IL33 in rheumatoid arthritis: potential contribution to pathogenesis

Macedo, Rafaela Bicalho Viana; Kakehasi, Adriana María; Andrade, Marcus Vinícius Melo de

doi:10.1016/j.rbre.2016.03.009

Cited by 15 publications

(21 citation statements)

References 53 publications

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“…115 In addition to a role for IL-33 in the Th2 paradigm, there are also studies revealing a role for IL-33 in classic Th1 diseases such as inflammatory bowel disease 116 and rheumatoid arthritis. 117,118 IL-33 also increases the production of IFNγ. 119…”

Section: Nuclear Function Of Il-33mentioning

confidence: 95%

“…Another mechanism for the anti‐inflammatory properties of IL‐33 appears to be due to the requirement for IL‐1R8 . In addition to a role for IL‐33 in the Th2 paradigm, there are also studies revealing a role for IL‐33 in classic Th1 diseases such as inflammatory bowel disease and rheumatoid arthritis . IL‐33 also increases the production of IFN‐γ …”

Section: Il‐33mentioning

confidence: 99%

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Overview of the IL‐1 family in innate inflammation and acquired immunity

Dinarello

2017

Immunological Reviews

1,379

1,098

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Summary The interleukin-1 (IL-1) family of cytokines and receptors is unique in immunology because the IL-1 family and Toll-like receptor (TLR) families share similar functions. More than any other cytokine family, the IL-1 family is primarily associated with innate immunity. More than 95% of living organisms use innate immune mechanisms for survival whereas less than 5% depend on T-and B-cell functions. Innate immunity is manifested by inflammation, which can function as a mechanism of host defense but when uncontrolled is detrimental to survival. Each member of the IL-1 receptor and TLR family contains the cytoplasmic Toll-IL-1-Receptor (TIR) domain. The 50 amino acid TIR domains are highly homologous with the Toll protein in Drosophila. The TIR domain is nearly the same and present in each TLR and each IL-1 receptor family. Whereas IL-1 family cytokine members trigger innate inflammation via IL-1 family of receptors, TLRs trigger inflammation via bacteria, microbial products, viruses, nucleic acids, and damage-associated molecular patterns (DAMPs). In fact, IL-1 family member IL-1a and IL-33 also function as DAMPs. Although the inflammatory properties of the IL-1 family dominate in innate immunity, IL-1 family member can play a role in acquired immunity. This overview is a condensed update of the IL-1 family of cytokines and receptors.

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Section: Nuclear Function Of Il-33mentioning

confidence: 95%

Section: Il‐33mentioning

confidence: 99%

Overview of the IL‐1 family in innate inflammation and acquired immunity

Dinarello

2017

Immunological Reviews

1,379

1,098

View full text Add to dashboard Cite

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“…5,23 IL-33, mainly produced by airways epithelial cells, fibroblasts and endothelial cells as well as activated immune cells, 24 plays important roles in a range of autoimmune diseases. [25][26][27][28] In an attempt to link these findings, and in particular to provide a possible explanation for why lung function impairment and particularly alveolar damage may persist and progress despite apparent removal of the provoking stimulus, we hypothesized that the respiratory epithelial alarmin IL-33, known to be produced in response to inhaled environmental insults such as cigarette smoke, triggers a humoral autoimmune response directed against alveolar epithelial cells. Our aim was to explore whether antibodies can be induced in mice immunized with autologous (syngeneic) normal lung tissue while exposed to exogenous IL-33 delivered topically to the airways or systemically, and to examine their specificity in mice as well as their cross-specificity for human alveolar epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

“…It has also been shown that COPD is characterized by elevated production of the alarmin cytokine IL‐33, particularly with continued cigarette smoke exposure, to a degree that correlates with the rate of progression of the disease . IL‐33, mainly produced by airways epithelial cells, fibroblasts and endothelial cells as well as activated immune cells, plays important roles in a range of autoimmune diseases …”

Section: Introductionmentioning

confidence: 99%

IL‐33 induces production of autoantibody against autologous respiratory epithelial cells: a potential mechanism for the pathogenesis of COPD

Chen

et al. 2019

Immunology

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Summary The mechanisms underlying the chronic, progressive airways inflammation, remodelling and alveolar structural damage characteristic of human chronic obstructive pulmonary disease (COPD) remain unclear. In the present study, we address the hypothesis that these changes are at least in part mediated by respiratory epithelial alarmin (IL‐33)‐induced production of autoantibodies against airways epithelial cells. Mice immunized with homologous, syngeneic lung tissue lysate along with IL‐33 administered directly to the respiratory tract or systemically produced IgG autoantibodies binding predominantly to their own alveolar type II epithelial cells, along with increased percentages of Tfh cells and B2 B‐cells in their local, mediastinal lymph nodes. Consistent with its specificity for respiratory epithelial cells, this autoimmune inflammation was confined principally to the lung and not other organs such as the liver and kidney. Furthermore, the serum autoantibodies produced by the mice bound not only to murine, but also to human alveolar type II epithelial cells, suggesting specificity for common, cross‐species determinants. Finally, concentrations of antibodies against both human and murine alveolar epithelial cells were significantly elevated in the serum of patients with COPD compared with those of control subjects. These data are consistent with the hypothesis that IL‐33 contributes to the chronic, progressive airways obstruction, inflammation and alveolar destruction characteristic of phenotypes of COPD/emphysema through induction of autoantibodies against lung tissue, and particularly alveolar type II epithelial cells.

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“…Symmetry is a fundamental feature DOI 10.5935/2595-0118.20200003 ORIGINAL ARTICLE of the disease that evolves from asymmetric to symmetrical, with the progression of pathological manifestations. Initial inflammatory events affect the synovial membrane, presenting cellular hyperplasia and intense inflammatory process, denoting synovitis 2 . The synovial membrane has innervation marked by the presence of positive nerve fibers for proinflammatory neuropeptides, such as substance P (sP) and calcitonin gene-related peptide (CGRP), both in the intimal and subintimal layers and around the blood vessels 3 .…”

Section: Introductionmentioning

confidence: 99%

Low-level laser therapy in periarticular morphological aspects of the knee of Wistar rats in rheumatoid arthritis model

Neves¹,

Tavares²,

Retameiro³

et al. 2020

Brazilian Journal of Pain

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BACKGROUND AND OBJECTIVES: The deleterious effects of rheumatoid arthritis on periarticular tissues have not yet been fully elucidated. Therefore, the search for treatments that can modulate the inflammatory profile and tissue remodeling is pertinent. The present study evaluated the effects of low-level laser therapy (LLLT) on the morphology of periarticular tissues and synovial membrane of rats in a rheumatoid arthritis model. METHODS: Sixty-four male rats were divided into acute (7 days) and chronic (28 days) inflammatory periods, with four groups (n=8) each, being: CG (control group), LG (lesion group), CLaG (laser control group) and LLaG (laser lesion group). The animals of the lesion groups received two inoculations of Freund's Complete Adjuvant at a concentration of 50µL, the first at the base of the tail, and the second at the right knee. The animals in the control groups were injected with isotonic sodium chloride solution. The ClaG and LLaG were treated with 660nm LBI, 5J/cm 2 in the right knee. After the experimental period, the animals were euthanized, and the knees were processed for light microscopy. RESULTS: The CG and CLaG morphological analysis had normal aspects. The LG showed synovitis, femur, and tibia with changes in the periosteum, with inflammatory cells and bone modifications. In the LLaG, the synovial membrane showed signs of improvement. Bone tissue in the chronic period showed morphological aspects, denoting tissue remodeling. Low-level laser therapy in periarticular morphological aspects of the knee of Wistar rats in rheumatoid arthritis model Laser de baixa intensidade nos aspectos morfológicos periarticulares do joelho de ratos Wistar em modelo de artrite reumatoide

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IL33 in rheumatoid arthritis: potential contribution to pathogenesis

Cited by 15 publications

References 53 publications

Overview of the IL‐1 family in innate inflammation and acquired immunity

Overview of the IL‐1 family in innate inflammation and acquired immunity

IL‐33 induces production of autoantibody against autologous respiratory epithelial cells: a potential mechanism for the pathogenesis of COPD

Low-level laser therapy in periarticular morphological aspects of the knee of Wistar rats in rheumatoid arthritis model

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