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Article ; Online: IL-9 exerts biological function on antigen-experienced murine T cells and exacerbates colitis induced by adoptive transfer.

de Heusch, Magali / Steenwinckel, Valérie / Cochez, Perrine M / Louahed, Jamila / Warnier, Guy / Lemaire, Muriel M / Renauld, Jean-Christophe / Dumoutier, Laure

European journal of immunology

2020 Volume 50, Issue 7, Page(s) 1034–1043

Abstract: IL-9 is involved in various T cell-dependent inflammatory models including colitis, encepahlitis, and asthma. However, the regulation and specificity of IL-9 responsiveness by T cells during immune responses remains poorly understood. Here, we addressed ... ...

Abstract	IL-9 is involved in various T cell-dependent inflammatory models including colitis, encepahlitis, and asthma. However, the regulation and specificity of IL-9 responsiveness by T cells during immune responses remains poorly understood. Here, we addressed this question using two different models: experimental colitis induced by transfer of naive CD4
MeSH term(s)	Adoptive Transfer/adverse effects ; Animals ; Colitis/etiology ; Colitis/genetics ; Colitis/immunology ; Colitis/pathology ; Disease Models, Animal ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/immunology ; Interleukin-2/genetics ; Interleukin-2/immunology ; Interleukin-9/genetics ; Interleukin-9/immunology ; Mice ; Mice, Knockout ; Mice, SCID ; Receptors, Interleukin-9/genetics ; Receptors, Interleukin-9/immunology ; Th17 Cells/immunology ; Th17 Cells/pathology ; Th17 Cells/transplantation ; Th2 Cells/immunology ; Th2 Cells/pathology ; Th2 Cells/transplantation
Chemical Substances	Cd44 protein, mouse ; Hyaluronan Receptors ; Il9r protein, mouse ; Interleukin-2 ; Interleukin-9 ; Receptors, Interleukin-9
Language	English
Publishing date	2020-03-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201948430
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Induction of autoantibodies against mouse soluble proteins after immunization with living cells presenting the autoantigen at the cell surface in fusion with a human type 2 transmembrane protein

Lemaire, Muriel M / Vanhaudenarde, Aurélie / Nizet, Yannick / Dumoutier, Laure / Renauld, Jean-Christophe

Journal of immunological methods. 2011 Mar. 31, v. 367, no. 1-2

2011

Abstract: Induction of autoantibodies towards immune regulatory proteins, such as cytokines or their receptors, is a powerful strategy for functional studies on the role of these factors in vivo. Here we describe a new procedure to elicit autoantibodies by taking ... ...

Abstract	Induction of autoantibodies towards immune regulatory proteins, such as cytokines or their receptors, is a powerful strategy for functional studies on the role of these factors in vivo. Here we describe a new procedure to elicit autoantibodies by taking advantage of tumor cells as a vaccine against peptides presented at their surface in fusion with the human CD134L transmembrane protein. P1.HTR, an immunogenic variant of the P815 mastocytoma cell line, was used to generate stably transfected cell clones with expression vectors encoding the human CD134L transmembrane protein fused with either mouse IL-22BP or IL-9. Following repeated injections of living tumor cells expressing the mIL-22BP construct, mice developed autoantibodies that bind to mIL-22BP and inhibit its interaction with IL-22 in vitro. Mice similarly immunized against mIL-9 produced high titers of autoantibodies that block the activity of this cytokine in the TS1 bioassay. This procedure also inhibits IL-9 activity in vivo as no increase of serum MMCP-1 mast cell protease concentration was observed following IL-9 administration to immunized mice. As an alternative to the injection of living tumor cells expressing the CD134L-antigen fusion protein, intramuscular electrotransfer of the corresponding DNA construct also induced autoantibodies. These results validate this method as a simple and convenient approach to knock down the in vivo activity of soluble regulatory proteins, including cytokines and their receptors.
Keywords	DNA ; autoantibodies ; bioassays ; blood serum ; clones ; humans ; immunization ; interleukin-9 ; mice ; neoplasm cells ; peptides ; proteinases ; receptors ; regulatory proteins ; vaccines
Language	English
Dates of publication	2011-0331
Size	p. 56-62.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	120142-6
ISSN	1872-7905 ; 0022-1759
ISSN (online)	1872-7905
ISSN	0022-1759
DOI	10.1016/j.jim.2011.02.001
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Induction of autoantibodies against mouse soluble proteins after immunization with living cells presenting the autoantigen at the cell surface in fusion with a human type 2 transmembrane protein.

Lemaire, Muriel M / Vanhaudenarde, Aurélie / Nizet, Yannick / Dumoutier, Laure / Renauld, Jean-Christophe

Journal of immunological methods

2011 Volume 367, Issue 1-2, Page(s) 56–62

Abstract	Induction of autoantibodies towards immune regulatory proteins, such as cytokines or their receptors, is a powerful strategy for functional studies on the role of these factors in vivo. Here we describe a new procedure to elicit autoantibodies by taking advantage of tumor cells as a vaccine against peptides presented at their surface in fusion with the human CD134L transmembrane protein. P1.HTR, an immunogenic variant of the P815 mastocytoma cell line, was used to generate stably transfected cell clones with expression vectors encoding the human CD134L transmembrane protein fused with either mouse IL-22BP or IL-9. Following repeated injections of living tumor cells expressing the mIL-22BP construct, mice developed autoantibodies that bind to mIL-22BP and inhibit its interaction with IL-22 in vitro. Mice similarly immunized against mIL-9 produced high titers of autoantibodies that block the activity of this cytokine in the TS1 bioassay. This procedure also inhibits IL-9 activity in vivo as no increase of serum MMCP-1 mast cell protease concentration was observed following IL-9 administration to immunized mice. As an alternative to the injection of living tumor cells expressing the CD134L-antigen fusion protein, intramuscular electrotransfer of the corresponding DNA construct also induced autoantibodies. These results validate this method as a simple and convenient approach to knock down the in vivo activity of soluble regulatory proteins, including cytokines and their receptors.
MeSH term(s)	Animals ; Autoantibodies/biosynthesis ; Autoantigens/immunology ; Histocompatibility ; Humans ; Immunization ; Interleukin-9/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred DBA ; OX40 Ligand/genetics ; OX40 Ligand/immunology ; Receptors, Interleukin/immunology ; Recombinant Fusion Proteins/immunology ; Vaccines, DNA/immunology
Chemical Substances	Autoantibodies ; Autoantigens ; IL22RA2 protein, human ; Interleukin-9 ; OX40 Ligand ; Receptors, Interleukin ; Recombinant Fusion Proteins ; TNFSF4 protein, human ; Vaccines, DNA
Language	English
Publishing date	2011-03-31
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120142-6
ISSN	1872-7905 ; 0022-1759
ISSN (online)	1872-7905
ISSN	0022-1759
DOI	10.1016/j.jim.2011.02.001
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Article ; Online: Mucosal and systemic immune responses to Mycobacterium tuberculosis antigen 85A following its co-delivery with CpG, MPLA or LTB to the lungs in mice.

Todoroff, Julie / Lemaire, Muriel M / Fillee, Catherine / Jurion, Fabienne / Renauld, Jean-Christophe / Huygen, Kris / Vanbever, Rita

PloS one

2013 Volume 8, Issue 5, Page(s) e63344

Abstract: Pulmonary vaccination is a promising route for immunization against tuberculosis because the lung is the natural site of infection with Mycobacterium tuberculosis. Yet, adjuvants with a suitable safety profile need to be found to enhance mucosal immunity ...

Abstract	Pulmonary vaccination is a promising route for immunization against tuberculosis because the lung is the natural site of infection with Mycobacterium tuberculosis. Yet, adjuvants with a suitable safety profile need to be found to enhance mucosal immunity to recombinant antigens. The aim of this study was to evaluate the immunogenicity, the safety and the protective efficacy of a subunit vaccine composed of the immunodominant mycolyl-transferase antigen 85A (Ag85A) and one of three powerful mucosal adjuvants: the oligodeoxynucleotide containing unmethylated cytosine-phosphate-guanine motifs (CpG), the monophosphoryl lipid A of Salmonella minnesota (MPLA) or the B subunit of heat-labile enterotoxin of Escherichia coli (LTB). BALB/c mice were vaccinated in the deep lungs. Our results showed that lung administration of these adjuvants could specifically induce different types of T cell immunity. Both CpG and MPLA induced a Th-1 type immune response with significant antigen-specific IFN-γ production by spleen mononuclear cells in vitro and a tendency of increased IFN-γ in the lungs. Moreover, MPLA triggered a Th-17 response reflected by high IL-17A levels in the spleen and lungs. By contrast, LTB promoted a Th-2 biased immune response, with a production of IL-5 but not IFN-γ by spleen mononuclear cells in vitro. CpG did not induce inflammation in the lungs while LTB and MPLA showed a transient inflammation including a neutrophil influx one day after pulmonary administration. Pulmonary vaccination with Ag85A without or with MPLA or LTB tended to decrease bacterial counts in the spleen and lungs following a virulent challenge with M. tuberculosis H37Rv. In conclusion, CpG and MPLA were found to be potential adjuvants for pulmonary vaccination against tuberculosis, providing Th-1 and Th-17 immune responses and a good safety profile.
MeSH term(s)	Acyltransferases/administration & dosage ; Acyltransferases/immunology ; Adjuvants, Immunologic/administration & dosage ; Animals ; Antigens, Bacterial/administration & dosage ; Antigens, Bacterial/immunology ; Biomarkers/metabolism ; Female ; Immunity, Cellular ; Immunity, Humoral ; Immunity, Mucosal ; Inflammation/immunology ; Inflammation/metabolism ; Lipid A/administration & dosage ; Lipid A/analogs & derivatives ; Lung/immunology ; Lung/microbiology ; Mice ; Mycobacterium tuberculosis/immunology ; Spleen/immunology ; Tuberculosis/immunology ; Tuberculosis/prevention & control ; Tuberculosis Vaccines/administration & dosage ; Tuberculosis Vaccines/immunology ; Vaccines, Subunit/administration & dosage ; Vaccines, Subunit/immunology
Chemical Substances	Adjuvants, Immunologic ; Antigens, Bacterial ; Biomarkers ; Lipid A ; Tuberculosis Vaccines ; Vaccines, Subunit ; Acyltransferases (EC 2.3.-) ; antigen 85A, Mycobacterium tuberculosis (EC 2.3.1.-) ; monophosphoryl lipid A (MWC0ET1L2P)
Language	English
Publishing date	2013-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0063344
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Article ; Online: AhR modulates the IL-22-producing cell proliferation/recruitment in imiquimod-induced psoriasis mouse model.

Cochez, Perrine M / Michiels, Camille / Hendrickx, Emilie / Van Belle, Astrid B / Lemaire, Muriel M / Dauguet, Nicolas / Warnier, Guy / de Heusch, Magali / Togbe, Dieudonnée / Ryffel, Bernhard / Coulie, Pierre G / Renauld, Jean-Christophe / Dumoutier, Laure

European journal of immunology

2016 Volume 46, Issue 6, Page(s) 1449–1459

Abstract: IL-22 has a detrimental role in skin inflammatory processes, for example in psoriasis. As transcription factor, AhR controls the IL-22 production by several cell types (i.e. Th17 cells). Here, we analyzed the role of Ahr in IL-22 production by immune ... ...

Abstract	IL-22 has a detrimental role in skin inflammatory processes, for example in psoriasis. As transcription factor, AhR controls the IL-22 production by several cell types (i.e. Th17 cells). Here, we analyzed the role of Ahr in IL-22 production by immune cells in the inflamed skin, using an imiquimod-induced psoriasis mouse model. Our results indicate that IL-22 is expressed in the ear of imiquimod-treated Ahr(-/-) mice but less than in wild-type mice. We then studied the role of AhR on three cell populations known to produce IL-22 in the skin: γδ T cells, Th17 cells, and ILC3, and a novel IL-22-producing cell type identified in this setting: CD4(-) CD8(-) TCRβ(+) T cells. We showed that AhR is required for IL-22 production by Th17, but not by the three other cell types, in the imiquimod-treated ears. Moreover, AhR has a role in the recruitment of γδ T cells, ILC3, and CD4(-) CD8(-) TCRβ(+) T cells into the inflamed skin or in their local proliferation. Taken together, AhR has a direct role in IL-22 production by Th17 cells in the mouse ear skin, but not by γδ T cells, CD4(-) CD8(-) TCRβ(+) T cells and ILCs.
MeSH term(s)	Aminoquinolines/adverse effects ; Animals ; Cell Proliferation ; Chemotaxis/genetics ; Chemotaxis/immunology ; Disease Models, Animal ; Imiquimod ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Interleukins/biosynthesis ; Interleukins/genetics ; Mice ; Mice, Knockout ; Psoriasis/etiology ; Psoriasis/metabolism ; Psoriasis/pathology ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Receptors, Antigen, T-Cell, gamma-delta/genetics ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Receptors, Aryl Hydrocarbon/deficiency ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Th17 Cells/immunology ; Th17 Cells/metabolism ; Interleukin-22
Chemical Substances	Aminoquinolines ; Interleukins ; Receptors, Antigen, T-Cell, alpha-beta ; Receptors, Antigen, T-Cell, gamma-delta ; Receptors, Aryl Hydrocarbon ; Imiquimod (P1QW714R7M)
Language	English
Publishing date	2016-03-21
Publishing country	Germany
Document type	Journal Article
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201546070
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Article ; Online: Dual TCR expression biases lung inflammation in DO11.10 transgenic mice and promotes neutrophilia via microbiota-induced Th17 differentiation.

Lemaire, Muriel M / Dumoutier, Laure / Warnier, Guy / Uyttenhove, Catherine / Van Snick, Jacques / de Heusch, Magali / Stevens, Monique / Renauld, Jean-Christophe

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 187, Issue 7, Page(s) 3530–3537

Abstract: A commonly used mouse model of asthma is based on i.p. sensitization to OVA together with aluminum hydroxide (alum). In wild-type BALB/c mice, subsequent aerosol challenge using this protein generates an eosinophilic inflammation associated with Th2 ... ...

Abstract	A commonly used mouse model of asthma is based on i.p. sensitization to OVA together with aluminum hydroxide (alum). In wild-type BALB/c mice, subsequent aerosol challenge using this protein generates an eosinophilic inflammation associated with Th2 cytokine expression. By constrast, in DO11.10 mice, which are transgenic for an OVA-specific TCR, the same treatment fails to induce eosinophilia, but instead promotes lung neutrophilia. In this study, we show that this neutrophilic infiltration results from increased IL-17A and IL-17F production, whereas the eosinophilic response could be restored upon blockade of IFN-γ, independently of the Th17 response. In addition, we identified a CD4(+) cell population specifically present in DO11.10 mice that mediates the same inflammatory response upon transfer into RAG2(-/-) mice. This population contained a significant proportion of cells expressing an additional endogenous TCR α-chain and was not present in RAG2(-/-) DO11.10 mice, suggesting dual antigenic specificities. This particular cell population expressed markers of memory cells, secreted high levels of IL-17A, and other cytokines after short-term restimulation in vitro, and triggered a neutrophilic response in vivo upon OVA aerosol challenge. The relative numbers of these dual TCR lymphocytes increased with the age of the animals, and IL-17 production was abolished if mice were treated with large-spectrum antibiotics, suggesting that their differentiation depends on foreign Ags provided by gut microflora. Taken together, our data indicate that dual TCR expression biases the OVA-specific response in DO11.10 mice by inhibiting eosinophilic responses via IFN-γ and promoting a neutrophilic inflammation via microbiota-induced Th17 differentiation.
MeSH term(s)	Adoptive Transfer ; Animals ; Cell Differentiation/immunology ; Cell Separation ; Chemotaxis, Leukocyte/immunology ; Flow Cytometry ; Interferon-gamma/biosynthesis ; Interleukin-17/biosynthesis ; Lymphocyte Activation/immunology ; Mice ; Mice, Transgenic ; Neutrophils/immunology ; Neutrophils/metabolism ; Neutrophils/microbiology ; Ovalbumin/immunology ; Pneumonia/immunology ; Pneumonia/metabolism ; Receptors, Antigen, T-Cell/immunology ; Reverse Transcriptase Polymerase Chain Reaction ; Th17 Cells/immunology ; Th17 Cells/metabolism ; Th17 Cells/microbiology
Chemical Substances	Interleukin-17 ; Receptors, Antigen, T-Cell ; Interferon-gamma (82115-62-6) ; Ovalbumin (9006-59-1)
Language	English
Publishing date	2011-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1101720
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: ALL-associated JAK1 mutations confer hypersensitivity to the antiproliferative effect of type I interferon.

Hornakova, Tekla / Chiaretti, Sabina / Lemaire, Muriel M / Foà, Robin / Ben Abdelali, Raouf / Asnafi, Vahid / Tartaglia, Marco / Renauld, Jean-Christophe / Knoops, Laurent

Blood

2010 Volume 115, Issue 16, Page(s) 3287–3295

Abstract: Activating mutations in JAK1 have been reported in acute lymphoblastic leukemias (ALLs). In this study, we found a type I interferon (IFN) transcriptional signature in JAK1 mutation-positive human ALL samples. This signature was recapitulated in vitro by ...

Abstract	Activating mutations in JAK1 have been reported in acute lymphoblastic leukemias (ALLs). In this study, we found a type I interferon (IFN) transcriptional signature in JAK1 mutation-positive human ALL samples. This signature was recapitulated in vitro by the expression of JAK1 mutants in BW5147 and BaF3 hematopoietic cell lines. Binding of JAK1 to the IFN receptor was essential because mutations in the FERM domain abrogated this effect. Beside the constitutive activation of the type I IFN signaling cascade, JAK1 mutations also strongly potentiated the response to IFN in vitro. Typically, the proliferation of cell lines expressing JAK1(A634D) was abrogated by type I IFNs. Interestingly, we found that different JAK1 mutations differentially potentiate responses to type I IFNs or to interleukin-9, another cytokine using JAK1 to mediate its effects. This suggests that the type of mutation influences the specificity of the effect on distinct cytokine receptor signaling. Finally, we also showed in an in vivo leukemia model that cells expressing JAK1(A634D) are hypersensitive to the antiproliferative and antitumorigenic effect of type I IFN, suggesting that type I IFNs should be considered as a potential therapy for ALL with JAK1-activating mutations.
MeSH term(s)	Animals ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Clinical Trials as Topic ; Female ; Gene Expression ; Humans ; Interferon Type I/immunology ; Interferon Type I/metabolism ; Interferon Type I/pharmacology ; Janus Kinase 1/genetics ; Janus Kinase 1/metabolism ; Mice ; Mice, Knockout ; Mutation ; Oligonucleotide Array Sequence Analysis ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/physiology ; Transcription, Genetic ; Transfection
Chemical Substances	Interferon Type I ; JAK1 protein, human (EC 2.7.10.2) ; Janus Kinase 1 (EC 2.7.10.2)
Language	English
Publishing date	2010-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2009-09-245498
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Uh III Zs.140: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Crystal structure of a soluble decoy receptor IL-22BP bound to interleukin-22.

de Moura, Patricia Ribeiro / Watanabe, Leandra / Bleicher, Lucas / Colau, Didier / Dumoutier, Laure / Lemaire, Muriel M / Renauld, Jean-Christophe / Polikarpov, Igor

FEBS letters

2009 Volume 583, Issue 7, Page(s) 1072–1077

Abstract: Interleukin-22 (IL-22) plays an important role in the regulation of immune and inflammatory responses in mammals. The IL-22 binding protein (IL-22BP), a soluble receptor that specifically binds IL-22, prevents the IL-22/interleukin-22 receptor 1 (IL-22R1) ...

Abstract	Interleukin-22 (IL-22) plays an important role in the regulation of immune and inflammatory responses in mammals. The IL-22 binding protein (IL-22BP), a soluble receptor that specifically binds IL-22, prevents the IL-22/interleukin-22 receptor 1 (IL-22R1)/interleukin-10 receptor 2 (IL-10R2) complex assembly and blocks IL-22 biological activity. Here we present the crystal structure of the IL-22/IL-22BP complex at 2.75 A resolution. The structure reveals IL-22BP residues critical for IL-22 binding, which were confirmed by site-directed mutagenesis and functional studies. Comparison of IL-22/IL-22BP and IL-22/IL-22R1 crystal structures shows that both receptors display an overlapping IL-22 binding surface, which is consistent with the inhibitory role played by IL-22 binding protein.
MeSH term(s)	Binding Sites/physiology ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Interleukin-10 Receptor beta Subunit/chemistry ; Interleukin-10 Receptor beta Subunit/genetics ; Interleukin-10 Receptor beta Subunit/metabolism ; Interleukins/chemistry ; Interleukins/genetics ; Interleukins/metabolism ; Mutagenesis, Site-Directed ; Protein Binding/physiology ; Protein Structure, Quaternary/physiology ; Receptors, Interleukin/chemistry ; Receptors, Interleukin/genetics ; Receptors, Interleukin/metabolism ; Interleukin-22
Chemical Substances	IL22RA2 protein, human ; Interleukin-10 Receptor beta Subunit ; Interleukins ; Receptors, Interleukin ; interleukin-22 receptor
Language	English
Publishing date	2009-03-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2009.03.006
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Article ; Online: IL-22 is required for imiquimod-induced psoriasiform skin inflammation in mice.

Van Belle, Astrid B / de Heusch, Magali / Lemaire, Muriel M / Hendrickx, Emilie / Warnier, Guy / Dunussi-Joannopoulos, Kyri / Fouser, Lynette A / Renauld, Jean-Christophe / Dumoutier, Laure

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 188, Issue 1, Page(s) 462–469

Abstract: Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. IL-22 is a cytokine produced by the TH1, TH17, and TH22 subsets that are functionally implicated in the ... ...

Abstract	Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. IL-22 is a cytokine produced by the TH1, TH17, and TH22 subsets that are functionally implicated in the psoriatic pathology. We assessed the role of IL-22 in a mouse model where psoriasiform skin inflammation is triggered by topical application of the TLR7/8 agonist imiquimod. At the macroscopic level, scaly skin lesions induced by daily applications of imiquimod in wild-type mice were almost totally absent in IL-22-deficient mice or in mice treated with a blocking anti-IL-22 Ab. At the microscopic level, IL-22-deficient mice showed a dramatic decrease in the development of pustules and a partial decrease in acanthosis. At the molecular level, the absence or inhibition of IL-22 strongly decreased the expression of chemotactic factors such as CCL3 and CXCL3 and of biomarkers such as S100A8, S100A7, and keratin 14, which reflect the antimicrobial and hyperproliferative responses of keratinocytes. IL-22 also played a major role in neutrophil infiltration after imiquimod treatment. IL-23 was required for IL-22 production, and γδ TCR lymphocytes represented the major source of IL-22 in lymph nodes from imiquimod-treated mice. However, T cells were not absolutely required for IL-22 production because imiquimod-induced IL-22 expression in the skin is still preserved in Rag2(-/-) mice. Taken together, our data show that IL-22 is required for psoriasis-like lesions in the mouse imiquimod model and is produced by both T cells and innate immune cells.
MeSH term(s)	Adjuvants, Immunologic/adverse effects ; Adjuvants, Immunologic/pharmacology ; Aminoquinolines/adverse effects ; Aminoquinolines/pharmacology ; Animals ; Antigens, Differentiation/genetics ; Antigens, Differentiation/immunology ; Antigens, Differentiation/metabolism ; Chemokine CCL3/genetics ; Chemokine CCL3/immunology ; Chemokine CCL3/metabolism ; Dermatitis/etiology ; Dermatitis/immunology ; Dermatitis/metabolism ; Disease Models, Animal ; Gene Expression Regulation/genetics ; Gene Expression Regulation/immunology ; Imiquimod ; Immunity, Innate/drug effects ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Interleukins/biosynthesis ; Interleukins/genetics ; Interleukins/immunology ; Mice ; Mice, Knockout ; Neutrophil Infiltration/drug effects ; Neutrophil Infiltration/genetics ; Neutrophil Infiltration/immunology ; Neutrophils/immunology ; Neutrophils/metabolism ; Neutrophils/pathology ; Psoriasis/chemically induced ; Psoriasis/immunology ; Psoriasis/metabolism ; Psoriasis/pathology ; Receptors, Antigen, T-Cell, gamma-delta/genetics ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Skin/immunology ; Skin/metabolism ; Skin/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology ; Interleukin-22
Chemical Substances	Adjuvants, Immunologic ; Aminoquinolines ; Antigens, Differentiation ; Ccl3 protein, mouse ; Chemokine CCL3 ; Interleukins ; Receptors, Antigen, T-Cell, gamma-delta ; Imiquimod (P1QW714R7M)
Language	English
Publishing date	2011-11-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1102224
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: IL-9 promotes IL-13-dependent paneth cell hyperplasia and up-regulation of innate immunity mediators in intestinal mucosa.

Steenwinckel, Valérie / Louahed, Jamila / Lemaire, Muriel M / Sommereyns, Caroline / Warnier, Guy / McKenzie, Andrew / Brombacher, Frank / Van Snick, Jacques / Renauld, Jean-Christophe

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 182, Issue 8, Page(s) 4737–4743

Abstract: IL-9 contributes to lung inflammatory processes such as asthma, by promoting mast cell differentiation, B cell activation, eosinophilia, and mucus production by lung epithelial cells. The observation that IL-9 overexpressing mice show increased mast cell ...

Abstract	IL-9 contributes to lung inflammatory processes such as asthma, by promoting mast cell differentiation, B cell activation, eosinophilia, and mucus production by lung epithelial cells. The observation that IL-9 overexpressing mice show increased mast cell numbers in the intestinal mucosa suggests that this cytokine might also play a role in intestinal inflammation. In colons from IL-9 transgenic mice, the expression of Muc2, a major intestinal mucin gene, was up-regulated, together with that of CLCA3 chloride channel and resistin like alpha, which are goblet cell-associated genes. Additional IL-9 up-regulated genes were identified and included innate immunity genes such as angiogenin 4 and the PLA2g2a phospholipase A(2), which are typical Paneth cell markers. Histochemical staining of Paneth cells by phloxine/tartrazine showed that IL-9 induces Paneth cell hyperplasia in Lieberkühn glands of the small intestine, and in the colonic mucosa, where this cell type is normally absent. Expression of Paneth cell markers, including angiogenin 4, PLA2g2a, and cryptdins, was induced in the colon of wild-type mice after two to four daily administrations of IL-9. By crossing IL-9 transgenic mice with IL-13(-/-) mice, or by injecting IL-9 into IL-4R(-/-) mice, we showed that IL-13 was required for the up-regulation of these Paneth cell-specific genes by IL-9. Taken together, our data indicate that Paneth cell hyperplasia and expression of their various antimicrobial products contribute to the immune response driven by TH2 cytokines, such as IL-9 and IL-13 in the intestinal mucosa.
MeSH term(s)	Animals ; Biomarkers ; Hyperplasia/genetics ; Hyperplasia/immunology ; Hyperplasia/metabolism ; Hyperplasia/pathology ; Immunity, Innate/immunology ; Interleukin-13/deficiency ; Interleukin-13/genetics ; Interleukin-13/immunology ; Interleukin-13/metabolism ; Interleukin-9/genetics ; Interleukin-9/immunology ; Interleukin-9/metabolism ; Intestinal Mucosa/immunology ; Kinetics ; Mice ; Mice, Knockout ; Paneth Cells/immunology ; Phospholipases A2/metabolism ; Ribonuclease, Pancreatic/metabolism ; Up-Regulation/immunology
Chemical Substances	Biomarkers ; Interleukin-13 ; Interleukin-9 ; Phospholipases A2 (EC 3.1.1.4) ; Ang4 protein, mouse (EC 3.1.27.5) ; Ribonuclease, Pancreatic (EC 3.1.27.5)
Language	English
Publishing date	2009-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.0801941
Database	MEDical Literature Analysis and Retrieval System OnLINE

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