Identification of TNF-related apoptosis-inducing ligand and other molecules that distinguish inflammatory from resident dendritic cells in patients with psoriasis

Lisa C. Zaba, Judilyn Fuentes-Duculan, Narat John Eungdamrong, Leanne M. Johnson-Huang, Kristine E. Nograles, Traci R. White, Katherine C. Pierson, Tim Lentini, Mayte Suárez-Fariñas, Michelle A. Lowes, James G. Krueger

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

Background: Previous work has identified CD11c+CD1c- dendritic cells (DCs) as the major "inflammatory" dermal DC population in patients with psoriasis vulgaris and CD1c+ DCs as the "resident" cutaneous DC population. Objective: We sought to further define molecular differences between these 2 myeloid dermal DC populations. Methods: Inflammatory and resident DCs were single-cell sorted from lesional skin biopsy specimens of patients with psoriasis, and the transcriptome of CD11c+CD1c- versus CD1c+ DCs was determined. Results were confirmed with RT-PCR, flow cytometry, immunohistochemistry, and double-labeled immunofluorescence. Human keratinocytes were cultured for functional studies. Results: TNF-related apoptosis-inducing ligand (TRAIL), Toll-like receptors 1 and 2, S100A12/ENRAGE, CD32, and many other inflammatory products were differentially expressed in inflammatory DCs compared with resident DCs. Flow cytometry and immunofluorescence confirmed higher protein expression on CD1c- versus CD1c+ DCs. TRAIL receptors, death receptor 4, and decoy receptor 2 were expressed in keratinocytes and dermal cells. In vitro culture of keratinocytes with TRAIL induced CCL20 chemokine. Conclusions: CD11c+CD1c- inflammatory DCs in psoriatic lesional skin express a wide range of inflammatory molecules compared with skin-resident CD1c+ DCs. Some molecules made by inflammatory DCs, including TRAIL, could have direct effects on keratinocytes or other skin cell types to promote disease pathogenesis.

Original languageEnglish (US)
JournalJournal of Allergy and Clinical Immunology
Volume125
Issue number6
DOIs
StatePublished - Jun 2010
Externally publishedYes

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TNF-Related Apoptosis-Inducing Ligand
Psoriasis
Dendritic Cells
Keratinocytes
Langerhans Cells
Skin
TNF-Related Apoptosis-Inducing Ligand Receptors
Fluorescent Antibody Technique
Chemokine CCL20
Flow Cytometry
Toll-Like Receptor 1
Population
Toll-Like Receptor 2
Transcriptome
Immunohistochemistry

Keywords

  • CCL20
  • CD32
  • dendritic cell
  • inflammation
  • psoriasis
  • S100A12
  • Toll-like receptor 1
  • Toll-like receptor 2
  • TRAIL

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Identification of TNF-related apoptosis-inducing ligand and other molecules that distinguish inflammatory from resident dendritic cells in patients with psoriasis. / Zaba, Lisa C.; Fuentes-Duculan, Judilyn; Eungdamrong, Narat John; Johnson-Huang, Leanne M.; Nograles, Kristine E.; White, Traci R.; Pierson, Katherine C.; Lentini, Tim; Suárez-Fariñas, Mayte; Lowes, Michelle A.; Krueger, James G.

In: Journal of Allergy and Clinical Immunology, Vol. 125, No. 6, 06.2010.

Research output: Contribution to journalArticle

Zaba, LC, Fuentes-Duculan, J, Eungdamrong, NJ, Johnson-Huang, LM, Nograles, KE, White, TR, Pierson, KC, Lentini, T, Suárez-Fariñas, M, Lowes, MA & Krueger, JG 2010, 'Identification of TNF-related apoptosis-inducing ligand and other molecules that distinguish inflammatory from resident dendritic cells in patients with psoriasis', Journal of Allergy and Clinical Immunology, vol. 125, no. 6. https://doi.org/10.1016/j.jaci.2010.03.018
Zaba, Lisa C. ; Fuentes-Duculan, Judilyn ; Eungdamrong, Narat John ; Johnson-Huang, Leanne M. ; Nograles, Kristine E. ; White, Traci R. ; Pierson, Katherine C. ; Lentini, Tim ; Suárez-Fariñas, Mayte ; Lowes, Michelle A. ; Krueger, James G. / Identification of TNF-related apoptosis-inducing ligand and other molecules that distinguish inflammatory from resident dendritic cells in patients with psoriasis. In: Journal of Allergy and Clinical Immunology. 2010 ; Vol. 125, No. 6.
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T1 - Identification of TNF-related apoptosis-inducing ligand and other molecules that distinguish inflammatory from resident dendritic cells in patients with psoriasis

AU - Zaba, Lisa C.

AU - Fuentes-Duculan, Judilyn

AU - Eungdamrong, Narat John

AU - Johnson-Huang, Leanne M.

AU - Nograles, Kristine E.

AU - White, Traci R.

AU - Pierson, Katherine C.

AU - Lentini, Tim

AU - Suárez-Fariñas, Mayte

AU - Lowes, Michelle A.

AU - Krueger, James G.

PY - 2010/6

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N2 - Background: Previous work has identified CD11c+CD1c- dendritic cells (DCs) as the major "inflammatory" dermal DC population in patients with psoriasis vulgaris and CD1c+ DCs as the "resident" cutaneous DC population. Objective: We sought to further define molecular differences between these 2 myeloid dermal DC populations. Methods: Inflammatory and resident DCs were single-cell sorted from lesional skin biopsy specimens of patients with psoriasis, and the transcriptome of CD11c+CD1c- versus CD1c+ DCs was determined. Results were confirmed with RT-PCR, flow cytometry, immunohistochemistry, and double-labeled immunofluorescence. Human keratinocytes were cultured for functional studies. Results: TNF-related apoptosis-inducing ligand (TRAIL), Toll-like receptors 1 and 2, S100A12/ENRAGE, CD32, and many other inflammatory products were differentially expressed in inflammatory DCs compared with resident DCs. Flow cytometry and immunofluorescence confirmed higher protein expression on CD1c- versus CD1c+ DCs. TRAIL receptors, death receptor 4, and decoy receptor 2 were expressed in keratinocytes and dermal cells. In vitro culture of keratinocytes with TRAIL induced CCL20 chemokine. Conclusions: CD11c+CD1c- inflammatory DCs in psoriatic lesional skin express a wide range of inflammatory molecules compared with skin-resident CD1c+ DCs. Some molecules made by inflammatory DCs, including TRAIL, could have direct effects on keratinocytes or other skin cell types to promote disease pathogenesis.

AB - Background: Previous work has identified CD11c+CD1c- dendritic cells (DCs) as the major "inflammatory" dermal DC population in patients with psoriasis vulgaris and CD1c+ DCs as the "resident" cutaneous DC population. Objective: We sought to further define molecular differences between these 2 myeloid dermal DC populations. Methods: Inflammatory and resident DCs were single-cell sorted from lesional skin biopsy specimens of patients with psoriasis, and the transcriptome of CD11c+CD1c- versus CD1c+ DCs was determined. Results were confirmed with RT-PCR, flow cytometry, immunohistochemistry, and double-labeled immunofluorescence. Human keratinocytes were cultured for functional studies. Results: TNF-related apoptosis-inducing ligand (TRAIL), Toll-like receptors 1 and 2, S100A12/ENRAGE, CD32, and many other inflammatory products were differentially expressed in inflammatory DCs compared with resident DCs. Flow cytometry and immunofluorescence confirmed higher protein expression on CD1c- versus CD1c+ DCs. TRAIL receptors, death receptor 4, and decoy receptor 2 were expressed in keratinocytes and dermal cells. In vitro culture of keratinocytes with TRAIL induced CCL20 chemokine. Conclusions: CD11c+CD1c- inflammatory DCs in psoriatic lesional skin express a wide range of inflammatory molecules compared with skin-resident CD1c+ DCs. Some molecules made by inflammatory DCs, including TRAIL, could have direct effects on keratinocytes or other skin cell types to promote disease pathogenesis.

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KW - CD32

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KW - S100A12

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KW - Toll-like receptor 2

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