Infliximab induces downregulation of the IL-12/IL-23 axis in 6-sulfo-LacNac (slan)+ dendritic cells and macrophages
The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined. We sought to analyze the effects of anti–TNF-α treatment on TNF-α+ cells in the skin and blood of patients with psoriasis. Lesional psoriatic skin...
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| Published in | Journal of allergy and clinical immunology Vol. 132; no. 5; pp. 1184 - 1193.e8 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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New York, NY
Mosby, Inc
01.11.2013
Elsevier Elsevier Limited |
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| Abstract | The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined.
We sought to analyze the effects of anti–TNF-α treatment on TNF-α+ cells in the skin and blood of patients with psoriasis.
Lesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling.
By using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45+HLA-DR+ leukocytes consisting of CD11c+ dendritic cells and CD163+ macrophages. In peripheral blood we observed an increase in the TNF-α–producing myeloid subsets of CD14− 6-sulfo-LacNac+ dendritic cells and CD14+CD16+ “intermediate” monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers.
Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α+ cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment.
The decrease in tissue inflammation during anti–TNF-α therapy is not due to immediate killing of TNF-α–producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23–driven immune response. |
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| AbstractList | Background The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined. Objective We sought to analyze the effects of anti–TNF-α treatment on TNF-α+ cells in the skin and blood of patients with psoriasis. Methods Lesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling. Results By using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45+ HLA-DR+ leukocytes consisting of CD11c+ dendritic cells and CD163+ macrophages. In peripheral blood we observed an increase in the TNF-α–producing myeloid subsets of CD14− 6-sulfo-LacNac+ dendritic cells and CD14+ CD16+ “intermediate” monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers. Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α+ cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment. Conclusion The decrease in tissue inflammation during anti–TNF-α therapy is not due to immediate killing of TNF-α–producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23–driven immune response. The spectrum of TNF-α-producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined.BACKGROUNDThe spectrum of TNF-α-producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined.We sought to analyze the effects of anti-TNF-α treatment on TNF-α(+) cells in the skin and blood of patients with psoriasis.OBJECTIVEWe sought to analyze the effects of anti-TNF-α treatment on TNF-α(+) cells in the skin and blood of patients with psoriasis.Lesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling.METHODSLesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling.By using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45(+)HLA-DR(+) leukocytes consisting of CD11c(+) dendritic cells and CD163(+) macrophages. In peripheral blood we observed an increase in the TNF-α-producing myeloid subsets of CD14(-) 6-sulfo-LacNac(+) dendritic cells and CD14(+)CD16(+) "intermediate" monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers. Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α(+) cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment.RESULTSBy using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45(+)HLA-DR(+) leukocytes consisting of CD11c(+) dendritic cells and CD163(+) macrophages. In peripheral blood we observed an increase in the TNF-α-producing myeloid subsets of CD14(-) 6-sulfo-LacNac(+) dendritic cells and CD14(+)CD16(+) "intermediate" monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers. Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α(+) cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment.The decrease in tissue inflammation during anti-TNF-α therapy is not due to immediate killing of TNF-α-producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23-driven immune response.CONCLUSIONThe decrease in tissue inflammation during anti-TNF-α therapy is not due to immediate killing of TNF-α-producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23-driven immune response. The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined. We sought to analyze the effects of anti–TNF-α treatment on TNF-α+ cells in the skin and blood of patients with psoriasis. Lesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling. By using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45+HLA-DR+ leukocytes consisting of CD11c+ dendritic cells and CD163+ macrophages. In peripheral blood we observed an increase in the TNF-α–producing myeloid subsets of CD14− 6-sulfo-LacNac+ dendritic cells and CD14+CD16+ “intermediate” monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers. Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α+ cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment. The decrease in tissue inflammation during anti–TNF-α therapy is not due to immediate killing of TNF-α–producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23–driven immune response. Background The spectrum of TNF-α-producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined. Objective We sought to analyze the effects of anti-TNF-α treatment on TNF-α+cells in the skin and blood of patients with psoriasis. Methods Lesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling. Results By using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45+HLA-DR+leukocytes consisting of CD11c+dendritic cells and CD163+macrophages. In peripheral blood we observed an increase in the TNF-α-producing myeloid subsets of CD14-6-sulfo-LacNac+dendritic cells and CD14+CD16+"intermediate" monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers. Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α+cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade duringin vitrostimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment. Conclusion The decrease in tissue inflammation during anti-TNF-α therapy is not due to immediate killing of TNF-α-producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23-driven immune response. The spectrum of TNF-α-producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined. We sought to analyze the effects of anti-TNF-α treatment on TNF-α(+) cells in the skin and blood of patients with psoriasis. Lesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling. By using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45(+)HLA-DR(+) leukocytes consisting of CD11c(+) dendritic cells and CD163(+) macrophages. In peripheral blood we observed an increase in the TNF-α-producing myeloid subsets of CD14(-) 6-sulfo-LacNac(+) dendritic cells and CD14(+)CD16(+) "intermediate" monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers. Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α(+) cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment. The decrease in tissue inflammation during anti-TNF-α therapy is not due to immediate killing of TNF-α-producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23-driven immune response. BACKGROUND: The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined. OBJECTIVE: We sought to analyze the effects of anti–TNF-α treatment on TNF-α⁺ cells in the skin and blood of patients with psoriasis. METHODS: Lesional psoriatic skin was analyzed by means of immunohistologic staining and quantitative RT-PCR, and peripheral blood cells were phenotypically characterized by means of multicolor immunofluorescence labeling. RESULTS: By using a tyramide-based signal amplification system, TNF-α was detected in dermal CD45⁺HLA-DR⁺ leukocytes consisting of CD11c⁺ dendritic cells and CD163⁺ macrophages. In peripheral blood we observed an increase in the TNF-α–producing myeloid subsets of CD14⁻ 6-sulfo-LacNac⁺ dendritic cells and CD14⁺CD16⁺ “intermediate” monocytes compared with healthy control subjects. Strikingly, we did not find detectable levels of TNF-α in other cells, including keratinocytes or T cells, making these cell types unlikely targets of TNF-α blockers. Up to 48 hours after the intravenous administration of the TNF-α antagonist infliximab, we encountered no overt changes in numbers of TNF-α⁺ cells or signs of apoptosis in lesional psoriatic skin. Yet we observed a rapid decrease in IL-12p40, IL-1β, CCL20, and IL12RB1 mRNA levels. Consistently, TNF-α blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-12 and IL-23 but not IL-6. In a mixed leukocyte reaction infliximab led to significantly decreased proliferation rates of T cells independent of the Fc antibody fragment. CONCLUSION: The decrease in tissue inflammation during anti–TNF-α therapy is not due to immediate killing of TNF-α–producing cells but rather results from a rapid downregulation of the pathogenic IL-12/IL-23–driven immune response. |
| Author | Brunner, Patrick M. Reininger, Bärbel Koszik, Frieder Stingl, Georg Kalb, Madeleine L. Bauer, Wolfgang |
| Author_xml | – sequence: 1 givenname: Patrick M. surname: Brunner fullname: Brunner, Patrick M. – sequence: 2 givenname: Frieder surname: Koszik fullname: Koszik, Frieder – sequence: 3 givenname: Bärbel surname: Reininger fullname: Reininger, Bärbel – sequence: 4 givenname: Madeleine L. surname: Kalb fullname: Kalb, Madeleine L. – sequence: 5 givenname: Wolfgang surname: Bauer fullname: Bauer, Wolfgang – sequence: 6 givenname: Georg surname: Stingl fullname: Stingl, Georg email: georg.stingl@meduniwien.ac.at |
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| Keywords | 6-sulfo-LacNac tmTNF-α TNFR PASI Psoriasis IL-12p40 PMA MACS myeloid dendritic cells mDC slan TUNEL TNF-α iNOS sTNF-α NK BDCA DC Terminal deoxynucleotidyl transferase dUTP nick end labeling Psoriasis Area and Severity Index Magnetic cell sorting Inducible nitric oxide synthase Myeloid dendritic cell Transmembrane TNF-α (26 kDa) Dendritic cell Blood dendritic cell antigen Soluble TNF-α (17 kDa) Natural killer TNF receptor Phorbol 12-myristate 13-acetate Immunopathology Skin disease Cytokine Interleukin 12 Interleukin 23 Monoclonal antibody Anti-Tumor Necrosis Factor-alpha Interleukin 6 Immunology Infliximab Antigen presenting cell Anticytokine Tumor necrosis factor α Macrophage 6-Sulfo-LacNac |
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| PublicationPlace_xml | – name: New York, NY – name: United States – name: St. Louis |
| PublicationTitle | Journal of allergy and clinical immunology |
| PublicationTitleAlternate | J Allergy Clin Immunol |
| PublicationYear | 2013 |
| Publisher | Mosby, Inc Elsevier Elsevier Limited |
| Publisher_xml | – name: Mosby, Inc – name: Elsevier – name: Elsevier Limited |
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| Snippet | The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined.
We... Background The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly... The spectrum of TNF-α-producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly defined. We... Background The spectrum of TNF-α-producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly... The spectrum of TNF-α-producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly... BACKGROUND: The spectrum of TNF-α–producing cells in patients with psoriasis, as well as their fate during treatment with TNF-α antagonists, is not clearly... |
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| SubjectTerms | 6-sulfo-LacNac Adult Allergy and Immunology Amino Sugars - metabolism antagonists antibodies Antibodies, Monoclonal - pharmacology Antigens, CD - metabolism Apoptosis Biological and medical sciences Case-Control Studies chemokine CCL20 Cloning dendritic cells Dendritic Cells - drug effects Dendritic Cells - immunology Dendritic Cells - metabolism Dermatology Disease fluorescent antibody technique Fundamental and applied biological sciences. Psychology Fundamental immunology Gene Expression Humans IL-12p40 immune response Immune system Immunopathology Immunophenotyping inflammation Inflammation Mediators - metabolism Infliximab interleukin-12 Interleukin-12 - metabolism interleukin-1beta interleukin-23 Interleukin-23 - metabolism intravenous injection keratinocytes Leukocyte Count Leukocytes, Mononuclear - immunology Leukocytes, Mononuclear - metabolism macrophages Macrophages - drug effects Macrophages - immunology Macrophages - metabolism Medical sciences messenger RNA Metabolic disorders Middle Aged monocytes Monocytes - immunology Monocytes - metabolism myeloid dendritic cells patients Proteins Psoriasis Psoriasis - immunology Psoriasis - metabolism Psoriasis. Parapsoriasis. Lichen reverse transcriptase polymerase chain reaction RNA, Messenger - genetics RNA, Messenger - metabolism Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Skin T-lymphocytes TNF-α tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - genetics |
| Title | Infliximab induces downregulation of the IL-12/IL-23 axis in 6-sulfo-LacNac (slan)+ dendritic cells and macrophages |
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