Loading…
Cutting Edge: Low-Affinity, Smith Antigen-Specific B Cells Are Tolerized by Dendritic Cells and Macrophages1
Polyclonal B cell activation promotes immunity without the loss of tolerance. Our data show that during activation of the innate immune system, B cell tolerance to Smith Ag Sm is maintained by dendritic cells (DCs) and macrophages ( M Φ ). TLR4-activated myeloid DCs and M Φ , but not plasmacytoid or...
Saved in:
| Published in: | The Journal of immunology (1950) 2005-07, Vol.175 (1), p.37-41 |
|---|---|
| Main Authors: | , , , |
| Format: | Article |
| Language: | English |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | |
|---|---|
| cites | |
| container_end_page | 41 |
| container_issue | 1 |
| container_start_page | 37 |
| container_title | The Journal of immunology (1950) |
| container_volume | 175 |
| creator | Kilmon, Michelle A. Rutan, Jennifer A. Clarke, Stephen H. Vilen, Barbara J. |
| description | Polyclonal B cell activation promotes immunity without the loss of tolerance. Our data show that during activation of the innate immune system, B cell tolerance to Smith Ag Sm is maintained by dendritic cells (DCs) and macrophages (
M
Φ
). TLR4-activated myeloid DCs and
M
Φ
, but not plasmacytoid or lymphoid DCs, repressed autoreactive B cells through the secretion of soluble mediators, including IL-6. Although IL-6 promotes plasma cell differentiation of B cells acutely stimulated by Ag, we show that it repressed cells that were chronically exposed to self-Ag. This mechanism of tolerance was not limited to Smith Ag-specific B cells as hen egg lysozyme-and p-azophenylarsonate-specific B cells were similarly affected. Our data define a tolerogenic role for
M
Φ
and DCs in regulating autoreactive B cells during activation of the innate immune system. |
| format | article |
| fullrecord | <record><control><sourceid>pubmedcentral</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3724409</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>pubmedcentral_primary_oai_pubmedcentral_nih_gov_3724409</sourcerecordid><originalsourceid>FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_37244093</originalsourceid><addsrcrecordid>eNqljLFOwzAUAC1ERUPhH94HYMlxE0dhQAqhqANM7R65yYvzkONEtgsKXw8SLMxMN9zpLliS5rngSgl1yRIhpORpoYo1uw7hTQihhMyu2DrNy0IqWSbM1ucYyRnYdQbv4WX64FXfk6O43MFhpDhA5SIZdPwwY0s9tfAINVoboPIIx8mip0_s4LTAE7rOU_xOfgLtOnjVrZ_mQRsM6Q1b9doGvP3lhj087471ns_n04hdiy56bZvZ06j90kyamr_G0dCY6b3ZFjLLRLn99-ALZ8thqg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Cutting Edge: Low-Affinity, Smith Antigen-Specific B Cells Are Tolerized by Dendritic Cells and Macrophages1</title><source>EZB Electronic Journals Library</source><creator>Kilmon, Michelle A. ; Rutan, Jennifer A. ; Clarke, Stephen H. ; Vilen, Barbara J.</creator><creatorcontrib>Kilmon, Michelle A. ; Rutan, Jennifer A. ; Clarke, Stephen H. ; Vilen, Barbara J.</creatorcontrib><description>Polyclonal B cell activation promotes immunity without the loss of tolerance. Our data show that during activation of the innate immune system, B cell tolerance to Smith Ag Sm is maintained by dendritic cells (DCs) and macrophages (
M
Φ
). TLR4-activated myeloid DCs and
M
Φ
, but not plasmacytoid or lymphoid DCs, repressed autoreactive B cells through the secretion of soluble mediators, including IL-6. Although IL-6 promotes plasma cell differentiation of B cells acutely stimulated by Ag, we show that it repressed cells that were chronically exposed to self-Ag. This mechanism of tolerance was not limited to Smith Ag-specific B cells as hen egg lysozyme-and p-azophenylarsonate-specific B cells were similarly affected. Our data define a tolerogenic role for
M
Φ
and DCs in regulating autoreactive B cells during activation of the innate immune system.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>PMID: 15972629</identifier><language>eng</language><ispartof>The Journal of immunology (1950), 2005-07, Vol.175 (1), p.37-41</ispartof><rights>Copyright © 2005 by The American Association of Immunologists All rights reserved. 2005</rights><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</link.rule.ids></links><search><creatorcontrib>Kilmon, Michelle A.</creatorcontrib><creatorcontrib>Rutan, Jennifer A.</creatorcontrib><creatorcontrib>Clarke, Stephen H.</creatorcontrib><creatorcontrib>Vilen, Barbara J.</creatorcontrib><title>Cutting Edge: Low-Affinity, Smith Antigen-Specific B Cells Are Tolerized by Dendritic Cells and Macrophages1</title><title>The Journal of immunology (1950)</title><description>Polyclonal B cell activation promotes immunity without the loss of tolerance. Our data show that during activation of the innate immune system, B cell tolerance to Smith Ag Sm is maintained by dendritic cells (DCs) and macrophages (
M
Φ
). TLR4-activated myeloid DCs and
M
Φ
, but not plasmacytoid or lymphoid DCs, repressed autoreactive B cells through the secretion of soluble mediators, including IL-6. Although IL-6 promotes plasma cell differentiation of B cells acutely stimulated by Ag, we show that it repressed cells that were chronically exposed to self-Ag. This mechanism of tolerance was not limited to Smith Ag-specific B cells as hen egg lysozyme-and p-azophenylarsonate-specific B cells were similarly affected. Our data define a tolerogenic role for
M
Φ
and DCs in regulating autoreactive B cells during activation of the innate immune system.</description><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqljLFOwzAUAC1ERUPhH94HYMlxE0dhQAqhqANM7R65yYvzkONEtgsKXw8SLMxMN9zpLliS5rngSgl1yRIhpORpoYo1uw7hTQihhMyu2DrNy0IqWSbM1ucYyRnYdQbv4WX64FXfk6O43MFhpDhA5SIZdPwwY0s9tfAINVoboPIIx8mip0_s4LTAE7rOU_xOfgLtOnjVrZ_mQRsM6Q1b9doGvP3lhj087471ns_n04hdiy56bZvZ06j90kyamr_G0dCY6b3ZFjLLRLn99-ALZ8thqg</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>Kilmon, Michelle A.</creator><creator>Rutan, Jennifer A.</creator><creator>Clarke, Stephen H.</creator><creator>Vilen, Barbara J.</creator><scope>5PM</scope></search><sort><creationdate>20050701</creationdate><title>Cutting Edge: Low-Affinity, Smith Antigen-Specific B Cells Are Tolerized by Dendritic Cells and Macrophages1</title><author>Kilmon, Michelle A. ; Rutan, Jennifer A. ; Clarke, Stephen H. ; Vilen, Barbara J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_37244093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kilmon, Michelle A.</creatorcontrib><creatorcontrib>Rutan, Jennifer A.</creatorcontrib><creatorcontrib>Clarke, Stephen H.</creatorcontrib><creatorcontrib>Vilen, Barbara J.</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>Kilmon, Michelle A.</au><au>Rutan, Jennifer A.</au><au>Clarke, Stephen H.</au><au>Vilen, Barbara J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cutting Edge: Low-Affinity, Smith Antigen-Specific B Cells Are Tolerized by Dendritic Cells and Macrophages1</atitle><jtitle>The Journal of immunology (1950)</jtitle><date>2005-07-01</date><risdate>2005</risdate><volume>175</volume><issue>1</issue><spage>37</spage><epage>41</epage><pages>37-41</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Polyclonal B cell activation promotes immunity without the loss of tolerance. Our data show that during activation of the innate immune system, B cell tolerance to Smith Ag Sm is maintained by dendritic cells (DCs) and macrophages (
M
Φ
). TLR4-activated myeloid DCs and
M
Φ
, but not plasmacytoid or lymphoid DCs, repressed autoreactive B cells through the secretion of soluble mediators, including IL-6. Although IL-6 promotes plasma cell differentiation of B cells acutely stimulated by Ag, we show that it repressed cells that were chronically exposed to self-Ag. This mechanism of tolerance was not limited to Smith Ag-specific B cells as hen egg lysozyme-and p-azophenylarsonate-specific B cells were similarly affected. Our data define a tolerogenic role for
M
Φ
and DCs in regulating autoreactive B cells during activation of the innate immune system.</abstract><pmid>15972629</pmid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-1767 |
| ispartof | The Journal of immunology (1950), 2005-07, Vol.175 (1), p.37-41 |
| issn | 0022-1767 1550-6606 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3724409 |
| source | EZB Electronic Journals Library |
| title | Cutting Edge: Low-Affinity, Smith Antigen-Specific B Cells Are Tolerized by Dendritic Cells and Macrophages1 |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-27T03%3A08%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmedcentral&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cutting%20Edge:%20Low-Affinity,%20Smith%20Antigen-Specific%20B%20Cells%20Are%20Tolerized%20by%20Dendritic%20Cells%20and%20Macrophages1&rft.jtitle=The%20Journal%20of%20immunology%20(1950)&rft.au=Kilmon,%20Michelle%20A.&rft.date=2005-07-01&rft.volume=175&rft.issue=1&rft.spage=37&rft.epage=41&rft.pages=37-41&rft.issn=0022-1767&rft.eissn=1550-6606&rft_id=info:doi/&rft_dat=%3Cpubmedcentral%3Epubmedcentral_primary_oai_pubmedcentral_nih_gov_3724409%3C/pubmedcentral%3E%3Cgrp_id%3Ecdi_FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_37244093%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_id=info:pmid/15972629&rfr_iscdi=true |