CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.
Identifieur interne : 001E46 ( PubMed/Curation ); précédent : 001E45; suivant : 001E47CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.
Auteurs : Jamie C. Zampell [États-Unis] ; Alan Yan ; Sonia Elhadad ; Tomer Avraham ; Evan Weitman ; Babak J. MehraraSource :
- PloS one [ 1932-6203 ] ; 2012.
Descripteurs français
- KwdFr :
- Analyse sur cellule unique, Animaux, Cytométrie en flux, Fibrose (anatomopathologie), Fibrose (immunologie), Humains, Immunité acquise, Inflammation (anatomopathologie), Inflammation (immunologie), Lymphangiogenèse (immunologie), Lymphocytes T CD4+ (immunologie), Lymphocytes T CD4+ (métabolisme), Lymphocytes T CD8+ (cytologie), Lymphocytes T CD8+ (immunologie), Lymphocytes T auxiliaires (cytologie), Lymphocytes T auxiliaires (immunologie), Lymphoedème (anatomopathologie), Lymphoedème (immunologie), Noeuds lymphatiques (), Noeuds lymphatiques (anatomopathologie), Queue (anatomopathologie), Queue (immunologie), Souris, Sous-unité alpha du récepteur à l'interleukine-2.
- MESH :
- anatomopathologie : Fibrose, Inflammation, Lymphoedème, Noeuds lymphatiques, Queue.
- cytologie : Lymphocytes T CD8+, Lymphocytes T auxiliaires.
- immunologie : Fibrose, Inflammation, Lymphangiogenèse, Lymphocytes T CD4+, Lymphocytes T CD8+, Lymphocytes T auxiliaires, Lymphoedème, Queue.
- métabolisme : Lymphocytes T CD4+.
- Analyse sur cellule unique, Animaux, Cytométrie en flux, Humains, Immunité acquise, Noeuds lymphatiques, Souris, Sous-unité alpha du récepteur à l'interleukine-2.
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
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pubmed:23185491Le document en format XML
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<term>CD8-Positive T-Lymphocytes (cytology)</term>
<term>CD8-Positive T-Lymphocytes (immunology)</term>
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<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>
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<term>Lymphedema (pathology)</term>
<term>Mice</term>
<term>Single-Cell Analysis</term>
<term>T-Lymphocytes, Helper-Inducer (cytology)</term>
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<term>Flow Cytometry</term>
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<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>
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<Issue>11</Issue>
<PubDate><Year>2012</Year>
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<Title>PloS one</Title>
<ISOAbbreviation>PLoS ONE</ISOAbbreviation>
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<ArticleTitle>CD4(+) cells regulate fibrosis and lymphangiogenesis in response to lymphatic fluid stasis.</ArticleTitle>
<Pagination><MedlinePgn>e49940</MedlinePgn>
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<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>
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<Author ValidYN="Y"><LastName>Yan</LastName>
<ForeName>Alan</ForeName>
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<Author ValidYN="Y"><LastName>Elhadad</LastName>
<ForeName>Sonia</ForeName>
<Initials>S</Initials>
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<Author ValidYN="Y"><LastName>Avraham</LastName>
<ForeName>Tomer</ForeName>
<Initials>T</Initials>
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<Author ValidYN="Y"><LastName>Weitman</LastName>
<ForeName>Evan</ForeName>
<Initials>E</Initials>
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<Author ValidYN="Y"><LastName>Mehrara</LastName>
<ForeName>Babak J</ForeName>
<Initials>BJ</Initials>
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<OtherID Source="NLM">PMC3502174</OtherID>
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