Hepatic stellate cell-conditioned myeloid cells provide a novel therapy for prevention of factor VIII antibody formation in mice.
Identifieur interne : 000476 ( Main/Exploration ); précédent : 000475; suivant : 000477Hepatic stellate cell-conditioned myeloid cells provide a novel therapy for prevention of factor VIII antibody formation in mice.
Auteurs : Sumantha Bhatt [États-Unis] ; Gong-Qing Shen [États-Unis] ; Yan Li [États-Unis] ; Shiguang Qian [États-Unis] ; Margaret V. Ragni [États-Unis] ; Lina Lu [États-Unis]Source :
- Experimental hematology [ 1873-2399 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- biosynthèse : Autoanticorps.
- cytologie : Cellules myéloïdes, Cellules étoilées du foie.
- immunologie : Facteur VIII, Hémophilie A.
- Amorces ADN, Animaux, Réaction de polymérisation en chaîne, Souris, Souris de lignée C57BL, Séquence nucléotidique.
English descriptors
- KwdEn :
- MESH :
- chemical , biosynthesis : Autoantibodies.
- chemical , immunology : Factor VIII.
- cytology : Hepatic Stellate Cells, Myeloid Cells.
- immunology : Hemophilia A.
- Animals, Base Sequence, DNA Primers, Mice, Mice, Inbred C57BL, Polymerase Chain Reaction.
Abstract
A major complication of factor VIII (F.VIII) infusion therapies for the treatment of hemophilia A is the formation of antibodies (inhibitors) against F.VIII, a T-cell-dependent, B-cell-mediated process. To date, attempts to inhibit formation of the inhibitors have been limited in success. We have shown that hepatic stellate cells (HSCs) promote the development of myeloid-derived suppressor cells (MDSCs). The HSC-induced MDSCs are potent regulators of T-cell and B-cell responses. Here we show that MDSCs can be propagated from hemophilia A mouse bone marrow cells in coculture with HSCs. These cells exhibit a suppressive phenotype and display a marked ability to inhibit T-cell proliferation induced by dendritic cells in response to F.VIII. MDSCs can also inhibit proliferation and activation of B cells stimulated by immunoglobulin M and interleukin 4. Administration of HSC-induced MDSCs induces CD4(+) T cell and B220(+) B-cell hyporesponsiveness to F.VIII and reduces inhibitor formation in hemophilia A mice. These results suggest that MDSCs could serve as a form of immunotherapy for preventing inhibitor formation via induction of immune tolerance.
DOI: 10.1016/j.exphem.2014.12.001
PubMed: 25534204
Affiliations:
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Ragni</name><affiliation wicri:level="2"><nlm:affiliation>Division of Hematology/Oncology, Department of Medicine, University of Pittsburgh and Hemophilia Center of Western Pennsylvania, Pittsburgh, PA, United States. 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Electronic address: lul2@ccf.org.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Molecular Medicine, Lerner College of Medicine, Case Western Reserve University, Cleveland, OH, United States; Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, United States; Department of General Surgery, Digestive Disease Institute, Cleveland Clinic, Cleveland, OH</wicri:regionArea><placeName><region type="state">Ohio</region></placeName></affiliation></author></analytic><series><title level="j">Experimental hematology</title><idno type="eISSN">1873-2399</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autoantibodies (biosynthesis)</term><term>Base Sequence</term><term>DNA Primers</term><term>Factor VIII (immunology)</term><term>Hemophilia A (immunology)</term><term>Hepatic Stellate Cells (cytology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Myeloid Cells (cytology)</term><term>Polymerase Chain Reaction</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Amorces ADN</term><term>Animaux</term><term>Autoanticorps (biosynthèse)</term><term>Cellules myéloïdes (cytologie)</term><term>Cellules étoilées du foie (cytologie)</term><term>Facteur VIII (immunologie)</term><term>Hémophilie A (immunologie)</term><term>Réaction de polymérisation en chaîne</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Séquence nucléotidique</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Autoantibodies</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Factor VIII</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Autoanticorps</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules myéloïdes</term><term>Cellules étoilées du foie</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Hepatic Stellate Cells</term><term>Myeloid Cells</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Facteur VIII</term><term>Hémophilie A</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Hemophilia A</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>DNA Primers</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Polymerase Chain Reaction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Amorces ADN</term><term>Animaux</term><term>Réaction de polymérisation en chaîne</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Séquence nucléotidique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A major complication of factor VIII (F.VIII) infusion therapies for the treatment of hemophilia A is the formation of antibodies (inhibitors) against F.VIII, a T-cell-dependent, B-cell-mediated process. To date, attempts to inhibit formation of the inhibitors have been limited in success. We have shown that hepatic stellate cells (HSCs) promote the development of myeloid-derived suppressor cells (MDSCs). The HSC-induced MDSCs are potent regulators of T-cell and B-cell responses. Here we show that MDSCs can be propagated from hemophilia A mouse bone marrow cells in coculture with HSCs. These cells exhibit a suppressive phenotype and display a marked ability to inhibit T-cell proliferation induced by dendritic cells in response to F.VIII. MDSCs can also inhibit proliferation and activation of B cells stimulated by immunoglobulin M and interleukin 4. Administration of HSC-induced MDSCs induces CD4(+) T cell and B220(+) B-cell hyporesponsiveness to F.VIII and reduces inhibitor formation in hemophilia A mice. These results suggest that MDSCs could serve as a form of immunotherapy for preventing inhibitor formation via induction of immune tolerance.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Ohio</li><li>Pennsylvanie</li></region></list><tree><country name="États-Unis"><region name="Ohio"><name sortKey="Bhatt, Sumantha" sort="Bhatt, Sumantha" uniqKey="Bhatt S" first="Sumantha" last="Bhatt">Sumantha Bhatt</name></region><name sortKey="Li, Yan" sort="Li, Yan" uniqKey="Li Y" first="Yan" last="Li">Yan Li</name><name sortKey="Lu, Lina" sort="Lu, Lina" uniqKey="Lu L" first="Lina" last="Lu">Lina Lu</name><name sortKey="Qian, Shiguang" sort="Qian, Shiguang" uniqKey="Qian S" first="Shiguang" last="Qian">Shiguang Qian</name><name sortKey="Ragni, Margaret V" sort="Ragni, Margaret V" uniqKey="Ragni M" first="Margaret V" last="Ragni">Margaret V. Ragni</name><name sortKey="Shen, Gong Qing" sort="Shen, Gong Qing" uniqKey="Shen G" first="Gong-Qing" last="Shen">Gong-Qing Shen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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