Replenishing Regulatory T Cells to Halt Depigmentation in Vitiligo.
Identifieur interne : 000752 ( Main/Exploration ); précédent : 000751; suivant : 000753Replenishing Regulatory T Cells to Halt Depigmentation in Vitiligo.
Auteurs : I Caroline Le Poole [États-Unis] ; Shikhar Mehrotra [États-Unis]Source :
- The journal of investigative dermatology. Symposium proceedings [ 1529-1774 ] ; 2017.
Descripteurs français
- KwdFr :
- MESH :
- immunologie : Vitiligo.
- métabolisme : Chimiokine CCL22, Lymphocytes T régulateurs.
- thérapie : Vitiligo.
- transplantation : Animaux, Humains, Lymphocytes T régulateurs, Modèles animaux de maladie humaine, Souris, Transfert adoptif.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Chemokine CCL22.
- immunology : Vitiligo.
- metabolism : T-Lymphocytes, Regulatory.
- therapy : Vitiligo.
- transplantation : T-Lymphocytes, Regulatory.
- Adoptive Transfer, Animals, Disease Models, Animal, Humans, Mice.
Abstract
Vitiligo is a cutaneous autoimmune disease, especially devastating to patients with darker skin tones because of the contrast between unaffected and lesional skin. We studied immune cells infiltrating vitiligo skin and found very few regulatory T cells (Tregs). Vitiligo was not associated with a reduced frequency or function of circulating Tregs. To manipulate Treg function, we used mouse models expressing melanocyte-reactive TCRs, following changes in pelage color. We also isolated splenocytes to measure Treg function and evaluated cutaneous Treg abundance. Even small numbers of Tregs transferred into depigmenting mice could effectively interfere with depigmentation. The same holds true for treatment with rapamycin, readily translatable for use in human patients; such treatment may be well tolerated. Because vitiligo skin is relatively devoid of cells that produce the chemokine CCL22, whereas circulating Tregs express normal levels of its receptor CCR4, we overexpressed Ccl22 in the skin of vitiligo-prone mice to assess the resulting levels of depigmentation. Markedly reduced depigmentation was accompanied by Treg infiltration to the skin. With several options available to support a healthy balance between Tregs and effector T cells, the next challenge will be to render such treatment antigen specific and avoid general immunosuppression.
DOI: 10.1016/j.jisp.2016.10.023
PubMed: 28941492
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Replenishing Regulatory T Cells to Halt Depigmentation in Vitiligo.</title><author><name sortKey="Le Poole, I Caroline" sort="Le Poole, I Caroline" uniqKey="Le Poole I" first="I Caroline" last="Le Poole">I Caroline Le Poole</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology and Microbiology/Immunology, Oncology Research Institute, Loyola University, Chicago, Illinois, USA. Electronic address: ilepool@luc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Microbiology/Immunology, Oncology Research Institute, Loyola University, Chicago, Illinois</wicri:regionArea><placeName><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Mehrotra, Shikhar" sort="Mehrotra, Shikhar" uniqKey="Mehrotra S" first="Shikhar" last="Mehrotra">Shikhar Mehrotra</name><affiliation wicri:level="4"><nlm:affiliation>Department of Surgery, Medical University of South Carolina, Charleston, South Carolina, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery, Medical University of South Carolina, Charleston, South Carolina</wicri:regionArea><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28941492</idno><idno type="pmid">28941492</idno><idno type="doi">10.1016/j.jisp.2016.10.023</idno><idno type="wicri:Area/Main/Corpus">000721</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000721</idno><idno type="wicri:Area/Main/Curation">000721</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000721</idno><idno type="wicri:Area/Main/Exploration">000721</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Replenishing Regulatory T Cells to Halt Depigmentation in Vitiligo.</title><author><name sortKey="Le Poole, I Caroline" sort="Le Poole, I Caroline" uniqKey="Le Poole I" first="I Caroline" last="Le Poole">I Caroline Le Poole</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology and Microbiology/Immunology, Oncology Research Institute, Loyola University, Chicago, Illinois, USA. Electronic address: ilepool@luc.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology and Microbiology/Immunology, Oncology Research Institute, Loyola University, Chicago, Illinois</wicri:regionArea><placeName><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Mehrotra, Shikhar" sort="Mehrotra, Shikhar" uniqKey="Mehrotra S" first="Shikhar" last="Mehrotra">Shikhar Mehrotra</name><affiliation wicri:level="4"><nlm:affiliation>Department of Surgery, Medical University of South Carolina, Charleston, South Carolina, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Surgery, Medical University of South Carolina, Charleston, South Carolina</wicri:regionArea><placeName><region type="state">Caroline du Sud</region><settlement type="city">Columbia (Caroline du Sud)</settlement></placeName><orgName type="university">Université de Caroline du Sud</orgName></affiliation></author></analytic><series><title level="j">The journal of investigative dermatology. Symposium proceedings</title><idno type="eISSN">1529-1774</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adoptive Transfer (MeSH)</term><term>Animals (MeSH)</term><term>Chemokine CCL22 (metabolism)</term><term>Disease Models, Animal (MeSH)</term><term>Humans (MeSH)</term><term>Mice (MeSH)</term><term>T-Lymphocytes, Regulatory (metabolism)</term><term>T-Lymphocytes, Regulatory (transplantation)</term><term>Vitiligo (immunology)</term><term>Vitiligo (therapy)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Chimiokine CCL22 (métabolisme)</term><term>Humains (MeSH)</term><term>Lymphocytes T régulateurs (métabolisme)</term><term>Lymphocytes T régulateurs (transplantation)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Souris (MeSH)</term><term>Transfert adoptif (MeSH)</term><term>Vitiligo (immunologie)</term><term>Vitiligo (thérapie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Chemokine CCL22</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Vitiligo</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Vitiligo</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>T-Lymphocytes, Regulatory</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Chimiokine CCL22</term><term>Lymphocytes T régulateurs</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Vitiligo</term></keywords><keywords scheme="MESH" qualifier="thérapie" xml:lang="fr"><term>Vitiligo</term></keywords><keywords scheme="MESH" qualifier="transplantation" xml:lang="en"><term>T-Lymphocytes, Regulatory</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adoptive Transfer</term><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" qualifier="transplantation" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Lymphocytes T régulateurs</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Transfert adoptif</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vitiligo is a cutaneous autoimmune disease, especially devastating to patients with darker skin tones because of the contrast between unaffected and lesional skin. We studied immune cells infiltrating vitiligo skin and found very few regulatory T cells (Tregs). Vitiligo was not associated with a reduced frequency or function of circulating Tregs. To manipulate Treg function, we used mouse models expressing melanocyte-reactive TCRs, following changes in pelage color. We also isolated splenocytes to measure Treg function and evaluated cutaneous Treg abundance. Even small numbers of Tregs transferred into depigmenting mice could effectively interfere with depigmentation. The same holds true for treatment with rapamycin, readily translatable for use in human patients; such treatment may be well tolerated. Because vitiligo skin is relatively devoid of cells that produce the chemokine CCL22, whereas circulating Tregs express normal levels of its receptor CCR4, we overexpressed Ccl22 in the skin of vitiligo-prone mice to assess the resulting levels of depigmentation. Markedly reduced depigmentation was accompanied by Treg infiltration to the skin. With several options available to support a healthy balance between Tregs and effector T cells, the next challenge will be to render such treatment antigen specific and avoid general immunosuppression.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28941492</PMID><DateCompleted><Year>2018</Year><Month>06</Month><Day>05</Day></DateCompleted><DateRevised><Year>2018</Year><Month>06</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1529-1774</ISSN><JournalIssue CitedMedium="Internet"><Volume>18</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>10</Month></PubDate></JournalIssue><Title>The journal of investigative dermatology. Symposium proceedings</Title><ISOAbbreviation>J Investig Dermatol Symp Proc</ISOAbbreviation></Journal><ArticleTitle>Replenishing Regulatory T Cells to Halt Depigmentation in Vitiligo.</ArticleTitle><Pagination><MedlinePgn>S38-S45</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1087-0024(16)30074-0</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jisp.2016.10.023</ELocationID><Abstract><AbstractText>Vitiligo is a cutaneous autoimmune disease, especially devastating to patients with darker skin tones because of the contrast between unaffected and lesional skin. We studied immune cells infiltrating vitiligo skin and found very few regulatory T cells (Tregs). Vitiligo was not associated with a reduced frequency or function of circulating Tregs. To manipulate Treg function, we used mouse models expressing melanocyte-reactive TCRs, following changes in pelage color. We also isolated splenocytes to measure Treg function and evaluated cutaneous Treg abundance. Even small numbers of Tregs transferred into depigmenting mice could effectively interfere with depigmentation. The same holds true for treatment with rapamycin, readily translatable for use in human patients; such treatment may be well tolerated. Because vitiligo skin is relatively devoid of cells that produce the chemokine CCL22, whereas circulating Tregs express normal levels of its receptor CCR4, we overexpressed Ccl22 in the skin of vitiligo-prone mice to assess the resulting levels of depigmentation. Markedly reduced depigmentation was accompanied by Treg infiltration to the skin. With several options available to support a healthy balance between Tregs and effector T cells, the next challenge will be to render such treatment antigen specific and avoid general immunosuppression.</AbstractText><CopyrightInformation>Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Le Poole</LastName><ForeName>I Caroline</ForeName><Initials>IC</Initials><AffiliationInfo><Affiliation>Department of Pathology and Microbiology/Immunology, Oncology Research Institute, Loyola University, Chicago, Illinois, USA. Electronic address: ilepool@luc.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mehrotra</LastName><ForeName>Shikhar</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Surgery, Medical University of South Carolina, Charleston, South Carolina, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AR057643</GrantID><Acronym>AR</Acronym><Agency>NIAMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Investig Dermatol Symp Proc</MedlineTA><NlmUniqueID>9609059</NlmUniqueID><ISSNLinking>1087-0024</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C515483">Ccl22 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054422">Chemokine CCL22</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D019264" MajorTopicYN="Y">Adoptive Transfer</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054422" MajorTopicYN="N">Chemokine CCL22</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050378" MajorTopicYN="Y">T-Lymphocytes, Regulatory</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000637" MajorTopicYN="N">transplantation</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014820" MajorTopicYN="N">Vitiligo</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>09</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>09</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>6</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28941492</ArticleId><ArticleId IdType="pii">S1087-0024(16)30074-0</ArticleId><ArticleId IdType="doi">10.1016/j.jisp.2016.10.023</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Caroline du Sud</li><li>Illinois</li></region><settlement><li>Columbia (Caroline du Sud)</li></settlement><orgName><li>Université de Caroline du Sud</li></orgName></list><tree><country name="États-Unis"><region name="Illinois"><name sortKey="Le Poole, I Caroline" sort="Le Poole, I Caroline" uniqKey="Le Poole I" first="I Caroline" last="Le Poole">I Caroline Le Poole</name></region><name sortKey="Mehrotra, Shikhar" sort="Mehrotra, Shikhar" uniqKey="Mehrotra S" first="Shikhar" last="Mehrotra">Shikhar Mehrotra</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/RapamycinFungusV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000752 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000752 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= RapamycinFungusV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:28941492
|texte= Replenishing Regulatory T Cells to Halt Depigmentation in Vitiligo.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:28941492" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a RapamycinFungusV1
| This area was generated with Dilib version V0.6.38. |  |