Specific roles for dendritic cell subsets during initiation and progression of psoriasis

Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the contribution of Langerhans cells (LCs) and plasmacytoid DCs (pDCs) in psoriasis. In human psoriatic lesions and in a psoriasis mouse model (DKO* mic...

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Published inEMBO molecular medicine Vol. 6; no. 10; pp. 1312 - 1327
Main Authors Glitzner, Elisabeth, Korosec, Ana, Brunner, Patrick M, Drobits, Barbara, Amberg, Nicole, Schonthaler, Helia B, Kopp, Tamara, Wagner, Erwin F, Stingl, Georg, Holcmann, Martin, Sibilia, Maria
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.10.2014
John Wiley & Sons, Inc
EMBO Press
BlackWell Publishing Ltd
Springer Nature
Subjects
Adjuvants, Immunologic - pharmacology
Aminoquinolines - pharmacology
Analysis
Animals
Antibodies, Monoclonal - immunology
Antibodies, Monoclonal - pharmacology
Antigen-Presenting Cells - immunology
Antigen-Presenting Cells - metabolism
AP‐1
Bone marrow
Bone Marrow Transplantation
Dendritic cells
Dendritic Cells - immunology
Dendritic Cells - metabolism
Development and progression
Disease Progression
EMBO19
EMBO38
Etiology
Experiments
Flow Cytometry
Humans
IL‐23
Inflammation
Interleukin-10 - immunology
Interleukin-10 - metabolism
Interleukin-23 - immunology
Interleukin-23 - metabolism
Langerhans cells
Langerhans Cells - immunology
Langerhans Cells - metabolism
Lymphocytes
Mice, Inbred C57BL
Mice, Knockout
Microscopy, Confocal
Patients
Phenotypes
plasmacytoid dendritic cells
Proto-Oncogene Proteins c-jun - deficiency
Proto-Oncogene Proteins c-jun - genetics
Proto-Oncogene Proteins c-jun - immunology
Psoriasis
Psoriasis - genetics
Psoriasis - immunology
Psoriasis - prevention & control
Receptors, Interleukin - immunology
Receptors, Interleukin - metabolism
Research Article
Roles
Signal Transduction - drug effects
Signal Transduction - immunology
Skin - drug effects
Skin - immunology
Skin - pathology
Transcription Factors - deficiency
Transcription Factors - genetics
Transcription Factors - immunology
Langerhans cells
IL‐23
AP‐1
plasmacytoid dendritic cells
psoriasis
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Abstract Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the contribution of Langerhans cells (LCs) and plasmacytoid DCs (pDCs) in psoriasis. In human psoriatic lesions and in a psoriasis mouse model (DKO* mice), LCs are severely reduced, whereas pDCs are increased. Depletion of pDCs in DKO* mice prior to psoriasis induction resulted in a milder phenotype, whereas depletion during active disease had no effect. In contrast, while depletion of Langerin‐expressing APCs before disease onset had no effect, depletion from diseased mice aggravated psoriasis symptoms. Disease aggravation was due to the absence of LCs, but not other Langerin‐expressing APCs. LCs derived from DKO* mice produced increased IL‐10 levels, suggesting an immunosuppressive function. Moreover, IL‐23 production was high in psoriatic mice and further increased in the absence of LCs. Conversely, pDC depletion resulted in reduced IL‐23 production, and therapeutic inhibition of IL‐23R signaling ameliorated disease symptoms. Therefore, LCs have an anti‐inflammatory role during active psoriatic disease, while pDCs exert an instigatory function during disease initiation. Synopsis Resident epidermal LCs, which are gradually lost from the epidermis in active disease phase psoriasis, are responsible for maintaining a suppressive skin environment by balancing the anti‐inflammatory IL‐10 and pro‐inflammatory IL‐23 axis. Langerhans cells (LCs) are severely reduced and plasmacytoid DCs (pDCs) are increased in human psoriasis as well as in mouse models of psoriasis Depletion of pDCs in mice prior to psoriasis induction results in disease amelioration whereas depletion during active disease has no effect Depletion of LCs during active psoriasis results in disease aggravation whereas depletion before disease initiation has no effect The anti‐inflammatory role of LCs is mediated by direct release of the immunosuppressive cytokine IL‐10 and by preventing excessive IL‐23 accumulation in the skin pDC depletion results in reduced IL‐23 levels and therapeutic inhibition of IL‐23 receptor ameliorates disease symptoms Graphical Abstract Resident epidermal LCs, which are gradually lost from the epidermis in active disease phase psoriasis, are responsible for maintaining a suppressive skin environment by balancing the anti‐inflammatory IL‐10 and pro‐inflammatory IL‐23 axis.
AbstractList Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the contribution of Langerhans cells (LCs) and plasmacytoid DCs (pDCs) in psoriasis. In human psoriatic lesions and in a psoriasis mouse model (DKO* mice), LCs are severely reduced, whereas pDCs are increased. Depletion of pDCs in DKO* mice prior to psoriasis induction resulted in a milder phenotype, whereas depletion during active disease had no effect. In contrast, while depletion of Langerin‐expressing APCs before disease onset had no effect, depletion from diseased mice aggravated psoriasis symptoms. Disease aggravation was due to the absence of LCs, but not other Langerin‐expressing APCs. LCs derived from DKO* mice produced increased IL‐10 levels, suggesting an immunosuppressive function. Moreover, IL‐23 production was high in psoriatic mice and further increased in the absence of LCs. Conversely, pDC depletion resulted in reduced IL‐23 production, and therapeutic inhibition of IL‐23R signaling ameliorated disease symptoms. Therefore, LCs have an anti‐inflammatory role during active psoriatic disease, while pDCs exert an instigatory function during disease initiation.
Abstract Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the contribution of Langerhans cells (LCs) and plasmacytoid DCs (pDCs) in psoriasis. In human psoriatic lesions and in a psoriasis mouse model (DKO* mice), LCs are severely reduced, whereas pDCs are increased. Depletion of pDCs in DKO* mice prior to psoriasis induction resulted in a milder phenotype, whereas depletion during active disease had no effect. In contrast, while depletion of Langerin‐expressing APCs before disease onset had no effect, depletion from diseased mice aggravated psoriasis symptoms. Disease aggravation was due to the absence of LCs, but not other Langerin‐expressing APCs. LCs derived from DKO* mice produced increased IL‐10 levels, suggesting an immunosuppressive function. Moreover, IL‐23 production was high in psoriatic mice and further increased in the absence of LCs. Conversely, pDC depletion resulted in reduced IL‐23 production, and therapeutic inhibition of IL‐23R signaling ameliorated disease symptoms. Therefore, LCs have an anti‐inflammatory role during active psoriatic disease, while pDCs exert an instigatory function during disease initiation.
Abstract Several subtypes of APC s are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the contribution of Langerhans cells ( LC s) and plasmacytoid DC s ( pDC s) in psoriasis. In human psoriatic lesions and in a psoriasis mouse model ( DKO * mice), LCs are severely reduced, whereas pDC s are increased. Depletion of pDC s in DKO * mice prior to psoriasis induction resulted in a milder phenotype, whereas depletion during active disease had no effect. In contrast, while depletion of Langerin‐expressing APC s before disease onset had no effect, depletion from diseased mice aggravated psoriasis symptoms. Disease aggravation was due to the absence of LC s, but not other Langerin‐expressing APC s. LC s derived from DKO * mice produced increased IL ‐10 levels, suggesting an immunosuppressive function. Moreover, IL ‐23 production was high in psoriatic mice and further increased in the absence of LC s. Conversely, pDC depletion resulted in reduced IL ‐23 production, and therapeutic inhibition of IL ‐23R signaling ameliorated disease symptoms. Therefore, LC s have an anti‐inflammatory role during active psoriatic disease, while pDC s exert an instigatory function during disease initiation. Synopsis image Resident epidermal LC s, which are gradually lost from the epidermis in active disease phase psoriasis, are responsible for maintaining a suppressive skin environment by balancing the anti‐inflammatory IL ‐10 and pro‐inflammatory IL ‐23 axis. Langerhans cells ( LC s) are severely reduced and plasmacytoid DCs ( pDC s) are increased in human psoriasis as well as in mouse models of psoriasis Depletion of pDC s in mice prior to psoriasis induction results in disease amelioration whereas depletion during active disease has no effect Depletion of LC s during active psoriasis results in disease aggravation whereas depletion before disease initiation has no effect The anti‐inflammatory role of LC s is mediated by direct release of the immunosuppressive cytokine IL ‐10 and by preventing excessive IL ‐23 accumulation in the skin pDC depletion results in reduced IL ‐23 levels and therapeutic inhibition of IL ‐23 receptor ameliorates disease symptoms
Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the contribution of Langerhans cells (LCs) and plasmacytoid DCs (pDCs) in psoriasis. In human psoriatic lesions and in a psoriasis mouse model (DKO* mice), LCs are severely reduced, whereas pDCs are increased. Depletion of pDCs in DKO* mice prior to psoriasis induction resulted in a milder phenotype, whereas depletion during active disease had no effect. In contrast, while depletion of Langerin‐expressing APCs before disease onset had no effect, depletion from diseased mice aggravated psoriasis symptoms. Disease aggravation was due to the absence of LCs, but not other Langerin‐expressing APCs. LCs derived from DKO* mice produced increased IL‐10 levels, suggesting an immunosuppressive function. Moreover, IL‐23 production was high in psoriatic mice and further increased in the absence of LCs. Conversely, pDC depletion resulted in reduced IL‐23 production, and therapeutic inhibition of IL‐23R signaling ameliorated disease symptoms. Therefore, LCs have an anti‐inflammatory role during active psoriatic disease, while pDCs exert an instigatory function during disease initiation. Synopsis Resident epidermal LCs, which are gradually lost from the epidermis in active disease phase psoriasis, are responsible for maintaining a suppressive skin environment by balancing the anti‐inflammatory IL‐10 and pro‐inflammatory IL‐23 axis. Langerhans cells (LCs) are severely reduced and plasmacytoid DCs (pDCs) are increased in human psoriasis as well as in mouse models of psoriasis Depletion of pDCs in mice prior to psoriasis induction results in disease amelioration whereas depletion during active disease has no effect Depletion of LCs during active psoriasis results in disease aggravation whereas depletion before disease initiation has no effect The anti‐inflammatory role of LCs is mediated by direct release of the immunosuppressive cytokine IL‐10 and by preventing excessive IL‐23 accumulation in the skin pDC depletion results in reduced IL‐23 levels and therapeutic inhibition of IL‐23 receptor ameliorates disease symptoms Resident epidermal LCs, which are gradually lost from the epidermis in active disease phase psoriasis, are responsible for maintaining a suppressive skin environment by balancing the anti‐inflammatory IL‐10 and pro‐inflammatory IL‐23 axis.
Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the contribution of Langerhans cells (LCs) and plasmacytoid DCs (pDCs) in psoriasis. In human psoriatic lesions and in a psoriasis mouse model (DKO* mice), LCs are severely reduced, whereas pDCs are increased. Depletion of pDCs in DKO* mice prior to psoriasis induction resulted in a milder phenotype, whereas depletion during active disease had no effect. In contrast, while depletion of Langerin‐expressing APCs before disease onset had no effect, depletion from diseased mice aggravated psoriasis symptoms. Disease aggravation was due to the absence of LCs, but not other Langerin‐expressing APCs. LCs derived from DKO* mice produced increased IL‐10 levels, suggesting an immunosuppressive function. Moreover, IL‐23 production was high in psoriatic mice and further increased in the absence of LCs. Conversely, pDC depletion resulted in reduced IL‐23 production, and therapeutic inhibition of IL‐23R signaling ameliorated disease symptoms. Therefore, LCs have an anti‐inflammatory role during active psoriatic disease, while pDCs exert an instigatory function during disease initiation. Synopsis Resident epidermal LCs, which are gradually lost from the epidermis in active disease phase psoriasis, are responsible for maintaining a suppressive skin environment by balancing the anti‐inflammatory IL‐10 and pro‐inflammatory IL‐23 axis. Langerhans cells (LCs) are severely reduced and plasmacytoid DCs (pDCs) are increased in human psoriasis as well as in mouse models of psoriasis Depletion of pDCs in mice prior to psoriasis induction results in disease amelioration whereas depletion during active disease has no effect Depletion of LCs during active psoriasis results in disease aggravation whereas depletion before disease initiation has no effect The anti‐inflammatory role of LCs is mediated by direct release of the immunosuppressive cytokine IL‐10 and by preventing excessive IL‐23 accumulation in the skin pDC depletion results in reduced IL‐23 levels and therapeutic inhibition of IL‐23 receptor ameliorates disease symptoms Graphical Abstract Resident epidermal LCs, which are gradually lost from the epidermis in active disease phase psoriasis, are responsible for maintaining a suppressive skin environment by balancing the anti‐inflammatory IL‐10 and pro‐inflammatory IL‐23 axis.
Audience Academic
Author Wagner, Erwin F
Schonthaler, Helia B
Stingl, Georg
Holcmann, Martin
Amberg, Nicole
Drobits, Barbara
Sibilia, Maria
Brunner, Patrick M
Glitzner, Elisabeth
Kopp, Tamara
Korosec, Ana
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  organization: Department of Medicine I, Comprehensive Cancer Center, Institute of Cancer Research, Medical University of Vienna
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  organization: Department of Dermatology, Division of Immunology, Allergy and Infectious Diseases, Medical University of Vienna
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/25216727$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
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Issue 10
Keywords Langerhans cells
IL‐23
AP‐1
plasmacytoid dendritic cells
psoriasis
Language English
License Attribution
2014 The Authors. Published under the terms of the CC BY 4.0 license.
This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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SSID ssj0065618
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Snippet Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated the...
Abstract Several subtypes of APC s are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated...
Abstract Several subtypes of APCs are found in psoriasis patients, but their involvement in disease pathogenesis is poorly understood. Here, we investigated...
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SubjectTerms Adjuvants, Immunologic - pharmacology
Aminoquinolines - pharmacology
Analysis
Animals
Antibodies, Monoclonal - immunology
Antibodies, Monoclonal - pharmacology
Antigen-Presenting Cells - immunology
Antigen-Presenting Cells - metabolism
AP‐1
Bone marrow
Bone Marrow Transplantation
Dendritic cells
Dendritic Cells - immunology
Dendritic Cells - metabolism
Development and progression
Disease Progression
EMBO19
EMBO38
Etiology
Experiments
Flow Cytometry
Humans
IL‐23
Inflammation
Interleukin-10 - immunology
Interleukin-10 - metabolism
Interleukin-23 - immunology
Interleukin-23 - metabolism
Langerhans cells
Langerhans Cells - immunology
Langerhans Cells - metabolism
Lymphocytes
Mice, Inbred C57BL
Mice, Knockout
Microscopy, Confocal
Patients
Phenotypes
plasmacytoid dendritic cells
Proto-Oncogene Proteins c-jun - deficiency
Proto-Oncogene Proteins c-jun - genetics
Proto-Oncogene Proteins c-jun - immunology
Psoriasis
Psoriasis - genetics
Psoriasis - immunology
Psoriasis - prevention & control
Receptors, Interleukin - immunology
Receptors, Interleukin - metabolism
Research Article
Roles
Signal Transduction - drug effects
Signal Transduction - immunology
Skin - drug effects
Skin - immunology
Skin - pathology
Transcription Factors - deficiency
Transcription Factors - genetics
Transcription Factors - immunology
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Title Specific roles for dendritic cell subsets during initiation and progression of psoriasis
URI https://link.springer.com/article/10.15252/emmm.201404114
https://onlinelibrary.wiley.com/doi/abs/10.15252%2Femmm.201404114
https://www.ncbi.nlm.nih.gov/pubmed/25216727
https://www.proquest.com/docview/2288228336
https://search.proquest.com/docview/1586095081
https://pubmed.ncbi.nlm.nih.gov/PMC4287934
https://doaj.org/article/0deedda89e6943ffb42d4008249c2cbb
Volume 6
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