance UI="C088327">plerixafor octahydrochloride</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000911" MajorTopicYN="N">Antibodies, Monoclonal</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015703" MajorTopicYN="N">Antigens, CD</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000945" MajorTopicYN="N">Antigens, Differentiation, 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PubStatus="medline"><Year>2019</Year><Month>4</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>2</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29483712</ArticleId><ArticleId IdType="doi">10.1038/s41375-018-0052-x</ArticleId><ArticleId IdType="pii">10.1038/s41375-018-0052-x</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Espagne</li></country><region><li>Catalogne</li><li>Communauté de Madrid</li></region><settlement><li>Barcelone</li><li>Madrid</li></settlement><orgName><li>Université Pompeu Fabra</li></orgName></list><tree><country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Notario, Laura" sort="Notario, Laura" uniqKey="Notario L" first="Laura" last="Notario">Laura Notario</name></region><name sortKey="Alari Pahissa, Elisenda" sort="Alari Pahissa, Elisenda" uniqKey="Alari Pahissa E" first="Elisenda" last="Alari-Pahissa">Elisenda Alari-Pahissa</name><name sortKey="Albentosa, Almudena" sort="Albentosa, Almudena" uniqKey="Albentosa A" first="Almudena" last="Albentosa">Almudena Albentosa</name><name sortKey="Lauzurica, Pilar" sort="Lauzurica, Pilar" uniqKey="Lauzurica P" first="Pilar" last="Lauzurica">Pilar Lauzurica</name><name sortKey="Leiva, Magdalena" sort="Leiva, Magdalena" uniqKey="Leiva M" first="Magdalena" last="Leiva">Magdalena Leiva</name><name sortKey="Sabio, Guadalupe" sort="Sabio, Guadalupe" uniqKey="Sabio G" first="Guadalupe" last="Sabio">Guadalupe Sabio</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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