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Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis
Langerhans cell histiocytosis (LCH) is characterized by a clonal proliferation and retention of cells with a Langerhans cell (LC)-like phenotype at various sites within the body. The present study set out to elucidate whether aberrant expression of chemokine receptors or dysregulation of chemokine p...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2003
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193776/ https://www.ncbi.nlm.nih.gov/pubmed/12743170 http://dx.doi.org/10.1084/jem.20030137 |
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author | Annels, Nicola E. da Costa, Cristiana E.T. Prins, Frans A. Willemze, Annemieke Hogendoorn, Pancras C.W. Egeler, R. Maarten |
author_facet | Annels, Nicola E. da Costa, Cristiana E.T. Prins, Frans A. Willemze, Annemieke Hogendoorn, Pancras C.W. Egeler, R. Maarten |
author_sort | Annels, Nicola E. |
collection | PubMed |
description | Langerhans cell histiocytosis (LCH) is characterized by a clonal proliferation and retention of cells with a Langerhans cell (LC)-like phenotype at various sites within the body. The present study set out to elucidate whether aberrant expression of chemokine receptors or dysregulation of chemokine production in LCH lesions could explain abnormal retention of these cells. Immunohistochemical analysis on 13 LCH biopsies of bone, skin, and lymph node all expressed the immature dendritic cell (DC) marker CCR6 on the lesional LCs and absence of the mature DC marker CCR7. Furthermore, regardless of the tissue site, LCH lesions markedly overexpressed CCL20/MIP-3α, the ligand for CCR6. The lesional LCs appeared to be the source of this CCL20/MIP-3α production as well as other inflammatory chemokines such as CCL5/RANTES and CXCL11/I-TAC. These may explain the recruitment of eosinophils and CD4(+)CD45RO(+) T cells commonly found in LCH lesions. The findings of this study emphasize that, despite abundant TNF-α, lesional LCs remain in an immature state and are induced to produce chemokines, which via autocrine and paracrine mechanisms cause not only the retention of the lesional LCs but also the recruitment and retention of other lesional cells. We postulate that the lesional LCs themselves control the persistence and progression of LCH. |
format | Text |
id | pubmed-2193776 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21937762008-04-11 Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis Annels, Nicola E. da Costa, Cristiana E.T. Prins, Frans A. Willemze, Annemieke Hogendoorn, Pancras C.W. Egeler, R. Maarten J Exp Med Brief Definitive Report Langerhans cell histiocytosis (LCH) is characterized by a clonal proliferation and retention of cells with a Langerhans cell (LC)-like phenotype at various sites within the body. The present study set out to elucidate whether aberrant expression of chemokine receptors or dysregulation of chemokine production in LCH lesions could explain abnormal retention of these cells. Immunohistochemical analysis on 13 LCH biopsies of bone, skin, and lymph node all expressed the immature dendritic cell (DC) marker CCR6 on the lesional LCs and absence of the mature DC marker CCR7. Furthermore, regardless of the tissue site, LCH lesions markedly overexpressed CCL20/MIP-3α, the ligand for CCR6. The lesional LCs appeared to be the source of this CCL20/MIP-3α production as well as other inflammatory chemokines such as CCL5/RANTES and CXCL11/I-TAC. These may explain the recruitment of eosinophils and CD4(+)CD45RO(+) T cells commonly found in LCH lesions. The findings of this study emphasize that, despite abundant TNF-α, lesional LCs remain in an immature state and are induced to produce chemokines, which via autocrine and paracrine mechanisms cause not only the retention of the lesional LCs but also the recruitment and retention of other lesional cells. We postulate that the lesional LCs themselves control the persistence and progression of LCH. The Rockefeller University Press 2003-05-19 /pmc/articles/PMC2193776/ /pubmed/12743170 http://dx.doi.org/10.1084/jem.20030137 Text en Copyright © 2003, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Brief Definitive Report Annels, Nicola E. da Costa, Cristiana E.T. Prins, Frans A. Willemze, Annemieke Hogendoorn, Pancras C.W. Egeler, R. Maarten Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis |
title | Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis |
title_full | Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis |
title_fullStr | Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis |
title_full_unstemmed | Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis |
title_short | Aberrant Chemokine Receptor Expression and Chemokine Production by Langerhans Cells Underlies the Pathogenesis of Langerhans Cell Histiocytosis |
title_sort | aberrant chemokine receptor expression and chemokine production by langerhans cells underlies the pathogenesis of langerhans cell histiocytosis |
topic | Brief Definitive Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193776/ https://www.ncbi.nlm.nih.gov/pubmed/12743170 http://dx.doi.org/10.1084/jem.20030137 |
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