STAT1-dependent IgG cell-surface expression in a human B cell line derived from a STAT1-deficient patient
A STAT1‐dependent surface expression of IgGs is revealed in a human B cell line derived from a STAT1‐deficient patient. STAT1 is a key effector of cytokines involved in the resistance to pathogens; its identified transcriptional targets mediate the innate immune response involved in the defense agai...
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| Veröffentlicht in: | Journal of leukocyte biology 2010-06, Vol.87 (6), p.1145-1152 |
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| creator | Najjar, Imen Deglesne, Pierre-Antoine Schischmanoff, Pierre Olivier Fabre, Emmanuelle E Boisson-Dupuis, Stéphanie Nimmerjahn, Falk Bornkamm, Georg W Dusanter-Fourt, Isabelle Fagard, Remi |
| description | A STAT1‐dependent surface expression of IgGs is revealed in a human B cell line derived from a STAT1‐deficient patient.
STAT1 is a key effector of cytokines involved in the resistance to pathogens; its identified transcriptional targets mediate the innate immune response involved in the defense against viruses and bacteria. Little is known about the role of STAT1 in adaptive immunity, including its impact on BCR or surface Ig expression. Analysis of this point is difficult in humans, as STAT1 deficiency is extremely rare. SD patients die early in childhood from a severe immunodeficiency. Herein, a SD B cell line obtained from a SD patient was compared with a B cell line from a STAT1‐proficient subject in search of differences in surface Ig expression. In this SD B cell line, a complete absence of surface IgG was noted. The mRNA encoding the surface form of IgG was detected only in STAT1‐proficient B cells; the mRNAs encoding the secreted and the surface forms were detected in SD and STAT1‐proficient B cells. Re‐expression of STAT1 in SD B cells restored surface IgG expression and a functional BCR. Conversely, shRNA silencing of STAT1 in B cells reduced considerably the expression of the surface IgG. Although limited to one B cell line, these results suggest that STAT1 may play an essential role in surface IgG expression in human B cells. Possible mechanisms involve regulation of mRNA splicing, transcription, or both. These observations extend the role of STAT1 further in adaptive immunity, including the regulation of BCR expression. |
| doi_str_mv | 10.1189/jlb.1109714 |
| format | Article |
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STAT1 is a key effector of cytokines involved in the resistance to pathogens; its identified transcriptional targets mediate the innate immune response involved in the defense against viruses and bacteria. Little is known about the role of STAT1 in adaptive immunity, including its impact on BCR or surface Ig expression. Analysis of this point is difficult in humans, as STAT1 deficiency is extremely rare. SD patients die early in childhood from a severe immunodeficiency. Herein, a SD B cell line obtained from a SD patient was compared with a B cell line from a STAT1‐proficient subject in search of differences in surface Ig expression. In this SD B cell line, a complete absence of surface IgG was noted. The mRNA encoding the surface form of IgG was detected only in STAT1‐proficient B cells; the mRNAs encoding the secreted and the surface forms were detected in SD and STAT1‐proficient B cells. Re‐expression of STAT1 in SD B cells restored surface IgG expression and a functional BCR. Conversely, shRNA silencing of STAT1 in B cells reduced considerably the expression of the surface IgG. Although limited to one B cell line, these results suggest that STAT1 may play an essential role in surface IgG expression in human B cells. Possible mechanisms involve regulation of mRNA splicing, transcription, or both. These observations extend the role of STAT1 further in adaptive immunity, including the regulation of BCR expression.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1189/jlb.1109714</identifier><identifier>PMID: 20200400</identifier><language>eng</language><publisher>United States: Society for Leukocyte Biology</publisher><subject>adaptive immunity ; B-Lymphocytes - metabolism ; B-Lymphocytes - pathology ; Blotting, Western ; Cell Line, Transformed ; Flow Cytometry ; Fluorescent Antibody Technique ; Humans ; Immunoglobulin G - genetics ; Immunoglobulin G - metabolism ; innate immunity ; Phosphorylation ; Receptors, Antigen, B-Cell - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; STAT1 Transcription Factor - antagonists & inhibitors ; STAT1 Transcription Factor - deficiency ; STAT1 Transcription Factor - genetics</subject><ispartof>Journal of leukocyte biology, 2010-06, Vol.87 (6), p.1145-1152</ispartof><rights>2010 Society for Leukocyte Biology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3605-ecb7903874444f1735baaf99c3c1d6e6865274aee0bf1f2b03a915fc6221f9963</citedby><cites>FETCH-LOGICAL-c3605-ecb7903874444f1735baaf99c3c1d6e6865274aee0bf1f2b03a915fc6221f9963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1189%2Fjlb.1109714$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1189%2Fjlb.1109714$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20200400$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Najjar, Imen</creatorcontrib><creatorcontrib>Deglesne, Pierre-Antoine</creatorcontrib><creatorcontrib>Schischmanoff, Pierre Olivier</creatorcontrib><creatorcontrib>Fabre, Emmanuelle E</creatorcontrib><creatorcontrib>Boisson-Dupuis, Stéphanie</creatorcontrib><creatorcontrib>Nimmerjahn, Falk</creatorcontrib><creatorcontrib>Bornkamm, Georg W</creatorcontrib><creatorcontrib>Dusanter-Fourt, Isabelle</creatorcontrib><creatorcontrib>Fagard, Remi</creatorcontrib><title>STAT1-dependent IgG cell-surface expression in a human B cell line derived from a STAT1-deficient patient</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>A STAT1‐dependent surface expression of IgGs is revealed in a human B cell line derived from a STAT1‐deficient patient.
STAT1 is a key effector of cytokines involved in the resistance to pathogens; its identified transcriptional targets mediate the innate immune response involved in the defense against viruses and bacteria. Little is known about the role of STAT1 in adaptive immunity, including its impact on BCR or surface Ig expression. Analysis of this point is difficult in humans, as STAT1 deficiency is extremely rare. SD patients die early in childhood from a severe immunodeficiency. Herein, a SD B cell line obtained from a SD patient was compared with a B cell line from a STAT1‐proficient subject in search of differences in surface Ig expression. In this SD B cell line, a complete absence of surface IgG was noted. The mRNA encoding the surface form of IgG was detected only in STAT1‐proficient B cells; the mRNAs encoding the secreted and the surface forms were detected in SD and STAT1‐proficient B cells. Re‐expression of STAT1 in SD B cells restored surface IgG expression and a functional BCR. Conversely, shRNA silencing of STAT1 in B cells reduced considerably the expression of the surface IgG. Although limited to one B cell line, these results suggest that STAT1 may play an essential role in surface IgG expression in human B cells. Possible mechanisms involve regulation of mRNA splicing, transcription, or both. These observations extend the role of STAT1 further in adaptive immunity, including the regulation of BCR expression.</description><subject>adaptive immunity</subject><subject>B-Lymphocytes - metabolism</subject><subject>B-Lymphocytes - pathology</subject><subject>Blotting, Western</subject><subject>Cell Line, Transformed</subject><subject>Flow Cytometry</subject><subject>Fluorescent Antibody Technique</subject><subject>Humans</subject><subject>Immunoglobulin G - genetics</subject><subject>Immunoglobulin G - metabolism</subject><subject>innate immunity</subject><subject>Phosphorylation</subject><subject>Receptors, Antigen, B-Cell - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>STAT1 Transcription Factor - antagonists & inhibitors</subject><subject>STAT1 Transcription Factor - deficiency</subject><subject>STAT1 Transcription Factor - genetics</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P3DAQhq2KqmxpT71XPsGhCoztxE6OgICCVuqB7dlynDFrlK_aGwL_Hi-79IgvY42eeWb0EvKDwSljZXX22NbpA5Vi-SeyYJUoMyGVOCALUDnLihzgkHyN8REABJfwhRxy4ACpvyD-fnW-YlmDI_YN9ht6-3BDLbZtFqfgjEWKz2PAGP3QU99TQ9dTZ3p68QbR1vdIGwz-CRvqwtAl4N3ovPVb42g22_qNfHamjfh9X4_I3-ur1eXvbPnn5vbyfJlZIaHI0NaqAlGqPD3HlChqY1xVWWFZI1GWsuAqN4hQO-Z4DcJUrHBWcs4SJsUROdl5xzD8mzBudOfj9ljT4zBFrYRgvGQVT-SvHWnDEGNAp8fgOxNeNAO9jVanaPU-2kT_3HunusPmP_ueZQJgB8y-xZePXPpuecFYXqSR493I2j-sZx9Qx860bdrA9TzPpdJSv4GveGGOuw</recordid><startdate>201006</startdate><enddate>201006</enddate><creator>Najjar, Imen</creator><creator>Deglesne, Pierre-Antoine</creator><creator>Schischmanoff, Pierre Olivier</creator><creator>Fabre, Emmanuelle E</creator><creator>Boisson-Dupuis, Stéphanie</creator><creator>Nimmerjahn, Falk</creator><creator>Bornkamm, Georg W</creator><creator>Dusanter-Fourt, Isabelle</creator><creator>Fagard, Remi</creator><general>Society for Leukocyte Biology</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>201006</creationdate><title>STAT1-dependent IgG cell-surface expression in a human B cell line derived from a STAT1-deficient patient</title><author>Najjar, Imen ; Deglesne, Pierre-Antoine ; Schischmanoff, Pierre Olivier ; Fabre, Emmanuelle E ; Boisson-Dupuis, Stéphanie ; Nimmerjahn, Falk ; Bornkamm, Georg W ; Dusanter-Fourt, Isabelle ; Fagard, Remi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3605-ecb7903874444f1735baaf99c3c1d6e6865274aee0bf1f2b03a915fc6221f9963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>adaptive immunity</topic><topic>B-Lymphocytes - metabolism</topic><topic>B-Lymphocytes - pathology</topic><topic>Blotting, Western</topic><topic>Cell Line, Transformed</topic><topic>Flow Cytometry</topic><topic>Fluorescent Antibody Technique</topic><topic>Humans</topic><topic>Immunoglobulin G - genetics</topic><topic>Immunoglobulin G - metabolism</topic><topic>innate immunity</topic><topic>Phosphorylation</topic><topic>Receptors, Antigen, B-Cell - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>STAT1 Transcription Factor - antagonists & inhibitors</topic><topic>STAT1 Transcription Factor - deficiency</topic><topic>STAT1 Transcription Factor - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Najjar, Imen</creatorcontrib><creatorcontrib>Deglesne, Pierre-Antoine</creatorcontrib><creatorcontrib>Schischmanoff, Pierre Olivier</creatorcontrib><creatorcontrib>Fabre, Emmanuelle E</creatorcontrib><creatorcontrib>Boisson-Dupuis, Stéphanie</creatorcontrib><creatorcontrib>Nimmerjahn, Falk</creatorcontrib><creatorcontrib>Bornkamm, Georg W</creatorcontrib><creatorcontrib>Dusanter-Fourt, Isabelle</creatorcontrib><creatorcontrib>Fagard, Remi</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>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Najjar, Imen</au><au>Deglesne, Pierre-Antoine</au><au>Schischmanoff, Pierre Olivier</au><au>Fabre, Emmanuelle E</au><au>Boisson-Dupuis, Stéphanie</au><au>Nimmerjahn, Falk</au><au>Bornkamm, Georg W</au><au>Dusanter-Fourt, Isabelle</au><au>Fagard, Remi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>STAT1-dependent IgG cell-surface expression in a human B cell line derived from a STAT1-deficient patient</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2010-06</date><risdate>2010</risdate><volume>87</volume><issue>6</issue><spage>1145</spage><epage>1152</epage><pages>1145-1152</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>A STAT1‐dependent surface expression of IgGs is revealed in a human B cell line derived from a STAT1‐deficient patient.
STAT1 is a key effector of cytokines involved in the resistance to pathogens; its identified transcriptional targets mediate the innate immune response involved in the defense against viruses and bacteria. Little is known about the role of STAT1 in adaptive immunity, including its impact on BCR or surface Ig expression. Analysis of this point is difficult in humans, as STAT1 deficiency is extremely rare. SD patients die early in childhood from a severe immunodeficiency. Herein, a SD B cell line obtained from a SD patient was compared with a B cell line from a STAT1‐proficient subject in search of differences in surface Ig expression. In this SD B cell line, a complete absence of surface IgG was noted. The mRNA encoding the surface form of IgG was detected only in STAT1‐proficient B cells; the mRNAs encoding the secreted and the surface forms were detected in SD and STAT1‐proficient B cells. Re‐expression of STAT1 in SD B cells restored surface IgG expression and a functional BCR. Conversely, shRNA silencing of STAT1 in B cells reduced considerably the expression of the surface IgG. Although limited to one B cell line, these results suggest that STAT1 may play an essential role in surface IgG expression in human B cells. Possible mechanisms involve regulation of mRNA splicing, transcription, or both. These observations extend the role of STAT1 further in adaptive immunity, including the regulation of BCR expression.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>20200400</pmid><doi>10.1189/jlb.1109714</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of leukocyte biology, 2010-06, Vol.87 (6), p.1145-1152 |
| issn | 0741-5400 1938-3673 |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Wiley Online Library All Journals; Alma/SFX Local Collection |
| subjects | adaptive immunity B-Lymphocytes - metabolism B-Lymphocytes - pathology Blotting, Western Cell Line, Transformed Flow Cytometry Fluorescent Antibody Technique Humans Immunoglobulin G - genetics Immunoglobulin G - metabolism innate immunity Phosphorylation Receptors, Antigen, B-Cell - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism STAT1 Transcription Factor - antagonists & inhibitors STAT1 Transcription Factor - deficiency STAT1 Transcription Factor - genetics |
| title | STAT1-dependent IgG cell-surface expression in a human B cell line derived from a STAT1-deficient patient |
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