$node = stdClass Object (
[nid] => [16429]
[vid] => [16507]
[type] => [biblio]
[status] => [1]
[created] => [1226181129]
[changed] => [1226183513]
[comment] => [2]
[promote] => [1]
[sticky] => [0]
[revision_timestamp] => [1226183513]
[title] => [Conserved T cell receptor alpha-chain induces insulin autoantibodies.]
[body] => [<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rfr_id=info%3Asid%2Fwww.diabetescenters.org&rft.genre=article&rft.atitle=Conserved+T+cell+receptor+alpha-chain+induces+insulin+autoantibodies.&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.date=2008&rft.volume=105&rft.aulast=Kobayashi+M&rft.aufirst=Jasinski+Liu+Li+Miao+Zhang+Yu+Nakayama+Eisenbarth+GS&rft_id=http%3A%2F%2Fhwmaint.pnas.org%2Fcgi%2Fpmidlookup%3Fview%3Dlong%26pmid%3D18626021"></span><div class="biblio_type"><h3>Publication Type:</h3> Journal Article</div>
<div class="biblio_authors"><h3>Authors:</h3> <a href="/biblio/author/Kobayashi+M">Kobayashi M , Jasinski J , Liu E , Li M , Miao D , Zhang L , Yu L , Nakayama M , Eisenbarth GS ,</a></div>
<div class="biblio_source"><h3>Source: </h3> Proceedings of the National Academy of Sciences of the United States of America, Volume 105, p.10090-4 (2008)</div>
<h3>URL:</h3><a href="http://hwmaint.pnas.org/cgi/pmidlookup?view=long&pmid=18626021">http://hwmaint.pnas.org/cgi/pmidlookup?view=long&pmid=18626021</a>
<h3>Abstract:</h3> <p>A fundamental question is what are the molecular determinants that lead to spontaneous preferential targeting of specific autoantigens in autoimmune diseases, such as the insulin B:9-23 peptide sequence in type 1 diabetes. Anti-insulin B:9-23 T cell clones isolated from prediabetic NOD islets have a conserved Valpha-segment/Jalpha-segment, but no conservation of the alpha-chain N region and no conservation of the Vbeta-chain. Here, we show that the conserved T cell receptor alpha-chain generates insulin autoantibodies when transgenically or retrogenically introduced into mice without its corresponding Vbeta. We suggest that a major part of the mystery as to why islet autoimmunity develops relates to recognition of a primary insulin peptide by a conserved alpha chain T cell receptor.</p>
]
[log] => []
[format] => [1]
[uid] => [1]
[name] => [admin]
[picture] => []
[data] => [a:0:{}]
[biblio_type] => [102]
[biblio_number] => []
[biblio_section] => []
[biblio_other_number] => []
[biblio_secondary_title] => [Proceedings of the National Academy of Sciences of the United States of America]
[biblio_tertiary_title] => []
[biblio_short_title] => []
[biblio_alternate_title] => []
[biblio_translated_title] => []
[biblio_authors] => [Kobayashi M , Jasinski J , Liu E , Li M , Miao D , Zhang L , Yu L , Nakayama M , Eisenbarth GS ,]
[biblio_secondary_authors] => []
[biblio_tertiary_authors] => []
[biblio_corp_author] => []
[biblio_other_author_affiliations] => []
[biblio_edition] => []
[biblio_publisher] => []
[biblio_original_publication] => []
[biblio_reprint_edition] => []
[biblio_place_published] => []
[biblio_year] => [2008]
[biblio_volume] => [105]
[biblio_number_of_volumes] => []
[biblio_pages] => [10090-4]
[biblio_date] => []
[biblio_isbn] => []
[biblio_issn] => []
[biblio_lang] => [eng]
[biblio_abst_e] => [<p>A fundamental question is what are the molecular determinants that lead to spontaneous preferential targeting of specific autoantigens in autoimmune diseases, such as the insulin B:9-23 peptide sequence in type 1 diabetes. Anti-insulin B:9-23 T cell clones isolated from prediabetic NOD islets have a conserved Valpha-segment/Jalpha-segment, but no conservation of the alpha-chain N region and no conservation of the Vbeta-chain. Here, we show that the conserved T cell receptor alpha-chain generates insulin autoantibodies when transgenically or retrogenically introduced into mice without its corresponding Vbeta. We suggest that a major part of the mystery as to why islet autoimmunity develops relates to recognition of a primary insulin peptide by a conserved alpha chain T cell receptor.</p>]
[biblio_abst_f] => []
[biblio_full_text] => [0]
[biblio_keywords] => []
[biblio_url] => [http://hwmaint.pnas.org/cgi/pmidlookup?view=long&pmid=18626021]
[biblio_doi] => []
[biblio_issue] => []
[biblio_type_of_work] => []
[biblio_accession_number] => []
[biblio_call_number] => []
[biblio_notes] => []
[biblio_coins] => [<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rfr_id=info%3Asid%2Fwww.diabetescenters.org&rft.genre=article&rft.atitle=Conserved+T+cell+receptor+alpha-chain+induces+insulin+autoantibodies.&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.date=2008&rft.volume=105&rft.aulast=Kobayashi+M&rft.aufirst=Jasinski+Liu+Li+Miao+Zhang+Yu+Nakayama+Eisenbarth+GS&rft_id=http%3A%2F%2Fhwmaint.pnas.org%2Fcgi%2Fpmidlookup%3Fview%3Dlong%26pmid%3D18626021"></span>]
[biblio_research_notes] => []
[biblio_custom1] => [http://www.ncbi.nlm.nih.gov/pubmed/18626021?dopt=Abstract]
[biblio_custom2] => [DK057516]
[biblio_custom3] => [18626021]
[biblio_custom4] => []
[biblio_custom5] => []
[biblio_custom6] => []
[biblio_custom7] => []
[biblio_auth_address] => []
[biblio_remote_db_name] => []
[biblio_remote_db_provider] => []
[biblio_citekey] => [18626021]
[biblio_label] => []
[biblio_access_date] => []
[biblio_type_name] => [Journal Article]
[path] => [biblio/conserved-t-cell-receptor-alpha-chain-induces-insulin-autoantibodies]
[nodewords] => []
[last_comment_timestamp] => [1226181131]
[last_comment_name] => []
[comment_count] => [0]
[taxonomy] => array (
[89] => stdClass (
[0] => [**Recursion Detected**]
)
)
[files] => []
[page_title] => []
[content] => array (
[body] => array (
[#value] => [<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rfr_id=info%3Asid%2Fwww.diabetescenters.org&rft.genre=article&rft.atitle=Conserved+T+cell+receptor+alpha-chain+induces+insulin+autoantibodies.&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.date=2008&rft.volume=105&rft.aulast=Kobayashi+M&rft.aufirst=Jasinski+Liu+Li+Miao+Zhang+Yu+Nakayama+Eisenbarth+GS&rft_id=http%3A%2F%2Fhwmaint.pnas.org%2Fcgi%2Fpmidlookup%3Fview%3Dlong%26pmid%3D18626021"></span><div class="biblio_type"><h3>Publication Type:</h3> Journal Article</div>
<div class="biblio_authors"><h3>Authors:</h3> <a href="/biblio/author/Kobayashi+M">Kobayashi M , Jasinski J , Liu E , Li M , Miao D , Zhang L , Yu L , Nakayama M , Eisenbarth GS ,</a></div>
<div class="biblio_source"><h3>Source: </h3> Proceedings of the National Academy of Sciences of the United States of America, Volume 105, p.10090-4 (2008)</div>
<h3>URL:</h3><a href="http://hwmaint.pnas.org/cgi/pmidlookup?view=long&pmid=18626021">http://hwmaint.pnas.org/cgi/pmidlookup?view=long&pmid=18626021</a>
<h3>Abstract:</h3> <p>A fundamental question is what are the molecular determinants that lead to spontaneous preferential targeting of specific autoantigens in autoimmune diseases, such as the insulin B:9-23 peptide sequence in type 1 diabetes. Anti-insulin B:9-23 T cell clones isolated from prediabetic NOD islets have a conserved Valpha-segment/Jalpha-segment, but no conservation of the alpha-chain N region and no conservation of the Vbeta-chain. Here, we show that the conserved T cell receptor alpha-chain generates insulin autoantibodies when transgenically or retrogenically introduced into mice without its corresponding Vbeta. We suggest that a major part of the mystery as to why islet autoimmunity develops relates to recognition of a primary insulin peptide by a conserved alpha chain T cell receptor.</p>
]
[#printed] => [1]
)
[#children] => [<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rfr_id=info%3Asid%2Fwww.diabetescenters.org&rft.genre=article&rft.atitle=Conserved+T+cell+receptor+alpha-chain+induces+insulin+autoantibodies.&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.date=2008&rft.volume=105&rft.aulast=Kobayashi+M&rft.aufirst=Jasinski+Liu+Li+Miao+Zhang+Yu+Nakayama+Eisenbarth+GS&rft_id=http%3A%2F%2Fhwmaint.pnas.org%2Fcgi%2Fpmidlookup%3Fview%3Dlong%26pmid%3D18626021"></span><div class="biblio_type"><h3>Publication Type:</h3> Journal Article</div>
<div class="biblio_authors"><h3>Authors:</h3> <a href="/biblio/author/Kobayashi+M">Kobayashi M , Jasinski J , Liu E , Li M , Miao D , Zhang L , Yu L , Nakayama M , Eisenbarth GS ,</a></div>
<div class="biblio_source"><h3>Source: </h3> Proceedings of the National Academy of Sciences of the United States of America, Volume 105, p.10090-4 (2008)</div>
<h3>URL:</h3><a href="http://hwmaint.pnas.org/cgi/pmidlookup?view=long&pmid=18626021">http://hwmaint.pnas.org/cgi/pmidlookup?view=long&pmid=18626021</a>
<h3>Abstract:</h3> <p>A fundamental question is what are the molecular determinants that lead to spontaneous preferential targeting of specific autoantigens in autoimmune diseases, such as the insulin B:9-23 peptide sequence in type 1 diabetes. Anti-insulin B:9-23 T cell clones isolated from prediabetic NOD islets have a conserved Valpha-segment/Jalpha-segment, but no conservation of the alpha-chain N region and no conservation of the Vbeta-chain. Here, we show that the conserved T cell receptor alpha-chain generates insulin autoantibodies when transgenically or retrogenically introduced into mice without its corresponding Vbeta. We suggest that a major part of the mystery as to why islet autoimmunity develops relates to recognition of a primary insulin peptide by a conserved alpha chain T cell receptor.</p>
]
[#printed] => [1]
)
[links] => array (
[comment_forbidden] => array (
[title] => [<a href="/user/login?destination=comment/reply/16429%2523comment-form">Login</a> to post comments]
[html] => [1]
)
)
);
