CD23+CD21highCD1dhigh B cells in inflamed lymph nodes are a locally differentiated population with increased antigen capture and activation potential1
CD23 + CD21 high CD1d high B cells (Bin cells) accumulate in the LNs draining inflamed joints of the TNFα transgenic (TNFtg) mouse model of rheumatoid arthritis, and are primarily involved in the significant histological and functional LN alterations that accompany disease exacerbation in this strai...
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Veröffentlicht in: | The Journal of immunology (1950) 2012-05, Vol.188 (12), p.5944-5953 |
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creator | Moshkani, Safiehkhatoon Kuzin, Igor I. Adewale, Funmilola Jansson, Johan Sanz, Iñaki Schwarz, Edward M. Bottaro, Andrea |
description | CD23
+
CD21
high
CD1d
high
B cells (Bin cells) accumulate in the LNs draining inflamed joints of the TNFα transgenic (TNFtg) mouse model of rheumatoid arthritis, and are primarily involved in the significant histological and functional LN alterations that accompany disease exacerbation in this strain. Here we investigate the origin and function of Bin cells. We show that adoptively transferred GFP
+
sorted mature follicular B (FoB) cells home preferentially to inflamed LNs of TNFtg mice where they rapidly differentiate into Bin cells, with a close correlation with the endogenous Bin fraction. Bin cells are also induced in wild-type (WT) LNs after immunization with T-dependent antigens, and display a germinal center phenotype at higher rates compared to FoB cells. Furthermore, we show that Bin cells can capture and process antigen immune complexes in a CD21-dependent manner more efficiently than FoB cells, and express higher levels of MHCII and costimulatory antigens CD80 and CD86. We propose that Bin cells are a previously unrecognized inflammation-induced B cell population with increased antigen capture and activation potential, which may facilitate normal immune responses but may contribute to autoimmunity when chronic inflammation causes their accumulation and persistence in affected LNs. |
doi_str_mv | 10.4049/jimmunol.1103071 |
format | Article |
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+
CD21
high
CD1d
high
B cells (Bin cells) accumulate in the LNs draining inflamed joints of the TNFα transgenic (TNFtg) mouse model of rheumatoid arthritis, and are primarily involved in the significant histological and functional LN alterations that accompany disease exacerbation in this strain. Here we investigate the origin and function of Bin cells. We show that adoptively transferred GFP
+
sorted mature follicular B (FoB) cells home preferentially to inflamed LNs of TNFtg mice where they rapidly differentiate into Bin cells, with a close correlation with the endogenous Bin fraction. Bin cells are also induced in wild-type (WT) LNs after immunization with T-dependent antigens, and display a germinal center phenotype at higher rates compared to FoB cells. Furthermore, we show that Bin cells can capture and process antigen immune complexes in a CD21-dependent manner more efficiently than FoB cells, and express higher levels of MHCII and costimulatory antigens CD80 and CD86. We propose that Bin cells are a previously unrecognized inflammation-induced B cell population with increased antigen capture and activation potential, which may facilitate normal immune responses but may contribute to autoimmunity when chronic inflammation causes their accumulation and persistence in affected LNs.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.1103071</identifier><identifier>PMID: 22593620</identifier><language>eng</language><ispartof>The Journal of immunology (1950), 2012-05, Vol.188 (12), p.5944-5953</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids></links><search><creatorcontrib>Moshkani, Safiehkhatoon</creatorcontrib><creatorcontrib>Kuzin, Igor I.</creatorcontrib><creatorcontrib>Adewale, Funmilola</creatorcontrib><creatorcontrib>Jansson, Johan</creatorcontrib><creatorcontrib>Sanz, Iñaki</creatorcontrib><creatorcontrib>Schwarz, Edward M.</creatorcontrib><creatorcontrib>Bottaro, Andrea</creatorcontrib><title>CD23+CD21highCD1dhigh B cells in inflamed lymph nodes are a locally differentiated population with increased antigen capture and activation potential1</title><title>The Journal of immunology (1950)</title><description>CD23
+
CD21
high
CD1d
high
B cells (Bin cells) accumulate in the LNs draining inflamed joints of the TNFα transgenic (TNFtg) mouse model of rheumatoid arthritis, and are primarily involved in the significant histological and functional LN alterations that accompany disease exacerbation in this strain. Here we investigate the origin and function of Bin cells. We show that adoptively transferred GFP
+
sorted mature follicular B (FoB) cells home preferentially to inflamed LNs of TNFtg mice where they rapidly differentiate into Bin cells, with a close correlation with the endogenous Bin fraction. Bin cells are also induced in wild-type (WT) LNs after immunization with T-dependent antigens, and display a germinal center phenotype at higher rates compared to FoB cells. Furthermore, we show that Bin cells can capture and process antigen immune complexes in a CD21-dependent manner more efficiently than FoB cells, and express higher levels of MHCII and costimulatory antigens CD80 and CD86. We propose that Bin cells are a previously unrecognized inflammation-induced B cell population with increased antigen capture and activation potential, which may facilitate normal immune responses but may contribute to autoimmunity when chronic inflammation causes their accumulation and persistence in affected LNs.</description><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqljstOwzAQRS0EouGxZ-k9ahk7iUM3LEiL-AD20ZA4iSvHtmynKD_C9-ICG9ZIo7nS3KOjIeSOwaaAYvtwUNM0G6s3jEEOFTsjGStLWAsB4pxkAJyvWSWqFbkK4QAAAnhxSVacl9tccMjIZ73j-X1abFTDWO9Yd0r6TFupdaDKpOk1TrKjepncSI3tZKDoJUWqbYtaL7RTfS-9NFFhTKCzbtYYlTX0Q8UxGVovMaQGEzJIQ1t0cT4pTLq1UR1_aGfjt0SzG3LRow7y9jevydPL_q1-Xbv5Pf3SJsyjbpxXE_qlsaiav41RYzPYY5PnFcAj5P8WfAHcyXic</recordid><startdate>20120516</startdate><enddate>20120516</enddate><creator>Moshkani, Safiehkhatoon</creator><creator>Kuzin, Igor I.</creator><creator>Adewale, Funmilola</creator><creator>Jansson, Johan</creator><creator>Sanz, Iñaki</creator><creator>Schwarz, Edward M.</creator><creator>Bottaro, Andrea</creator><scope>5PM</scope></search><sort><creationdate>20120516</creationdate><title>CD23+CD21highCD1dhigh B cells in inflamed lymph nodes are a locally differentiated population with increased antigen capture and activation potential1</title><author>Moshkani, Safiehkhatoon ; Kuzin, Igor I. ; Adewale, Funmilola ; Jansson, Johan ; Sanz, Iñaki ; Schwarz, Edward M. ; Bottaro, Andrea</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_33700803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moshkani, Safiehkhatoon</creatorcontrib><creatorcontrib>Kuzin, Igor I.</creatorcontrib><creatorcontrib>Adewale, Funmilola</creatorcontrib><creatorcontrib>Jansson, Johan</creatorcontrib><creatorcontrib>Sanz, Iñaki</creatorcontrib><creatorcontrib>Schwarz, Edward M.</creatorcontrib><creatorcontrib>Bottaro, Andrea</creatorcontrib><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moshkani, Safiehkhatoon</au><au>Kuzin, Igor I.</au><au>Adewale, Funmilola</au><au>Jansson, Johan</au><au>Sanz, Iñaki</au><au>Schwarz, Edward M.</au><au>Bottaro, Andrea</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD23+CD21highCD1dhigh B cells in inflamed lymph nodes are a locally differentiated population with increased antigen capture and activation potential1</atitle><jtitle>The Journal of immunology (1950)</jtitle><date>2012-05-16</date><risdate>2012</risdate><volume>188</volume><issue>12</issue><spage>5944</spage><epage>5953</epage><pages>5944-5953</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>CD23
+
CD21
high
CD1d
high
B cells (Bin cells) accumulate in the LNs draining inflamed joints of the TNFα transgenic (TNFtg) mouse model of rheumatoid arthritis, and are primarily involved in the significant histological and functional LN alterations that accompany disease exacerbation in this strain. Here we investigate the origin and function of Bin cells. We show that adoptively transferred GFP
+
sorted mature follicular B (FoB) cells home preferentially to inflamed LNs of TNFtg mice where they rapidly differentiate into Bin cells, with a close correlation with the endogenous Bin fraction. Bin cells are also induced in wild-type (WT) LNs after immunization with T-dependent antigens, and display a germinal center phenotype at higher rates compared to FoB cells. Furthermore, we show that Bin cells can capture and process antigen immune complexes in a CD21-dependent manner more efficiently than FoB cells, and express higher levels of MHCII and costimulatory antigens CD80 and CD86. We propose that Bin cells are a previously unrecognized inflammation-induced B cell population with increased antigen capture and activation potential, which may facilitate normal immune responses but may contribute to autoimmunity when chronic inflammation causes their accumulation and persistence in affected LNs.</abstract><pmid>22593620</pmid><doi>10.4049/jimmunol.1103071</doi></addata></record> |
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title | CD23+CD21highCD1dhigh B cells in inflamed lymph nodes are a locally differentiated population with increased antigen capture and activation potential1 |
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