Cytokine-Induced CEACAM1 Expression on Keratinocytes Is Characteristic for Psoriatic Skin and Contributes to a Prolonged Lifespan of Neutrophils Massilva.

Slides:

Advertisements

Similar presentations

Volume 24, Issue 3, Pages (March 2006)

Advertisements

The CXC-chemokine platelet factor 4 promotes monocyte survival and induces monocyte differentiation into macrophages by Barbara Scheuerer, Martin Ernst,

Interleukin-10 Downregulates Anti-Microbial Peptide Expression in Atopic Dermatitis Michael D. Howell, Natalija Novak, Thomas Bieber, Saveria Pastore,

IL-21 May Promote Granzyme B-Dependent NK/Plasmacytoid Dendritic Cell Functional Interaction in Cutaneous Lupus Erythematosus Valentina Salvi, William.

Cathelicidin Antimicrobial Peptide LL-37 in Psoriasis Enables Keratinocyte Reactivity against TLR9 Ligands Shin Morizane, Kenshi Yamasaki, Beda Mühleisen,

Impaired Responses of Peripheral Blood Mononuclear Cells to Staphylococcal Superantigen in Patients with Severe Atopic Dermatitis: A Role of T Cell Apoptosis

Unprocessed Interleukin-36α Regulates Psoriasis-Like Skin Inflammation in Cooperation With Interleukin-1 Katelynn A. Milora, Hangfei Fu, Ornella Dubaz,

Natural Killer and Dendritic Cell Contact in Lesional Atopic Dermatitis Skin –Malassezia- Influenced Cell Interaction Eva Buentke, Lena C. Heffler, Annika.

Staphylococcus aureus Stimulates Neutrophil Targeting Chemokine Expression in Keratinocytes through an Autocrine IL-1α Signaling Loop Florina Olaru,

IL-32 is expressed by human primary keratinocytes and modulates keratinocyte apoptosis in atopic dermatitis Norbert Meyer, MD, Maya Zimmermann, PhD,

Differentiation, phenotype, and function of interleukin-17–producing human Vγ9Vδ2 T cells by Nadia Caccamo, Carmela La Mendola, Valentina Orlando, Serena.

Skin-Resident Effector Memory CD8+CD28– T Cells Exhibit a Profibrotic Phenotype in Patients with Systemic Sclerosis Gang Li, Adriana T. Larregina, Robyn.

The IL-17A-Producing CD8+ T-Cell Population in Psoriatic Lesional Skin Comprises Mucosa-Associated Invariant T Cells and Conventional T Cells Marcel.

Interferon-γ Protects from Staphylococcal Alpha Toxin-Induced Keratinocyte Death through Apolipoprotein L1 Anne M. Brauweiler, Elena Goleva, Donald Y.M.

Decreased Expression of Caveolin-1 Contributes to the Pathogenesis of Psoriasiform Dermatitis in Mice Yukie Yamaguchi, Yuko Watanabe, Tomoya Watanabe,

IL-13-Stimulated Human Keratinocytes Preferentially Attract CD4+CCR4+ T cells: Possible Role in Atopic Dermatitis Rahul Purwar, Thomas Werfel, Miriam.

Cytokine Effects Induced by the Human Autoallergen α-NAC

Myeloid-Derived Suppressor Cells in Psoriasis Are an Expanded Population Exhibiting Diverse T-Cell–Suppressor Mechanisms Lauren Y. Cao, Jin-Sung Chung,

Interleukin-17 and Interferon-γ Synergize in the Enhancement of Proinflammatory Cytokine Production by Human Keratinocytes Marcel B.M. Teunissen, Jan.

Increased Sensitivity to Interferon-α in Psoriatic T Cells

Propionibacterium acnes Induces an IL-17 Response in Acne Vulgaris that Is Regulated by Vitamin A and Vitamin D George W. Agak, Min Qin, Jennifer Nobe,

Streptococcus Induces Circulating CLA+ Memory T-Cell-Dependent Epidermal Cell Activation in Psoriasis Marta Ferran, Ana B. Galván, Catalina Rincón, Ester.

Increased Lipocalin-2 Contributes to the Pathogenesis of Psoriasis by Modulating Neutrophil Chemotaxis and Cytokine Secretion Shuai Shao, Tianyu Cao,

EGFR Regulates the Expression of Keratinocyte-Derived Granulocyte/Macrophage Colony-Stimulating Factor In Vitro and In Vivo Francesca Mascia, Christophe.

IL-22 Increases the Innate Immunity of Tissues

Age-Related Differences in Sensitivity of Peripheral Blood Monocytes to Lipopolysaccharide and Staphylococcus Aureus Toxin B in Atopic Dermatitis Marie.

Jasper G. van den Boorn, Debby Konijnenberg, Trees A. M. Dellemijn, J

IL-31 Receptor Alpha Expression in Epidermal Keratinocytes Is Modulated by Cell Differentiation and Interferon Gamma Ruth Heise, Mark M. Neis, Yvonne.

IL-1R1 Signaling Facilitates Munro’s Microabscess Formation in Psoriasiform Imiquimod-Induced Skin Inflammation Mireia Uribe-Herranz, Li-Hua Lian, Kirsten.

Regulation of IL-33 Expression by IFN-γ and Tumor Necrosis Factor-α in Normal Human Epidermal Keratinocytes Jitlada Meephansan, Hidetoshi Tsuda, Mayumi.

IL-10-Producing Langerhans Cells and Regulatory T Cells Are Responsible for Depressed Contact Hypersensitivity in Grafted Skin Ryutaro Yoshiki, Kenji.

Targeting PKC in Human T Cells Using Sotrastaurin (AEB071) Preserves Regulatory T Cells and Prevents IL-17 Production Xuehui He, Hans J.P.M. Koenen,

Dorothea Dijkstra, Holger Stark, Paul L. Chazot, Fiona C

IL-18, but Not IL-12, Induces Production of IFN-γ in the Immunosuppressive Environment of HPV16 E7 Transgenic Hyperplastic Skin Christina Gosmann, Ian.

The Antimicrobial Protein Psoriasin (S100A7) Is Upregulated in Atopic Dermatitis and after Experimental Skin Barrier Disruption Regine Gläser, Ulf Meyer-Hoffert,

Stimulation of Purinergic Receptors Modulates Chemokine Expression in Human Keratinocytes Saveria Pastore, Francesca Mascia, Sara Gulinelli, Sylvia Forchap,

Differential Effects of Corticosteroids and Pimecrolimus on the Developing Skin Immune System in Humans and Mice Simone Meindl, Christine Vaculik, Josef.

Poly(I:C)-Treated Human Langerhans Cells Promote the Differentiation of CD4+ T Cells Producing IFN-γ and IL-10 Laetitia Furio, Hermine Billard, Jenny.

Skin CD4+ T Cells Produce Interferon-γIn Vitro in Response to Streptococcal Antigens in Chronic Plaque Psoriasis Dean W. Brown, Barbara S. Baker, Jean-Marc.

Increased Expression of Carbonic Anhydrase II (CA II) in Lesional Skin of Atopic Dermatitis: Regulation by Th2 Cytokines Marijke Kamsteeg, Patrick L.J.M.

Vitamin D Analog Calcipotriol Suppresses the Th17 Cytokine–Induced Proinflammatory S100 “Alarmins” Psoriasin (S100A7) and Koebnerisin (S100A15) in Psoriasis

Characterization of the CC Chemokine Receptor 3 on Human Keratinocytes

Inter-Regulation of Th17 Cytokines and the IL-36 Cytokines In Vitro and In Vivo: Implications in Psoriasis Pathogenesis Yijun Carrier, Hak-Ling Ma, Hilda.

Functional Characterization of IL-17F as a Selective Neutrophil Attractant in Psoriasis Hideaki Watanabe, Mio Kawaguchi, Sawa Fujishima, Miyoko Ogura,

Ekatherina Vassina, Martin Leverkus, Shida Yousefi, Lasse R

Identification of a Novel CD160+CD4+ T-Lymphocyte Subset in the Skin: A Possible Role for CD160 in Skin Inflammation Sofia Abecassis, Jérôme Giustiniani,

The relative contribution of IL-4 and IL-13 to human IgE synthesis induced by activated CD4+ or CD8+ T cells Juha Punnonen, MD, PhD, Hans Yssel, PhD,

Caspase-5 Expression Is Upregulated in Lesional Psoriatic Skin

TNF-α and IFN-γ Are Potential Inducers of Fas-Mediated Keratinocyte Apoptosis through Activation of Inducible Nitric Oxide Synthase in Toxic Epidermal.

UVB and Proinflammatory Cytokines Synergistically Activate TNF-α Production in Keratinocytes through Enhanced Gene Transcription Muhammad M. Bashir,

Anti-Mycotics Suppress Interleukin-4 and Interleukin-5 Production in Anti-CD3 Plus Anti- CD28-Stimulated T Cells from Patients with Atopic Dermatitis

Staphylococcal exotoxins are strong inducers of IL-22: A potential role in atopic dermatitis Margarete Niebuhr, MD, Helena Scharonow, MS, Merle Gathmann,

PPARδ Is a Type 1 IFN Target Gene and Inhibits Apoptosis in T Cells

Suprabasal Spongiosis in Acute Eczematous Dermatitis: cFLIP Maintains Resistance of Basal Keratinocytes to T-Cell-Mediated Apoptosis Nicole Armbruster,

Characterization of the Sensitizing Potential of Chemicals by In Vitro Analysis of Dendritic Cell Activation and Skin Penetration Pierre Aeby, Christoph.

Serotonin Activates Human Monocytes and Prevents Apoptosis

Possible Roles of IL-27 in the Pathogenesis of Psoriasis

IL-4 and IL-13 Alter Plasmacytoid Dendritic Cell Responsiveness to CpG DNA and Herpes Simplex Virus-1 Jurjen Tel, Ruurd Torensma, Carl G. Figdor, I.

A Comprehensive Analysis of Pattern Recognition Receptors in Normal and Inflamed Human Epidermis: Upregulation of Dectin-1 in Psoriasis Heleen D. de.

Human Langerhans Cells Are More Efficient Than CD14−CD1c+ Dermal Dendritic Cells at Priming Naive CD4+ T Cells Laetitia Furio, Isabelle Briotet, Alexandra.

AP-1-Controlled Hepatocyte Growth Factor Activation Promotes Keratinocyte Migration via CEACAM1 and Urokinase Plasminogen Activator/Urokinase Plasminogen.

Keratinocytes Inhibit Expression of Connective Tissue Growth Factor in Fibroblasts In Vitro by an Interleukin-1α-Dependent Mechanism Daniel Nowinski,

Foxp3+ Regulatory T Cells of Psoriasis Patients Easily Differentiate into IL-17A- Producing Cells and Are Found in Lesional Skin H. Jorn Bovenschen, Peter.

Volume 24, Issue 3, Pages (March 2006)

Regulation of IL-13 Receptors in Human Keratinocytes

Possible Pathogenic Role of Th17 Cells for Atopic Dermatitis

Increased Type 2 Cytokine Expression by Both CD4+ CD45RO+ T Cells and CD8+ CD45RO+ T Cells in Blood Circulation is Associated with High Serum IgE but.

Volume 126, Issue 5, Pages (May 2004)

The Activity of Caspase-1 Is Increased in Lesional Psoriatic Epidermis

The Majority of Epidermal T Cells in Psoriasis Vulgaris Lesions can Produce Type 1 Cytokines, Interferon-γ, Interleukin-2, and Tumor Necrosis Factor-α,

Presentation transcript:

Cytokine-Induced CEACAM1 Expression on Keratinocytes Is Characteristic for Psoriatic Skin and Contributes to a Prolonged Lifespan of Neutrophils Massilva Rahmoun, Jean-Pierre Molès, Nathalie Pedretti, Marc Mathieu, Isabelle Fremaux, Nadia Raison-Peyron, Jean-Claude Lecron, Hans Yssel, Jérôme Pène Journal of Investigative Dermatology Volume 129, Issue 3, Pages 671-681 (March 2009) DOI: 10.1038/jid.2008.303 Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 1 Keratinocytes in the outer epidermal layer of psoriatic lesions specifically express CEACAM1. CEACAM1 expression on cutaneous biopsies from individuals with (a) melanoma, from (b) healthy individuals, or patients with (c) psoriasis, (d) atopic dermatitis, or (e) nummular dermatitis was determined by immunohistochemistry analysis as described in ‘Materials and Methods’. The presence of the Munro-Saboureau microabscess in the outer layer of psoriatic skin (c) is indicated by *. Arrows indicate CEACAM1 expression in the dermis of (b) healthy individuals or patients with (d) atopic or (e) nummular dermatitis. (f) CD3 expression in biopsies from patients with psoriasis. Controls are inserted in the relevant figures. Scale bars=100μm. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 2 Culture supernatants of activated skin-infiltrating T cells induce expression of CEACAM1 transcripts and protein by NHEK in an IFN-γ-dependent manner. (a) NHEK were cultured with different dilutions of supernatants of in vitro-activated skin-infiltrating T cells, depleted or not for the presence of IFN-γ, and the expression of CEACAM1 transcripts was analyzed by real-time RT-PCR following 24hours of incubation. (b) NHEK were cultured in medium only (Cont.) or in the presence of 30 or 5% culture supernatant, derived from psoriatic skin-infiltrating T cells, that had been activated for 24hours in vitro with anti-CD3 and CD28 mAbs (30% ND and 5% ND). In addition, supernatants depleted for the presence of IFN-γ used at a concentration of 30% (30% D) or 5% (5% D) were added in parallel. As a control, NHEK were stimulated with anti-CD3 and CD28 mAbs (CD3CD28). Expression of CEACAM1 was determined by immunohistochemistry analysis after 48hours of incubation. Scale bar=100μm. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 3 IFN-γ induces cell-surface expression of CEACAM1 by NHEK. NHEK were cultured for 48hours in the (a) absence or (b) presence of IFN-γ. Cell-surface expression of CEACAM1 was determined by immunohistochemistry (a, b) or western blotting analysis (c). Negative control for immunohistochemical analysis is inserted in (b). Scale bar=100μm. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 4 OSM induces cell-surface expression of CEACAM1 on human reconstituted epidermis. Human reconstituted epidermis was cultured for 48hours in (a) the absence or (b) the presence of 30% T-cell-derived culture supernatant, with (c) OSM or (d) IL-17, both at a concentration of 10ngml−1. The expression of CEACAM1 was determined by immunohistochemistry analysis. Scale bar=100μm. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 5 IL-17 does not induce CEACAM1 expression on NHEK. NHEK were cultured in medium only (Cont.) or in the presence of either a culture supernatant (30%, T-cell SN) of in vitro-activated psoriatic skin-infiltrating T cells, IFN-γ (10ngml−1), or IL-17 and the expression of CEACAM1 was analyzed by immunohistochemistry after 48hours of incubation. Negative controls for the two conditions that induce CEACAM1 expression are inserted in the figures. Scale bars=100μm. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 6 Cytokines produced by activated skin-infiltrating T cells induce the expression of CEACAM1-S and -L isoform transcripts on primary keratinocytes. (a) NHEK were cultured for 24hours with a combinations of cytokines, each used at a concentration of 10ngml−1 or with a culture supernatant (30%) of in vitro-activated psoriatic skin-infiltrating T cells, in the presence or absence of neutralizing mAbs specific for IFN-γ or IL-17 and the expression of transcripts for the short (3S and 4S) and long (3L and 4L) isoforms of CEACAM1 was analyzed by real-time RT-PCR. (b) The specificity of the primers for the different isoforms was validated by classic PCR on NHEK, cultured in the presence of T-cell culture supernatant. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 7 IFN-γ-induced expression of CEACAM1 on keratinocytes protects neutrophils from spontaneous apoptosis. (a) One million of freshly isolated peripheral blood neutrophils were cultured for 24hours in medium alone or (b) 200ngml−1 GM-CSF or were cocultured with either NHEK that had been preincubated for 48hours (c) in medium, (d) with 10ngml−1 IFN-γ, or with (e) wild type CHO cells or with CHO cells expressing (f) the long or (g) the short isoform of CEACAM1. Frequencies of viable and early or late apoptotic cells were determined by measuring Annexin-V binding (x axis) and PI incorporation (y axis) using flow cytometry. Results shown in (a) to (g) are representative of three independent experiments with neutrophils from different donors and the percentages of cells in the quadrants are indicated in each graph. (h) Percentages of viable cells are represented as the mean±SD. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions

Figure 8 CEACAM1 engagement delays neutrophil apoptosis. One million of freshly isolated peripheral blood neutrophils were either cultured (a) in medium only, (b) with 200ngml−1 GM-CSF, (c) with 30μgml−1 of the anti-CEACAM1 mAb 19.6, or (d) with 30μgml−1 of an isotype control mAb for various periods of time. Frequencies of viable and early or late apoptotic cells were determined by measuring Annexin-V binding and PI incorporation using flow cytometry. Representative results from four independent experiments with neutrophils from different donors. Percentages of cells in the quadrants are indicated. (e) Kinetics of viable cell frequencies are expressed as the mean±SD of the values obtained in the four experiments. Journal of Investigative Dermatology 2009 129, 671-681DOI: (10.1038/jid.2008.303) Copyright © 2009 The Society for Investigative Dermatology, Inc Terms and Conditions