Measurement of Interleukin-33 (IL-33) and IL-33 Receptors (sST2 and ST2L) in Patients with Rheumatoid Arthritis
The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its...
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Published in | Journal of Korean medical science Vol. 26; no. 9; pp. 1132 - 1139 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
The Korean Academy of Medical Sciences
01.09.2011
대한의학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1011-8934 1598-6357 1598-6357 |
DOI | 10.3346/jkms.2011.26.9.1132 |
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Abstract | The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA. |
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AbstractList | The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA.The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA. The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen–allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL,P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional diseasemodifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA. KCI Citation Count: 32 The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA. |
Author | Moon, Su-Jin Hong, Yeon-Sik Park, Sung-Hwan Kim, Ho-Youn Min, Jun-Ki Cho, Mi-La Jeon, Chan-Hong Ju, Ji Hyeon Joo, Young-Bin Oh, Hye-Jwa Heo, Yu-Jung |
AuthorAffiliation | 2 Department of Internal medicine, Soonchunhyang University College of Medicine, Bucheon, Korea 3 The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea 1 Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea |
AuthorAffiliation_xml | – name: 1 Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea – name: 2 Department of Internal medicine, Soonchunhyang University College of Medicine, Bucheon, Korea – name: 3 The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea |
Author_xml | – sequence: 1 givenname: Yeon-Sik surname: Hong fullname: Hong, Yeon-Sik organization: Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea – sequence: 2 givenname: Su-Jin surname: Moon fullname: Moon, Su-Jin organization: Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea – sequence: 3 givenname: Young-Bin surname: Joo fullname: Joo, Young-Bin organization: Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea – sequence: 4 givenname: Chan-Hong surname: Jeon fullname: Jeon, Chan-Hong organization: Department of Internal medicine, Soonchunhyang University College of Medicine, Bucheon, Korea – sequence: 5 givenname: Mi-La surname: Cho fullname: Cho, Mi-La organization: The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea – sequence: 6 givenname: Ji Hyeon surname: Ju fullname: Ju, Ji Hyeon organization: Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea – sequence: 7 givenname: Hye-Jwa surname: Oh fullname: Oh, Hye-Jwa organization: The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea – sequence: 8 givenname: Yu-Jung surname: Heo fullname: Heo, Yu-Jung organization: The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea – sequence: 9 givenname: Sung-Hwan surname: Park fullname: Park, Sung-Hwan organization: Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea – sequence: 10 givenname: Ho-Youn surname: Kim fullname: Kim, Ho-Youn organization: Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea – sequence: 11 givenname: Jun-Ki surname: Min fullname: Min, Jun-Ki organization: Division of Rheumatology, Department of Internal Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21935266$$D View this record in MEDLINE/PubMed https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART001586190$$DAccess content in National Research Foundation of Korea (NRF) |
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Keywords | Interleukin-33 sST2, ST2L Arthritis, Rheumatoid |
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Snippet | The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and... The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen–allergen response, autoimmunity and... |
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SubjectTerms | Adult Aged Antirheumatic Agents - therapeutic use Arthritis, Rheumatoid - blood Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - pathology C-Reactive Protein - analysis Female Humans Interleukin-1 Receptor-Like 1 Protein Interleukin-1beta - analysis Interleukin-1beta - blood Interleukin-33 Interleukin-6 - analysis Interleukin-6 - blood Interleukins - analysis Interleukins - blood Male Middle Aged Original Osteoarthritis - blood Osteoarthritis - pathology Receptors, Cell Surface - analysis Receptors, Cell Surface - blood Synovial Fluid - metabolism 의학일반 |
Title | Measurement of Interleukin-33 (IL-33) and IL-33 Receptors (sST2 and ST2L) in Patients with Rheumatoid Arthritis |
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