Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis
Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. I...
| Autor principal: | Manfredo Vieira, Silvio |
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| Outros Autores: | Cunha, Thiago Mattar, França, Rafael Freitas de Oliveira, Pinto, Larissa Garcia, Talbot, Jhimmy, Turato, Walter Miguel, Lemos, Henrique Paula, Lima, Jonilson Berlink, Verri, Waldiceu A., Almeida, Sërgio C.L., Ferreira, Seérgio Henrique, Louzada-Jünior, Paulo, Zamboni, Darío Simões, Cunha, Fernando Queiroz |
| Grau: | Artigo |
| Idioma: | English |
| Publicado em: |
Journal of Immunology
2020
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| Acesso em linha: |
https://repositorio.inpa.gov.br/handle/1/16128 |
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oai:repositorio:1-16128 |
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oai:repositorio:1-16128 Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis Manfredo Vieira, Silvio Cunha, Thiago Mattar França, Rafael Freitas de Oliveira Pinto, Larissa Garcia Talbot, Jhimmy Turato, Walter Miguel Lemos, Henrique Paula Lima, Jonilson Berlink Verri, Waldiceu A. Almeida, Sërgio C.L. Ferreira, Seérgio Henrique Louzada-Jünior, Paulo Zamboni, Darío Simões Cunha, Fernando Queiroz Caspase Recruitment Domain Protein 15 Caspase Recruitment Domain Protein 4 Cd4 Antigen Cxcl1 Chemokine Interleukin-17 Interleukin-1beta Interleukin-23 Interleukin-6 Proteoglycan Receptor Interacting Protein Serine Threonine Kinase 2 Tumor Necrosis Factor Animals Cell Animals Experiment Animals Model Animals Tissue Arthritis Cartilage Degeneration Controlled Study Enzyme Activity Enzyme-linked Immunosorbent Assay Enzyme Regulation Histopathology Immune Response Mouse Neutrophil Nociception Nonhuman Priority Journal Protein Expression Protein Function Reverse Transcription Polymerase Chain Reaction Arthritis, Rheumatoid Signal Transduction Synovium Animal Arthritis, Experimental Cattle Cells, Cultured Interleukin-17 Knee Joint Mice Mice, Inbred C57bl Mice, Knockout Nod1 Signaling Adaptor Protein Nod2 Signaling Adaptor Protein Receptor-interacting Protein Serine-threonine Kinases Serum Albumin, Bovine Signal Transduction Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. In this study, we evaluated the role of NOD1 and NOD2 on development of experimental arthritis. Ag-induced arthritis was generated in wild-type, NOD1 -/-, NOD2 -/-, or receptor-interacting serine-threonine kinase 2 -/- (RIPK2 -/-) immunized mice challenged intra-articularly with methylated BSA. Nociception was determined by electronic Von Frey test. Neutrophil recruitment and histopathological analysis of proteoglycan lost was evaluated in inflamed joints. Joint levels of inflammatory cytokine/chemokine were measured by ELISA. Cytokine (IL-6 and IL-23) and NOD2 expressions were determined in mice synovial tissue by RT-PCR. The NOD2 -/- and RIPK2 -/-, but not NOD1 -/-, mice are protected from Ag-induced arthritis, which was characterized by a reduction in neutrophil recruitment, nociception, and cartilage degradation. NOD2/RIPK2 signaling impairment was associated with a reduction in proinflammatory cytokines and chemokines (TNF, IL-1b, and CXCL1/KC). IL-17 and IL-17 triggering cytokines (IL-6 and IL-23) were also reduced in the joint, but there is no difference in the percentage of CD4 + IL-17 + cells in the lymph node between arthritic wild-type and NOD2 -/- mice. Altogether, these findings point to a pivotal role of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17-dependent joint immune response. Therefore, we could propose that NOD2 signaling is a target for the development of new therapies for the control of rheumatoid arthritis. Copyright © 2012 by The American Association of Immunologists, Inc. 2020-05-24T22:15:12Z 2020-05-24T22:15:12Z 2012 Artigo https://repositorio.inpa.gov.br/handle/1/16128 10.4049/jimmunol.1004190 en Volume 188, Número 10, Pags. 5116-5122 Attribution-NonCommercial-NoDerivs 3.0 Brazil http://creativecommons.org/licenses/by-nc-nd/3.0/br/ application/pdf Journal of Immunology |
| institution |
Instituto Nacional de Pesquisas da Amazônia - Repositório Institucional |
| collection |
INPA-RI |
| language |
English |
| topic |
Caspase Recruitment Domain Protein 15 Caspase Recruitment Domain Protein 4 Cd4 Antigen Cxcl1 Chemokine Interleukin-17 Interleukin-1beta Interleukin-23 Interleukin-6 Proteoglycan Receptor Interacting Protein Serine Threonine Kinase 2 Tumor Necrosis Factor Animals Cell Animals Experiment Animals Model Animals Tissue Arthritis Cartilage Degeneration Controlled Study Enzyme Activity Enzyme-linked Immunosorbent Assay Enzyme Regulation Histopathology Immune Response Mouse Neutrophil Nociception Nonhuman Priority Journal Protein Expression Protein Function Reverse Transcription Polymerase Chain Reaction Arthritis, Rheumatoid Signal Transduction Synovium Animal Arthritis, Experimental Cattle Cells, Cultured Interleukin-17 Knee Joint Mice Mice, Inbred C57bl Mice, Knockout Nod1 Signaling Adaptor Protein Nod2 Signaling Adaptor Protein Receptor-interacting Protein Serine-threonine Kinases Serum Albumin, Bovine Signal Transduction |
| spellingShingle |
Caspase Recruitment Domain Protein 15 Caspase Recruitment Domain Protein 4 Cd4 Antigen Cxcl1 Chemokine Interleukin-17 Interleukin-1beta Interleukin-23 Interleukin-6 Proteoglycan Receptor Interacting Protein Serine Threonine Kinase 2 Tumor Necrosis Factor Animals Cell Animals Experiment Animals Model Animals Tissue Arthritis Cartilage Degeneration Controlled Study Enzyme Activity Enzyme-linked Immunosorbent Assay Enzyme Regulation Histopathology Immune Response Mouse Neutrophil Nociception Nonhuman Priority Journal Protein Expression Protein Function Reverse Transcription Polymerase Chain Reaction Arthritis, Rheumatoid Signal Transduction Synovium Animal Arthritis, Experimental Cattle Cells, Cultured Interleukin-17 Knee Joint Mice Mice, Inbred C57bl Mice, Knockout Nod1 Signaling Adaptor Protein Nod2 Signaling Adaptor Protein Receptor-interacting Protein Serine-threonine Kinases Serum Albumin, Bovine Signal Transduction Manfredo Vieira, Silvio Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis |
| topic_facet |
Caspase Recruitment Domain Protein 15 Caspase Recruitment Domain Protein 4 Cd4 Antigen Cxcl1 Chemokine Interleukin-17 Interleukin-1beta Interleukin-23 Interleukin-6 Proteoglycan Receptor Interacting Protein Serine Threonine Kinase 2 Tumor Necrosis Factor Animals Cell Animals Experiment Animals Model Animals Tissue Arthritis Cartilage Degeneration Controlled Study Enzyme Activity Enzyme-linked Immunosorbent Assay Enzyme Regulation Histopathology Immune Response Mouse Neutrophil Nociception Nonhuman Priority Journal Protein Expression Protein Function Reverse Transcription Polymerase Chain Reaction Arthritis, Rheumatoid Signal Transduction Synovium Animal Arthritis, Experimental Cattle Cells, Cultured Interleukin-17 Knee Joint Mice Mice, Inbred C57bl Mice, Knockout Nod1 Signaling Adaptor Protein Nod2 Signaling Adaptor Protein Receptor-interacting Protein Serine-threonine Kinases Serum Albumin, Bovine Signal Transduction |
| description |
Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. In this study, we evaluated the role of NOD1 and NOD2 on development of experimental arthritis. Ag-induced arthritis was generated in wild-type, NOD1 -/-, NOD2 -/-, or receptor-interacting serine-threonine kinase 2 -/- (RIPK2 -/-) immunized mice challenged intra-articularly with methylated BSA. Nociception was determined by electronic Von Frey test. Neutrophil recruitment and histopathological analysis of proteoglycan lost was evaluated in inflamed joints. Joint levels of inflammatory cytokine/chemokine were measured by ELISA. Cytokine (IL-6 and IL-23) and NOD2 expressions were determined in mice synovial tissue by RT-PCR. The NOD2 -/- and RIPK2 -/-, but not NOD1 -/-, mice are protected from Ag-induced arthritis, which was characterized by a reduction in neutrophil recruitment, nociception, and cartilage degradation. NOD2/RIPK2 signaling impairment was associated with a reduction in proinflammatory cytokines and chemokines (TNF, IL-1b, and CXCL1/KC). IL-17 and IL-17 triggering cytokines (IL-6 and IL-23) were also reduced in the joint, but there is no difference in the percentage of CD4 + IL-17 + cells in the lymph node between arthritic wild-type and NOD2 -/- mice. Altogether, these findings point to a pivotal role of the NOD2/RIPK2 signaling in the onset of experimental arthritis by triggering an IL-17-dependent joint immune response. Therefore, we could propose that NOD2 signaling is a target for the development of new therapies for the control of rheumatoid arthritis. Copyright © 2012 by The American Association of Immunologists, Inc. |
| format |
Artigo |
| author |
Manfredo Vieira, Silvio |
| author2 |
Cunha, Thiago Mattar França, Rafael Freitas de Oliveira Pinto, Larissa Garcia Talbot, Jhimmy Turato, Walter Miguel Lemos, Henrique Paula Lima, Jonilson Berlink Verri, Waldiceu A. Almeida, Sërgio C.L. Ferreira, Seérgio Henrique Louzada-Jünior, Paulo Zamboni, Darío Simões Cunha, Fernando Queiroz |
| author2Str |
Cunha, Thiago Mattar França, Rafael Freitas de Oliveira Pinto, Larissa Garcia Talbot, Jhimmy Turato, Walter Miguel Lemos, Henrique Paula Lima, Jonilson Berlink Verri, Waldiceu A. Almeida, Sërgio C.L. Ferreira, Seérgio Henrique Louzada-Jünior, Paulo Zamboni, Darío Simões Cunha, Fernando Queiroz |
| title |
Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis |
| title_short |
Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis |
| title_full |
Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis |
| title_fullStr |
Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis |
| title_full_unstemmed |
Joint NOD2/RIPK2 signaling regulates IL-17 axis and contributes to the development of experimental arthritis |
| title_sort |
joint nod2/ripk2 signaling regulates il-17 axis and contributes to the development of experimental arthritis |
| publisher |
Journal of Immunology |
| publishDate |
2020 |
| url |
https://repositorio.inpa.gov.br/handle/1/16128 |
| _version_ |
1787143549114908672 |
| score |
11.675608 |