A checkpoint in B-lymphopoiesis related to Notch resistance
► Delta-like 1 represses B-lymphopoiesis. ► Flt3+ Il7r+ B220+ Cd19+ cells generate B cells even in the presence of delta-like 1. ► They are present in the bone marrow and few in the thymus. ► The absence of them explains why the thymus does not support B-lymphopoiesis. While murine B- and T-lymphopo...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2012-01, Vol.417 (1), p.141-146 |
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| creator | Okuyama, Kazuki Murata, Akihiko Sudo, Tetsuo Yoshino, Miya Hayashi, Shin-Ichi |
| description | ► Delta-like 1 represses B-lymphopoiesis. ► Flt3+ Il7r+ B220+ Cd19+ cells generate B cells even in the presence of delta-like 1. ► They are present in the bone marrow and few in the thymus. ► The absence of them explains why the thymus does not support B-lymphopoiesis.
While murine B- and T-lymphopoiesis require overlapping molecules, they occur in separate organs: the bone marrow (BM) and the thymus, respectively. The BM microenvironment is incapable of supporting T-lymphopoiesis because of insufficient interactions of Notch1 with delta-like ligand (Dll). Notch1/Dll interactions also play a role in the suppression of B-lymphopoiesis in the thymus. However, it is still unclear whether the Notch1/Dll interaction alone explains why the thymus does not support B-lymphopoiesis. In this study, we compared the precursor population colonizing the thymus with that in the BM by culturing them on stromal cells expressing abundant Dll1. We demonstrated that Flt3+ Il7r+ B220+ Cd19+ BM cells gave rise to B cells under this condition. We defined them as resistant to Dll1. In the thymus, Dll1-resistant cells were undetectable. This suggested that the absence of Dll1-resistant cells might explain the absence of B-lymphopoiesis in the thymus. |
| doi_str_mv | 10.1016/j.bbrc.2011.11.072 |
| format | Article |
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While murine B- and T-lymphopoiesis require overlapping molecules, they occur in separate organs: the bone marrow (BM) and the thymus, respectively. The BM microenvironment is incapable of supporting T-lymphopoiesis because of insufficient interactions of Notch1 with delta-like ligand (Dll). Notch1/Dll interactions also play a role in the suppression of B-lymphopoiesis in the thymus. However, it is still unclear whether the Notch1/Dll interaction alone explains why the thymus does not support B-lymphopoiesis. In this study, we compared the precursor population colonizing the thymus with that in the BM by culturing them on stromal cells expressing abundant Dll1. We demonstrated that Flt3+ Il7r+ B220+ Cd19+ BM cells gave rise to B cells under this condition. We defined them as resistant to Dll1. In the thymus, Dll1-resistant cells were undetectable. This suggested that the absence of Dll1-resistant cells might explain the absence of B-lymphopoiesis in the thymus.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2011.11.072</identifier><identifier>PMID: 22138652</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antigens, CD19 - metabolism ; B-Lymphocytes - immunology ; B-lymphopoiesis ; Bone marrow (BM) ; Cells, Cultured ; Delta-like ligand (Dll) ; fms-Like Tyrosine Kinase 3 - metabolism ; Intracellular Signaling Peptides and Proteins - metabolism ; Leukocyte Common Antigens - metabolism ; Lymphopoiesis ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Notch ; Receptor, Notch1 - metabolism ; Receptors, Interleukin-7 - metabolism ; Thymus ; Thymus Gland - immunology</subject><ispartof>Biochemical and biophysical research communications, 2012-01, Vol.417 (1), p.141-146</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3802-77b1bb59382ddae95eb3ffaa7514c582b4a204eb6c76d0b5dda2ca799dad4faa3</citedby><cites>FETCH-LOGICAL-c3802-77b1bb59382ddae95eb3ffaa7514c582b4a204eb6c76d0b5dda2ca799dad4faa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2011.11.072$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22138652$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okuyama, Kazuki</creatorcontrib><creatorcontrib>Murata, Akihiko</creatorcontrib><creatorcontrib>Sudo, Tetsuo</creatorcontrib><creatorcontrib>Yoshino, Miya</creatorcontrib><creatorcontrib>Hayashi, Shin-Ichi</creatorcontrib><title>A checkpoint in B-lymphopoiesis related to Notch resistance</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>► Delta-like 1 represses B-lymphopoiesis. ► Flt3+ Il7r+ B220+ Cd19+ cells generate B cells even in the presence of delta-like 1. ► They are present in the bone marrow and few in the thymus. ► The absence of them explains why the thymus does not support B-lymphopoiesis.
While murine B- and T-lymphopoiesis require overlapping molecules, they occur in separate organs: the bone marrow (BM) and the thymus, respectively. The BM microenvironment is incapable of supporting T-lymphopoiesis because of insufficient interactions of Notch1 with delta-like ligand (Dll). Notch1/Dll interactions also play a role in the suppression of B-lymphopoiesis in the thymus. However, it is still unclear whether the Notch1/Dll interaction alone explains why the thymus does not support B-lymphopoiesis. In this study, we compared the precursor population colonizing the thymus with that in the BM by culturing them on stromal cells expressing abundant Dll1. We demonstrated that Flt3+ Il7r+ B220+ Cd19+ BM cells gave rise to B cells under this condition. We defined them as resistant to Dll1. In the thymus, Dll1-resistant cells were undetectable. This suggested that the absence of Dll1-resistant cells might explain the absence of B-lymphopoiesis in the thymus.</description><subject>Animals</subject><subject>Antigens, CD19 - metabolism</subject><subject>B-Lymphocytes - immunology</subject><subject>B-lymphopoiesis</subject><subject>Bone marrow (BM)</subject><subject>Cells, Cultured</subject><subject>Delta-like ligand (Dll)</subject><subject>fms-Like Tyrosine Kinase 3 - metabolism</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Leukocyte Common Antigens - metabolism</subject><subject>Lymphopoiesis</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Notch</subject><subject>Receptor, Notch1 - metabolism</subject><subject>Receptors, Interleukin-7 - metabolism</subject><subject>Thymus</subject><subject>Thymus Gland - immunology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LxDAQhoMo7rr6BzxIb55ak7RNG_Sii1-w6EXBW8jHlM3aNjXpCvvvzbKrR2Fg4OWZF-ZB6JzgjGDCrlaZUl5nFBOSxcEVPUBTgjlOKcHFIZpijFlKOfmYoJMQVjiCBePHaEIpyWtW0im6vk30EvTn4Gw_JrZP7tJ20w1LFwMINiQeWjmCSUaXvLhRL2MQ41H2Gk7RUSPbAGf7PUPvD_dv86d08fr4PL9dpDqvMU2rShGlSp7X1BgJvASVN42UVUkKXdZUFZLiAhTTFTNYlRGiWlacG2mKyOUzdLnrHbz7WkMYRWeDhraVPbh1EJzEVzBjLJJ0R2rvQvDQiMHbTvqNIFhsnYmV2DoTW2ciTnQWjy729WvVgfk7-ZUUgZsdAPHJbwteBG0hCjDWgx6Fcfa__h9GSH12</recordid><startdate>20120106</startdate><enddate>20120106</enddate><creator>Okuyama, Kazuki</creator><creator>Murata, Akihiko</creator><creator>Sudo, Tetsuo</creator><creator>Yoshino, Miya</creator><creator>Hayashi, Shin-Ichi</creator><general>Elsevier Inc</general><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>20120106</creationdate><title>A checkpoint in B-lymphopoiesis related to Notch resistance</title><author>Okuyama, Kazuki ; Murata, Akihiko ; Sudo, Tetsuo ; Yoshino, Miya ; Hayashi, Shin-Ichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3802-77b1bb59382ddae95eb3ffaa7514c582b4a204eb6c76d0b5dda2ca799dad4faa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Antigens, CD19 - metabolism</topic><topic>B-Lymphocytes - immunology</topic><topic>B-lymphopoiesis</topic><topic>Bone marrow (BM)</topic><topic>Cells, Cultured</topic><topic>Delta-like ligand (Dll)</topic><topic>fms-Like Tyrosine Kinase 3 - metabolism</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Leukocyte Common Antigens - metabolism</topic><topic>Lymphopoiesis</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Notch</topic><topic>Receptor, Notch1 - metabolism</topic><topic>Receptors, Interleukin-7 - metabolism</topic><topic>Thymus</topic><topic>Thymus Gland - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okuyama, Kazuki</creatorcontrib><creatorcontrib>Murata, Akihiko</creatorcontrib><creatorcontrib>Sudo, Tetsuo</creatorcontrib><creatorcontrib>Yoshino, Miya</creatorcontrib><creatorcontrib>Hayashi, Shin-Ichi</creatorcontrib><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>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okuyama, Kazuki</au><au>Murata, Akihiko</au><au>Sudo, Tetsuo</au><au>Yoshino, Miya</au><au>Hayashi, Shin-Ichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A checkpoint in B-lymphopoiesis related to Notch resistance</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2012-01-06</date><risdate>2012</risdate><volume>417</volume><issue>1</issue><spage>141</spage><epage>146</epage><pages>141-146</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>► Delta-like 1 represses B-lymphopoiesis. ► Flt3+ Il7r+ B220+ Cd19+ cells generate B cells even in the presence of delta-like 1. ► They are present in the bone marrow and few in the thymus. ► The absence of them explains why the thymus does not support B-lymphopoiesis.
While murine B- and T-lymphopoiesis require overlapping molecules, they occur in separate organs: the bone marrow (BM) and the thymus, respectively. The BM microenvironment is incapable of supporting T-lymphopoiesis because of insufficient interactions of Notch1 with delta-like ligand (Dll). Notch1/Dll interactions also play a role in the suppression of B-lymphopoiesis in the thymus. However, it is still unclear whether the Notch1/Dll interaction alone explains why the thymus does not support B-lymphopoiesis. In this study, we compared the precursor population colonizing the thymus with that in the BM by culturing them on stromal cells expressing abundant Dll1. We demonstrated that Flt3+ Il7r+ B220+ Cd19+ BM cells gave rise to B cells under this condition. We defined them as resistant to Dll1. In the thymus, Dll1-resistant cells were undetectable. This suggested that the absence of Dll1-resistant cells might explain the absence of B-lymphopoiesis in the thymus.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22138652</pmid><doi>10.1016/j.bbrc.2011.11.072</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigens, CD19 - metabolism B-Lymphocytes - immunology B-lymphopoiesis Bone marrow (BM) Cells, Cultured Delta-like ligand (Dll) fms-Like Tyrosine Kinase 3 - metabolism Intracellular Signaling Peptides and Proteins - metabolism Leukocyte Common Antigens - metabolism Lymphopoiesis Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mice, Transgenic Notch Receptor, Notch1 - metabolism Receptors, Interleukin-7 - metabolism Thymus Thymus Gland - immunology |
| title | A checkpoint in B-lymphopoiesis related to Notch resistance |
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