Langerhans-cell histiocytosis 'insight into DC biology'

Jon D. Laman; Pieter J.M. Leenen; Nicola E. Annels; Pancras C.W. Hogendoorn; R. Maarten Egeler

doi:10.1016/S1471-4906(03)00063-2

Langerhans-cell histiocytosis 'insight into DC biology'

Jon D. Laman
, Pieter J.M. Leenen
, Nicola E. Annels
, Pancras C.W. Hogendoorn
, R. Maarten Egeler^*

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

145 Citations (Scopus)

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Abstract

Langerhans-cell histiocytosis (LCH) is caused by an uncontrolled pathogenic clonal proliferation of dendritic cells (DCs) with Langerhans-cell (LC) characteristics. LCH cells are arrested in an immature, partially activated stage and show a deviant regulation of cell division. Their aberrant interactions with T cells and the lesional microenvironment are typified by high level production of diverse cytokines. Chemokine and chemokine receptor patterns probably explain LCH predilection sites and lesion composition, reminiscent of chronic granulomatous inflammation. Recent advances in LCH immunology suggest that clonal changes in DCs might underlie the aberrant immune interaction with T cells, leading to a unique pathological picture, which combines features of carcinogenesis and chronic inflammation.

Original language	English
Pages (from-to)	190-196
Number of pages	7
Journal	Trends in Immunology
Volume	24
Issue number	4
DOIs	https://doi.org/10.1016/S1471-4906(03)00063-2
Publication status	Published - 1-Apr-2003
Externally published	Yes

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@article{cfa93e5ee17a4377a7e5b803dc8b1b1e,

title = "Langerhans-cell histiocytosis 'insight into DC biology'",

abstract = "Langerhans-cell histiocytosis (LCH) is caused by an uncontrolled pathogenic clonal proliferation of dendritic cells (DCs) with Langerhans-cell (LC) characteristics. LCH cells are arrested in an immature, partially activated stage and show a deviant regulation of cell division. Their aberrant interactions with T cells and the lesional microenvironment are typified by high level production of diverse cytokines. Chemokine and chemokine receptor patterns probably explain LCH predilection sites and lesion composition, reminiscent of chronic granulomatous inflammation. Recent advances in LCH immunology suggest that clonal changes in DCs might underlie the aberrant immune interaction with T cells, leading to a unique pathological picture, which combines features of carcinogenesis and chronic inflammation.",

author = "Laman, \{Jon D.\} and Leenen, \{Pieter J.M.\} and Annels, \{Nicola E.\} and Hogendoorn, \{Pancras C.W.\} and Egeler, \{R. Maarten\}",

note = "Funding Information: This article is dedicated to Elizabeth and Paul Kontoyannis, whose longstanding support, including the yearly Nikolas Symposium on LCH in Athens, Greece, is a driving stimulus in this field. This work was supported by the Histiocytosis Association of America and the Stichting LCH in The Netherlands. We thank Errol Prens for critical reading of the manuscript, and colleagues at the Nikolas Symposium for intense discussions and valuable suggestions and apologize to those whose studies were not cited because of space constraints.",

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doi = "10.1016/S1471-4906(03)00063-2",

language = "English",

volume = "24",

pages = "190--196",

journal = "Trends in Immunology",

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T1 - Langerhans-cell histiocytosis 'insight into DC biology'

AU - Laman, Jon D.

AU - Leenen, Pieter J.M.

AU - Annels, Nicola E.

AU - Hogendoorn, Pancras C.W.

AU - Egeler, R. Maarten

N1 - Funding Information: This article is dedicated to Elizabeth and Paul Kontoyannis, whose longstanding support, including the yearly Nikolas Symposium on LCH in Athens, Greece, is a driving stimulus in this field. This work was supported by the Histiocytosis Association of America and the Stichting LCH in The Netherlands. We thank Errol Prens for critical reading of the manuscript, and colleagues at the Nikolas Symposium for intense discussions and valuable suggestions and apologize to those whose studies were not cited because of space constraints.

PY - 2003/4/1

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N2 - Langerhans-cell histiocytosis (LCH) is caused by an uncontrolled pathogenic clonal proliferation of dendritic cells (DCs) with Langerhans-cell (LC) characteristics. LCH cells are arrested in an immature, partially activated stage and show a deviant regulation of cell division. Their aberrant interactions with T cells and the lesional microenvironment are typified by high level production of diverse cytokines. Chemokine and chemokine receptor patterns probably explain LCH predilection sites and lesion composition, reminiscent of chronic granulomatous inflammation. Recent advances in LCH immunology suggest that clonal changes in DCs might underlie the aberrant immune interaction with T cells, leading to a unique pathological picture, which combines features of carcinogenesis and chronic inflammation.

AB - Langerhans-cell histiocytosis (LCH) is caused by an uncontrolled pathogenic clonal proliferation of dendritic cells (DCs) with Langerhans-cell (LC) characteristics. LCH cells are arrested in an immature, partially activated stage and show a deviant regulation of cell division. Their aberrant interactions with T cells and the lesional microenvironment are typified by high level production of diverse cytokines. Chemokine and chemokine receptor patterns probably explain LCH predilection sites and lesion composition, reminiscent of chronic granulomatous inflammation. Recent advances in LCH immunology suggest that clonal changes in DCs might underlie the aberrant immune interaction with T cells, leading to a unique pathological picture, which combines features of carcinogenesis and chronic inflammation.

U2 - 10.1016/S1471-4906(03)00063-2

DO - 10.1016/S1471-4906(03)00063-2

M3 - Review article

C2 - 12697451

AN - SCOPUS:0037385291

SN - 1471-4906

VL - 24

SP - 190

EP - 196

JO - Trends in Immunology

JF - Trends in Immunology

IS - 4

ER -

Langerhans-cell histiocytosis 'insight into DC biology'

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