CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.
Identifieur interne : 001E46 ( PubMed/Corpus ); précédent : 001E45; suivant : 001E47CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.
Auteurs : Jamie C. Zampell ; Alan Yan ; Sonia Elhadad ; Tomer Avraham ; Evan Weitman ; Babak J. MehraraSource :
- PloS one [ 1932-6203 ] ; 2012.
English descriptors
- KwdEn :
- Adaptive Immunity, Animals, CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (metabolism), CD8-Positive T-Lymphocytes (cytology), CD8-Positive T-Lymphocytes (immunology), Fibrosis (immunology), Fibrosis (pathology), Flow Cytometry, Humans, Inflammation (immunology), Inflammation (pathology), Interleukin-2 Receptor alpha Subunit, Lymph Nodes (pathology), Lymph Nodes (surgery), Lymphangiogenesis (immunology), Lymphedema (immunology), Lymphedema (pathology), Mice, Single-Cell Analysis, T-Lymphocytes, Helper-Inducer (cytology), T-Lymphocytes, Helper-Inducer (immunology), Tail (immunology), Tail (pathology).
- MESH :
- chemical : Interleukin-2 Receptor alpha Subunit.
- cytology : CD8-Positive T-Lymphocytes, T-Lymphocytes, Helper-Inducer.
- immunology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Fibrosis, Inflammation, Lymphangiogenesis, Lymphedema, T-Lymphocytes, Helper-Inducer, Tail.
- metabolism : CD4-Positive T-Lymphocytes.
- pathology : Fibrosis, Inflammation, Lymph Nodes, Lymphedema, Tail.
- surgery : Lymph Nodes.
- Adaptive Immunity, Animals, Flow Cytometry, Humans, Mice, Single-Cell Analysis.
Abstract
Lymphedema is a chronic disorder that occurs commonly after lymph node removal for cancer treatment and is characterized by swelling, fibrosis, inflammation, and adipose deposition. Although previous histological studies have investigated inflammatory changes that occur in lymphedema, the precise cellular make up of the inflammatory infiltrate remains unknown. It is also unclear if this inflammatory response plays a causal role in the pathology of lymphedema. The purpose of this study was therefore to characterize the inflammatory response to lymphatic stasis and determine if these responses are necessary for the pathological changes that occur in lymphedema.
DOI: 10.1371/journal.pone.0049940
PubMed: 23185491
Links to Exploration step
pubmed:23185491Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.</title><author><name sortKey="Zampell, Jamie C" sort="Zampell, Jamie C" uniqKey="Zampell J" first="Jamie C" last="Zampell">Jamie C. Zampell</name><affiliation><nlm:affiliation>The Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Yan, Alan" sort="Yan, Alan" uniqKey="Yan A" first="Alan" last="Yan">Alan Yan</name></author><author><name sortKey="Elhadad, Sonia" sort="Elhadad, Sonia" uniqKey="Elhadad S" first="Sonia" last="Elhadad">Sonia Elhadad</name></author><author><name sortKey="Avraham, Tomer" sort="Avraham, Tomer" uniqKey="Avraham T" first="Tomer" last="Avraham">Tomer Avraham</name></author><author><name sortKey="Weitman, Evan" sort="Weitman, Evan" uniqKey="Weitman E" first="Evan" last="Weitman">Evan Weitman</name></author><author><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J" last="Mehrara">Babak J. Mehrara</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:23185491</idno><idno type="pmid">23185491</idno><idno type="doi">10.1371/journal.pone.0049940</idno><idno type="wicri:Area/PubMed/Corpus">001E46</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001E46</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.</title><author><name sortKey="Zampell, Jamie C" sort="Zampell, Jamie C" uniqKey="Zampell J" first="Jamie C" last="Zampell">Jamie C. Zampell</name><affiliation><nlm:affiliation>The Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Yan, Alan" sort="Yan, Alan" uniqKey="Yan A" first="Alan" last="Yan">Alan Yan</name></author><author><name sortKey="Elhadad, Sonia" sort="Elhadad, Sonia" uniqKey="Elhadad S" first="Sonia" last="Elhadad">Sonia Elhadad</name></author><author><name sortKey="Avraham, Tomer" sort="Avraham, Tomer" uniqKey="Avraham T" first="Tomer" last="Avraham">Tomer Avraham</name></author><author><name sortKey="Weitman, Evan" sort="Weitman, Evan" uniqKey="Weitman E" first="Evan" last="Weitman">Evan Weitman</name></author><author><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J" last="Mehrara">Babak J. Mehrara</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptive Immunity</term><term>Animals</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>CD4-Positive T-Lymphocytes (metabolism)</term><term>CD8-Positive T-Lymphocytes (cytology)</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>Fibrosis (immunology)</term><term>Fibrosis (pathology)</term><term>Flow Cytometry</term><term>Humans</term><term>Inflammation (immunology)</term><term>Inflammation (pathology)</term><term>Interleukin-2 Receptor alpha Subunit</term><term>Lymph Nodes (pathology)</term><term>Lymph Nodes (surgery)</term><term>Lymphangiogenesis (immunology)</term><term>Lymphedema (immunology)</term><term>Lymphedema (pathology)</term><term>Mice</term><term>Single-Cell Analysis</term><term>T-Lymphocytes, Helper-Inducer (cytology)</term><term>T-Lymphocytes, Helper-Inducer (immunology)</term><term>Tail (immunology)</term><term>Tail (pathology)</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Interleukin-2 Receptor alpha Subunit</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term><term>T-Lymphocytes, Helper-Inducer</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>CD8-Positive T-Lymphocytes</term><term>Fibrosis</term><term>Inflammation</term><term>Lymphangiogenesis</term><term>Lymphedema</term><term>T-Lymphocytes, Helper-Inducer</term><term>Tail</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Fibrosis</term><term>Inflammation</term><term>Lymph Nodes</term><term>Lymphedema</term><term>Tail</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Lymph Nodes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adaptive Immunity</term><term>Animals</term><term>Flow Cytometry</term><term>Humans</term><term>Mice</term><term>Single-Cell Analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphedema is a chronic disorder that occurs commonly after lymph node removal for cancer treatment and is characterized by swelling, fibrosis, inflammation, and adipose deposition. Although previous histological studies have investigated inflammatory changes that occur in lymphedema, the precise cellular make up of the inflammatory infiltrate remains unknown. It is also unclear if this inflammatory response plays a causal role in the pathology of lymphedema. The purpose of this study was therefore to characterize the inflammatory response to lymphatic stasis and determine if these responses are necessary for the pathological changes that occur in lymphedema.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23185491</PMID><DateCreated><Year>2012</Year><Month>11</Month><Day>27</Day></DateCreated><DateCompleted><Year>2013</Year><Month>05</Month><Day>30</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>11</Issue><PubDate><Year>2012</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.</ArticleTitle><Pagination><MedlinePgn>e49940</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0049940</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Lymphedema is a chronic disorder that occurs commonly after lymph node removal for cancer treatment and is characterized by swelling, fibrosis, inflammation, and adipose deposition. Although previous histological studies have investigated inflammatory changes that occur in lymphedema, the precise cellular make up of the inflammatory infiltrate remains unknown. It is also unclear if this inflammatory response plays a causal role in the pathology of lymphedema. The purpose of this study was therefore to characterize the inflammatory response to lymphatic stasis and determine if these responses are necessary for the pathological changes that occur in lymphedema.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">We used mouse-tail lymphedema and axillary lymph node dissection (ANLD) models in order to study tissue inflammatory changes. Single cell suspensions were created and analyzed using multi-color flow cytometry to identify individual cell types. We utilized antibody depletion techniques to analyze the causal role of CD4+, CD8+, and CD25+ cells in the regulation of inflammation, fibrosis, adipose deposition, and lymphangiogenesis.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Lymphedema in the mouse-tail resulted in a mixed inflammatory cell response with significant increases in T-helper, T-regulatory, neutrophils, macrophages, and dendritic cell populations. Interestingly, we found that ALND resulted in significant increases in T-helper cells suggesting that these adaptive immune responses precede changes in macrophage and dendritic cell infiltration. In support of this we found that depletion of CD4+, but not CD8 or CD25+ cells, significantly decreased tail lymphedema, inflammation, fibrosis, and adipose deposition. In addition, depletion of CD4+ cells significantly increased lymphangiogenesis both in our tail model and also in an inflammatory lymphangiogenesis model.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Lymphedema and lymphatic stasis result in CD4+ cell inflammation and infiltration of mature T-helper cells. Loss of CD4+ but not CD8+ or CD25+ cell inflammation markedly decreases the pathological changes associated with lymphedema. In addition, CD4+ cells regulate lymphangiogenesis during wound repair and inflammatory lymphangiogenesis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zampell</LastName><ForeName>Jamie C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>The Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Alan</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Elhadad</LastName><ForeName>Sonia</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Avraham</LastName><ForeName>Tomer</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Weitman</LastName><ForeName>Evan</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Mehrara</LastName><ForeName>Babak J</ForeName><Initials>BJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL111130</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01HL111130</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>11</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053645">Interleukin-2 Receptor alpha Subunit</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Arthritis Rheum. 2003 May;48(5):1452-60</RefSource><PMID Version="1">12746920</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lymphology. 1978 Dec;11(4):174-80</RefSource><PMID Version="1">739790</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lymphology. 1986 Dec;19(4):139-45</RefSource><PMID Version="1">2951567</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lymphology. 1990 Mar;23(1):23-33</RefSource><PMID Version="1">2352440</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lymphology. 1992 Dec;25(4):166-71</RefSource><PMID Version="1">1284085</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trop Med Parasitol. 1993 Mar;44(1):40-4</RefSource><PMID Version="1">8516632</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer. 1998 Dec 15;83(12 Suppl American):2776-81</RefSource><PMID Version="1">9874397</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Surg. 1965 Sep;110:394-7</RefSource><PMID Version="1">14337995</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lymphat Res Biol. 2003;1(3):235-43</RefSource><PMID Version="1">15624440</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Microvasc Res. 2006 Nov;72(3):161-71</RefSource><PMID Version="1">16876204</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS Med. 2006 Jul;3(7):e254</RefSource><PMID Version="1">16834456</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Pathol. 2008 Jan;214(2):199-210</RefSource><PMID Version="1">18161745</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann N Y Acad Sci. 2008;1131:147-54</RefSource><PMID Version="1">18519968</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Oncol. 2008 Jul 20;26(21):3536-42</RefSource><PMID Version="1">18640935</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Heart Circ Physiol. 2008 Nov;295(5):H2113-27</RefSource><PMID Version="1">18849330</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Plast Reconstr Surg. 2009 Aug;124(2):438-50</RefSource><PMID Version="1">19644258</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Med. 2009 Aug;15(8):921-9</RefSource><PMID Version="1">19633657</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2009 Oct;175(4):1733-45</RefSource><PMID Version="1">19762711</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2009;4(12):e8380</RefSource><PMID Version="1">20027220</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Cell Physiol. 2010 Sep;299(3):C589-605</RefSource><PMID Version="1">20519446</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer. 2010 Nov 15;116(22):5138-49</RefSource><PMID Version="1">20665892</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2010;5(11):e15404</RefSource><PMID Version="1">21072213</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2010 Dec;177(6):3202-14</RefSource><PMID Version="1">21056998</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2010 Dec;24(12):4877-88</RefSource><PMID Version="1">20720160</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Immunity. 2011 Jan 28;34(1):96-107</RefSource><PMID Version="1">21256057</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Cell Physiol. 2011 May;300(5):C1107-21</RefSource><PMID Version="1">21248077</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Cell Physiol. 2012 Jan 15;302(2):C392-404</RefSource><PMID Version="1">21940662</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2012 Mar;26(3):1027-39</RefSource><PMID Version="1">22067482</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Plast Reconstr Surg. 2012 Apr;129(4):825-34</RefSource><PMID Version="1">22456354</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Immunol Cell Biol. 2012 Sep;90(8):755-62</RefSource><PMID Version="1">22231651</PMID></CommentsCorrections><CommentsCorrections RefType="ErratumIn"><RefSource>PLoS One. 2013;8(5). doi:10.1371/annotation/158f757f-7d51-40b8-a3a4-550811bf0267</RefSource></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D056704" MajorTopicYN="Y">Adaptive Immunity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015496" MajorTopicYN="Y">CD4-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005355" MajorTopicYN="N">Fibrosis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="Y">Inflammation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053645" MajorTopicYN="N">Interleukin-2 Receptor alpha Subunit</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008198" MajorTopicYN="N">Lymph Nodes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000601" MajorTopicYN="Y">surgery</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="Y">Lymphedema</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059010" MajorTopicYN="N">Single-Cell Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006377" MajorTopicYN="N">T-Lymphocytes, Helper-Inducer</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013623" MajorTopicYN="N">Tail</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3502174</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>07</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>10</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>11</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>11</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>6</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23185491</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0049940</ArticleId><ArticleId IdType="pii">PONE-D-12-22076</ArticleId><ArticleId IdType="pmc">PMC3502174</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001E46 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 001E46 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= LymphedemaV1
|flux= PubMed
|étape= Corpus
|type= RBID
|clé= pubmed:23185491
|texte= CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:23185491" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a LymphedemaV1
| This area was generated with Dilib version V0.6.31. |  |