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Article ; Online: Allogeneic Chondrogenic Mesenchymal Stromal Cells Alter Helper T Cell Subsets in CD4+ Memory T Cells.

Kiernan, Caoimhe H / Asmawidjaja, Patrick S / Fahy, Niamh / Witte-Bouma, Janneke / Wolvius, Eppo B / Brama, Pieter A J / Lubberts, Erik / Farrell, Eric

Tissue engineering. Part A

2020 Volume 26, Issue 9-10, Page(s) 490–502

Abstract: Implantation of chondrogenically differentiated mesenchymal stromal cells (MSCs) leads to bone ... ...

Abstract	Implantation of chondrogenically differentiated mesenchymal stromal cells (MSCs) leads to bone formation
MeSH term(s)	CD4-Positive T-Lymphocytes/metabolism ; Cell Differentiation/physiology ; Cells, Cultured ; Chondrogenesis/genetics ; Chondrogenesis/physiology ; Coculture Techniques ; Humans ; Interleukin-6/metabolism ; Leukocytes, Mononuclear/cytology ; Leukocytes, Mononuclear/metabolism ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells/cytology ; Mesenchymal Stem Cells/metabolism ; T-Lymphocytes/cytology ; T-Lymphocytes/metabolism ; T-Lymphocytes, Helper-Inducer/metabolism
Chemical Substances	Interleukin-6
Language	English
Publishing date	2020-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2420582-5
ISSN	1937-335X ; 1937-3341
ISSN (online)	1937-335X
ISSN	1937-3341
DOI	10.1089/ten.TEA.2019.0177
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Article ; Online: IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation.

Razawy, Wida / Alves, Celso H / Koedam, Marijke / Asmawidjaja, Patrick S / Mus, Adriana M C / Oukka, Mohamed / Leenen, Pieter J M / Visser, Jenny A / van der Eerden, Bram C J / Lubberts, Erik

Scientific reports

2021 Volume 11, Issue 1, Page(s) 10244

Abstract: The IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the ... ...

Abstract	The IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the regulation of bone homeostasis remains elusive. Therefore, we studied the role of IL-23R signaling in physiological bone remodeling using IL-23R deficient mice. Using µCT, we demonstrate that 7-week-old IL-23R
MeSH term(s)	Animals ; Bone Density ; Bone Development ; Bone Remodeling ; Bone and Bones/metabolism ; Bone and Bones/physiology ; Cell Differentiation ; Cells, Cultured ; Female ; Femur/metabolism ; Gene Knock-In Techniques/methods ; Interleukin-23/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Osteogenesis/genetics ; Osteogenesis/physiology ; Receptors, Interleukin/deficiency ; Receptors, Interleukin/genetics ; Receptors, Interleukin/metabolism
Chemical Substances	Interleukin-23 ; Receptors, Interleukin ; interleukin-23 receptor, mouse
Language	English
Publishing date	2021-05-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-89625-2
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Article ; Online: CD4

Razawy, Wida / Asmawidjaja, Patrick S / Mus, Anne-Marie / Salioska, Nazike / Davelaar, Nadine / Kops, Nicole / Oukka, Mohamed / Alves, C Henrique / Lubberts, Erik

European journal of immunology

2019 Volume 50, Issue 2, Page(s) 245–255

Abstract: IL-23 plays an important role in the development of arthritis and the IL-23 receptor (IL-23R) is expressed on different types of T cells. However, it is not fully clear which IL- ... ...

Abstract	IL-23 plays an important role in the development of arthritis and the IL-23 receptor (IL-23R) is expressed on different types of T cells. However, it is not fully clear which IL-23R
MeSH term(s)	Adoptive Transfer/methods ; Animals ; Arthritis/immunology ; CD4-Positive T-Lymphocytes/immunology ; Disease Models, Animal ; Female ; Inflammation/immunology ; Interleukin-17/immunology ; Interleukin-23/immunology ; Lymphoid Tissue/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, CCR6/immunology ; Receptors, Interleukin/immunology ; Th17 Cells/immunology
Chemical Substances	CCR6 protein, mouse ; Interleukin-17 ; Interleukin-23 ; Receptors, Antigen, T-Cell, gamma-delta ; Receptors, CCR6 ; Receptors, Interleukin ; interleukin-23 receptor, mouse
Language	English
Publishing date	2019-11-28
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.201948112
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Article ; Online: 1,25(OH)

Dankers, Wendy / González-Leal, Claudia / Davelaar, Nadine / Asmawidjaja, Patrick S / Mus, Adriana M C / Hazes, Johanna M W / Colin, Edgar M / Lubberts, Erik

Arthritis research & therapy

2018 Volume 20, Issue 1, Page(s) 212

Abstract: Background: Despite recent improvements in the treatment of rheumatoid arthritis (RA), an insufficient treatment response and the development of treatment resistance in many patients illustrates the need for new therapeutic strategies. Chronic synovial ... ...

Abstract	Background: Despite recent improvements in the treatment of rheumatoid arthritis (RA), an insufficient treatment response and the development of treatment resistance in many patients illustrates the need for new therapeutic strategies. Chronic synovial inflammation could be suppressed by targeting RA synovial fibroblast (RASF) activation by, for example, interleukin (IL)-17A-producing CCR6 Methods: CCR6 Results: 1,25(OH) Conclusion: This study suggests that 1,25(OH)
MeSH term(s)	Calcitriol/administration & dosage ; Coculture Techniques ; Dexamethasone/administration & dosage ; Drug Synergism ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; Leukocytes, Mononuclear/drug effects ; Leukocytes, Mononuclear/metabolism ; Receptors, CCR6/biosynthesis ; Synovial Membrane/drug effects ; Synovial Membrane/metabolism ; T-Lymphocytes, Helper-Inducer/drug effects ; T-Lymphocytes, Helper-Inducer/metabolism ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	CCR6 protein, human ; Receptors, CCR6 ; Tumor Necrosis Factor-alpha ; Dexamethasone (7S5I7G3JQL) ; Calcitriol (FXC9231JVH)
Language	English
Publishing date	2018-09-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2107602-9
ISSN	1478-6362 ; 1478-6354
ISSN (online)	1478-6362
ISSN	1478-6354
DOI	10.1186/s13075-018-1706-9
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Article ; Online: Interleukin-17A Is Produced by CD4+ but Not CD8+ T Cells in Synovial Fluid Following T Cell Receptor Activation and Regulates Different Inflammatory Mediators Compared to Tumor Necrosis Factor in a Model of Psoriatic Arthritis Synovitis.

Xu, Xiaofei / Davelaar, Nadine / Mus, Anne-Marie / Asmawidjaja, Patrick S / Hazes, Johanna M W / Baeten, Dominique L P / Vis, Marijn / Bisoendial, Radjesh J / Prens, Errol P / Lubberts, Erik

Arthritis & rheumatology (Hoboken, N.J.)

2020 Volume 72, Issue 8, Page(s) 1303–1313

Abstract: Objective: Interleukin-17A (IL-17A) and tumor necrosis factor (TNF) contribute to the pathogenesis of psoriatic arthritis (PsA). However, their functional relationship in PsA synovitis has not been fully elucidated. Additionally, although CD8+ T cells ... ...

Abstract	Objective: Interleukin-17A (IL-17A) and tumor necrosis factor (TNF) contribute to the pathogenesis of psoriatic arthritis (PsA). However, their functional relationship in PsA synovitis has not been fully elucidated. Additionally, although CD8+ T cells in PsA have been recognized via flow cytometry as a source of IL-17A production, it is not clear whether CD8+ T cells secrete IL-17A under more physiologically relevant conditions in the context from PsA synovitis. This study was undertaken to clarify the roles of IL-17A and TNF in the synovial fluid (SF) from patients with PsA and investigate the impact of CD8+ T cells on IL-17A production. Methods: IL-17A+ T cells were identified by flow cytometry in SF samples from 20 patients with active PsA, blood samples from 22 treatment-naive patients with PsA, and blood samples from 22 healthy donors. IL-17A+ T cells were sorted from 12 PsA SF samples and stimulated using anti-CD3/anti-CD28 or phorbol myristate acetate (PMA) and ionomycin ex vivo, alone (n = 3) or together with autologous monocytes (n = 3) or PsA fibroblast-like synoviocytes (FLS) (n = 5-6). To evaluate the differential allogeneic effects of neutralizing IL-17A and TNF, SF CD4+ T cells and PsA FLS cocultures were also used (n = 5-6). Results: Flow cytometry analyses of SF samples from patients with PsA showed IL-17A positivity for CD4+ and CD8+ T cells (IL-17A, median 0.71% [interquartile range 0.35-1.50%] in CD4+ cells; median 0.44% [interquartile range 0.17-1.86%] in CD8+ T cells). However, only CD4+ T cells secreted IL-17A after anti-CD3/anti-CD28 activation, when cultured alone and in cocultures with PsA monocytes or PsA FLS (each P < 0.05). Remarkably, CD8+ T cells only secreted IL-17A after 4- or 72-hour stimulation with PMA/ionomycin. Anti-IL-17A and anti-TNF treatments both inhibited PsA synovitis ex vivo. Neutralizing IL-17A strongly inhibited IL-6 (P < 0.05) and IL-1β (P < 0.01), while anti-TNF treatment was more potent in reducing matrix metalloproteinase 3 (MMP-3) (P < 0.05) and MMP-13. Conclusion: CD8+ T cells, in contrast to CD4+ T cells, in SF specimens obtained from PsA patients did not secrete IL-17A following T cell receptor activation. Overlapping, but distinct, effects at the level of inflammatory cytokines and MMPs were found after neutralizing IL-17A or TNF ex vivo in a human model of PsA synovitis.
MeSH term(s)	Adult ; Arthritis, Psoriatic/drug therapy ; Arthritis, Psoriatic/immunology ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; Cell Culture Techniques ; Female ; Flow Cytometry ; Humans ; Inflammation Mediators/metabolism ; Interleukin-17/biosynthesis ; Ionomycin/pharmacology ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Male ; Receptors, Antigen, T-Cell/administration & dosage ; Receptors, Antigen, T-Cell/immunology ; Synovial Fluid ; Synoviocytes/drug effects ; Synoviocytes/immunology ; Synovitis/drug therapy ; Synovitis/immunology ; Tetradecanoylphorbol Acetate/pharmacology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	IL17A protein, human ; Inflammation Mediators ; Interleukin-17 ; Receptors, Antigen, T-Cell ; Tumor Necrosis Factor-alpha ; Ionomycin (56092-81-0) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2020-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.41271
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Article ; Online: JAK-inhibitor tofacitinib suppresses interferon alfa production by plasmacytoid dendritic cells and inhibits arthrogenic and antiviral effects of interferon alfa.

Boor, Patrick P C / de Ruiter, Petra E / Asmawidjaja, Patrick S / Lubberts, Erik / van der Laan, Luc J W / Kwekkeboom, Jaap

Translational research : the journal of laboratory and clinical medicine

2017 Volume 188, Page(s) 67–79

Abstract: Tofacitinib is an oral Janus kinase inhibitor that is effective for the treatment of rheumatoid arthritis and shows encouraging therapeutic effects in several other autoimmune diseases. A prominent adverse effect of tofacitinib therapy is the increased ... ...

Abstract	Tofacitinib is an oral Janus kinase inhibitor that is effective for the treatment of rheumatoid arthritis and shows encouraging therapeutic effects in several other autoimmune diseases. A prominent adverse effect of tofacitinib therapy is the increased risk of viral infections. Despite its advanced stage of clinical development, the modes of action that mediate the beneficial and adverse effects of tofacitinib in autoimmune diseases remain unclear. Interferon alfa (IFNα) produced by plasmacytoid dendritic cells (PDCs) is critically involved in the pathogenesis of many systemic autoimmune diseases and in immunity to viral infections. Using in vitro culture models with human cells, we studied the effects of tofacitinib on PDC survival and IFNα production, and on arthrogenic and antiviral effects of IFNα. Tofacitinib inhibited the expression of antiapoptotic BCL-A1 and BCL-XL in human PDC and induced PDC apoptosis. TLR7 stimulation upregulated the levels of antiapoptotic Bcl-2 family members and prevented the induction of PDC apoptosis by tofacitinib. However, tofacitinib robustly inhibited the production of IFNα by toll like receptor-stimulated PDC. In addition, tofacitinib profoundly suppressed IFNα-induced upregulation of TLR3 on synovial fibroblasts, thereby inhibiting their cytokine and protease production in response to TLR3 ligation. Finally, tofacitinib counteracted the suppressive effects of IFNα on viral replication. Tofacitinib inhibits PDC survival and IFNα production and suppresses arthrogenic and antiviral effects of IFNα signaling. Inhibition of the IFNα pathway at 2 levels may contribute to the beneficial effects of tofacitinib in autoimmune diseases and explain the increased viral infection rates observed during tofacitinib treatment.
MeSH term(s)	Apoptosis/physiology ; Cell Line, Tumor ; Dendritic Cells/drug effects ; Dendritic Cells/metabolism ; Dose-Response Relationship, Drug ; Gene Expression Regulation/drug effects ; Hepacivirus/physiology ; Humans ; Interferon-alpha/genetics ; Interferon-alpha/metabolism ; Interleukin-3/genetics ; Interleukin-3/metabolism ; Piperidines/administration & dosage ; Piperidines/pharmacology ; Protein Kinase Inhibitors/administration & dosage ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Pyrimidines/administration & dosage ; Pyrimidines/pharmacology ; Pyrroles/administration & dosage ; Pyrroles/pharmacology ; STAT Transcription Factors/genetics ; STAT Transcription Factors/metabolism ; Virus Replication
Chemical Substances	Interferon-alpha ; Interleukin-3 ; Piperidines ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins c-bcl-2 ; Pyrimidines ; Pyrroles ; STAT Transcription Factors ; tofacitinib (87LA6FU830)
Language	English
Publishing date	2017-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2016.11.006
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Article ; Online: Lack of IL-17 Receptor A signaling aggravates lymphoproliferation in C57BL/6 lpr mice.

Corneth, Odilia B J / Schaper, Fleur / Luk, Franka / Asmawidjaja, Patrick S / Mus, Adriana M C / Horst, Gerda / Heeringa, Peter / Hendriks, Rudi W / Westra, Johanna / Lubberts, Erik

Scientific reports

2019 Volume 9, Issue 1, Page(s) 4032

Abstract: Defects in Fas function correlate with susceptibility to systemic autoimmune diseases like autoimmune lymphoproliferative syndrome (ALPS) and systemic lupus erythematosus (SLE). C57BL/6 lpr (B6/lpr) mice are used as an animal model of ALPS and develop a ... ...

Abstract	Defects in Fas function correlate with susceptibility to systemic autoimmune diseases like autoimmune lymphoproliferative syndrome (ALPS) and systemic lupus erythematosus (SLE). C57BL/6 lpr (B6/lpr) mice are used as an animal model of ALPS and develop a mild SLE phenotype. Involvement of interleukin-17A (IL-17A) has been suggested in both phenotypes. Since IL-17 receptor A is part of the signaling pathway of many IL-17 family members we investigated the role of IL-17 receptor signaling in disease development in mice with a B6/lpr background. B6/lpr mice were crossed with IL-17 receptor A deficient (IL-17RA KO) mice and followed over time for disease development. IL-17RA KO/lpr mice presented with significantly enhanced lymphoproliferation compared with B6/lpr mice, which was characterized by dramatic lymphadenomegaly/splenomegaly and increased lymphocyte numbers, expansion of double-negative (DN) T-cells and enhanced plasma cell formation. However, the SLE phenotype was not enhanced, as anti-nuclear antibody (ANA) titers and induction of glomerulonephritis were not different. In contrast, levels of High Mobility Group Box 1 (HMGB1) and anti-HMGB1 autoantibodies were significantly increased in IL-17RA KO/lpr mice compared to B6/lpr mice. These data show that lack of IL-17RA signaling aggravates the lymphoproliferative phenotype in B6/lpr mice but does not affect the SLE phenotype.
MeSH term(s)	Animals ; Autoimmune Lymphoproliferative Syndrome/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Cell Proliferation ; HMGB1 Protein/metabolism ; Kidney/immunology ; Kidney/pathology ; Lupus Erythematosus, Systemic/immunology ; Lymph Nodes/immunology ; Lymph Nodes/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred MRL lpr ; Mice, Knockout ; Receptors, Interleukin-17/genetics ; Receptors, Interleukin-17/physiology ; Spleen/immunology ; Spleen/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
Chemical Substances	HMGB1 Protein ; HMGB1 protein, mouse ; Il17ra protein, mouse ; Receptors, Interleukin-17
Language	English
Publishing date	2019-03-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-39483-w
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Article ; Online: Enhanced Expression of Bruton's Tyrosine Kinase in B Cells Drives Systemic Autoimmunity by Disrupting T Cell Homeostasis.

Corneth, Odilia B J / de Bruijn, Marjolein J W / Rip, Jasper / Asmawidjaja, Patrick S / Kil, Laurens P / Hendriks, Rudi W

Journal of immunology (Baltimore, Md. : 1950)

2016 Volume 197, Issue 1, Page(s) 58–67

Abstract: Upon BCR stimulation, naive B cells increase protein levels of the key downstream signaling molecule Bruton's tyrosine kinase (BTK). Transgenic CD19-hBtk mice with B cell-specific BTK overexpression show spontaneous germinal center formation, anti- ... ...

Abstract	Upon BCR stimulation, naive B cells increase protein levels of the key downstream signaling molecule Bruton's tyrosine kinase (BTK). Transgenic CD19-hBtk mice with B cell-specific BTK overexpression show spontaneous germinal center formation, anti-nuclear autoantibodies, and systemic autoimmunity resembling lupus and Sjögren syndrome. However, it remains unknown how T cells are engaged in this pathology. In this study, we found that CD19-hBtk B cells were high in IL-6 and IL-10 and disrupted T cell homeostasis in vivo. CD19-hBtk B cells promoted IFN-γ production by T cells and expression of the immune-checkpoint protein ICOS on T cells and induced follicular Th cell differentiation. Crosses with CD40L-deficient mice revealed that increased IL-6 production and autoimmune pathology in CD19-hBtk mice was dependent on B-T cell interaction, whereas IL-10 production and IgM autoantibody formation were CD40L independent. Surprisingly, in Btk-overexpressing mice, naive B cells manifested increased CD86 expression, which was dependent on CD40L, suggesting that T cells interact with B cells in a very early stage of immune pathology. These findings indicate that increased BTK-mediated signaling in B cells involves a positive-feedback loop that establishes T cell-propagated autoimmune pathology, making BTK an attractive therapeutic target in autoimmune disease.
MeSH term(s)	Animals ; Antigens, CD19/genetics ; Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; Autoimmunity ; B-Lymphocytes/physiology ; CD40 Ligand/genetics ; CD40 Ligand/metabolism ; Cell Communication ; Homeostasis ; Humans ; Interferon-gamma/metabolism ; Interleukin-10/metabolism ; Interleukin-6/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mutation/genetics ; Promoter Regions, Genetic/genetics ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; T-Lymphocytes/immunology
Chemical Substances	Antigens, CD19 ; Interleukin-6 ; Interleukin-10 (130068-27-8) ; CD40 Ligand (147205-72-9) ; Interferon-gamma (82115-62-6) ; Agammaglobulinaemia tyrosine kinase (EC 2.7.10.1) ; Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2016-07-01
Publishing country	United States
Document type	Journal Article
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.1600208
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Article ; Online: IL-23 dependent and independent stages of experimental arthritis: no clinical effect of therapeutic IL-23p19 inhibition in collagen-induced arthritis.

Cornelissen, Ferry / Asmawidjaja, Patrick S / Mus, Adriana M C / Corneth, Odilia / Kikly, Kristine / Lubberts, Erik

PloS one

2013 Volume 8, Issue 2, Page(s) e57553

Abstract: IL-23p19 deficient mice have revealed a critical role of IL-23 in the development of experimental autoimmune diseases, such as collagen-induced arthritis (CIA). Neutralizing IL-23 after onset of CIA in rats has been shown to reduce paw volume, but the ... ...

Abstract	IL-23p19 deficient mice have revealed a critical role of IL-23 in the development of experimental autoimmune diseases, such as collagen-induced arthritis (CIA). Neutralizing IL-23 after onset of CIA in rats has been shown to reduce paw volume, but the effect on synovial inflammation and the immunological autoimmune response is not clear. In this study, we examined the role of IL-23 at different stages of CIA and during T cell memory mediated flare-up arthritis with focus on changes in B cell activity and Th1/Th17 modulation. Anti-IL-23p19 antibody (anti-IL23p19) treatment, starting 15 days after the type II collagen (CII)-immunization but before clinical signs of disease onset, significantly suppressed the severity of CIA. This was accompanied with significantly lower CII-specific IgG1 levels and lower IgG2a levels in the anti-IL-23p19 treated mice compared to the control group. Importantly, neutralizing IL-23 after the first signs of CIA did not ameliorate the disease. This was in contrast to arthritic mice that underwent an arthritis flare-up since a significantly lower disease score was observed in the IL-23p19 treated mice compared to the control group, accompanied by lower synovial IL-17A and IL-22 expression in the knee joints of these mice. These data show IL-23-dependent and IL-23-independent stages during autoimmune CIA. Furthermore, the memory T cell mediated flare-up arthritis is IL-23-mediated. These data suggest that specific neutralization of IL-23p19 after onset of autoimmune arthritis may not be beneficial as a therapeutic therapy for patients with rheumatoid arthritis (RA). However, T cell mediated arthritis relapses in patients with RA might be controlled by anti-IL-23p19 treatment.
MeSH term(s)	Animals ; Arthritis, Experimental/physiopathology ; Base Sequence ; CD4-Positive T-Lymphocytes/metabolism ; Collagen/toxicity ; DNA Primers ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Immunologic Memory ; Interleukin-23/biosynthesis ; Interleukin-23/immunology ; Interleukin-23/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Neutralization Tests ; Polymerase Chain Reaction
Chemical Substances	DNA Primers ; Interleukin-23 ; Collagen (9007-34-5)
Language	English
Publishing date	2013-02-28
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.0057553
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Article ; Online: IL-17/Th17 mediated synovial inflammation is IL-22 independent.

van Hamburg, Jan Piet / Corneth, Odilia B J / Paulissen, Sandra M J / Davelaar, Nadine / Asmawidjaja, Patrick S / Mus, Adriana M C / Lubberts, Erik

Annals of the rheumatic diseases

2013 Volume 72, Issue 10, Page(s) 1700–1707

Abstract: Background: Interleukin (IL)-17A and Th17 cells are critically involved in T cell-mediated synovial inflammation. Besides IL-17A, Th17 cells produce IL-22. Recently, Th22 cells were discovered, which produce IL-22 in the absence of IL-17. However, it ... ...

Abstract	Background: Interleukin (IL)-17A and Th17 cells are critically involved in T cell-mediated synovial inflammation. Besides IL-17A, Th17 cells produce IL-22. Recently, Th22 cells were discovered, which produce IL-22 in the absence of IL-17. However, it remains unclear whether IL-22 and Th22 cells contribute to T cell-mediated synovial inflammation. Therefore, we examined the potential of IL-22 and Th22 cells to induce synovial inflammation and whether IL-22 is required for T cell-mediated experimental arthritis. Methods: Peripheral and synovial Th17 and Th22 cells were identified and sorted from patients with rheumatoid arthritis (RA). Co-culture experiments of these primary T cell populations with RA synovial fibroblasts (RASF) were performed. The in vivo IL-22 contribution to synovial inflammation was investigated by inducing T cell-mediated arthritis in IL-22 deficient mice and wild-type mice. Results: Peripheral Th17 and Th22 cell populations were increased in patients with RA and present in RA synovial fluid. In T cell-RASF co-cultures, IL-22 in the presence of IL-17A had limited effects on IL-6, IL-8, matrix metalloproteinase-1 (MMP-1) and MMP-3 production. Furthermore, primary peripheral blood and synovial Th17 cells were more potent in the induction of these factors by RASF compared with Th22 cells. In line with this, similar synovial inflammation and disease severity was found between IL-22 deficient and wild-type mice in T cell-mediated experimental arthritis. Conclusions: These findings show that IL-17A/Th17 cell-mediated synovial inflammation is independent of IL-22 and Th22 cells. This implies that targeting IL-17A/Th17 cells, rather than IL-22/Th22 cells, should be the focus for treatment of T cell-mediated synovial inflammation.
MeSH term(s)	Adult ; Aged ; Animals ; Arthritis, Experimental/immunology ; Arthritis, Rheumatoid/immunology ; Coculture Techniques ; Female ; Humans ; Interleukin-17/biosynthesis ; Interleukin-17/immunology ; Interleukin-6/biosynthesis ; Interleukin-8/biosynthesis ; Interleukins/biosynthesis ; Interleukins/immunology ; Male ; Matrix Metalloproteinase 1/biosynthesis ; Matrix Metalloproteinase 3/biosynthesis ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Receptors, CCR6/analysis ; Synovitis/immunology ; Th17 Cells/immunology ; Up-Regulation/immunology ; Young Adult ; Interleukin-22
Chemical Substances	CCR6 protein, human ; IL17A protein, human ; Interleukin-17 ; Interleukin-6 ; Interleukin-8 ; Interleukins ; Receptors, CCR6 ; Matrix Metalloproteinase 3 (EC 3.4.24.17) ; Matrix Metalloproteinase 1 (EC 3.4.24.7)
Language	English
Publishing date	2013-01-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/annrheumdis-2012-202373
Database	MEDical Literature Analysis and Retrieval System OnLINE

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