Insights into IL‐29: Emerging role in inflammatory autoimmune diseases

Wang, Jia‐Min; Huang, An‐Fang; Xu, Wang‐Dong; Su, Lin‐Chong

doi:10.1111/jcmm.14697

Cited by 21 publications

(19 citation statements)

References 45 publications

(158 reference statements)

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“…Interleukin-29 (IL-29) is a newly identified inflammatory mediator belonging to a large IL-10 family. IL‐29 has emerged as a critical inflammation mediator in inflammatory autoimmune diseases [ 15 ]. A recent study shows that IL-29 plays a role in rheumatoid arthritis (RA) and is also involved in the pathogenesis of OA.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: The protective effects of Olmesartan against interleukin-29 (IL-29)-induced type 2 collagen degradation in human chondrocytes

Liu

et al. 2022

Bioengineered

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Osteoarthritis (OA) is a cartilage degenerative disease commonly observed in the elderly population and is pathologically characterized by the degradation of the cartilage extracellular matrix (ECM). Matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs) are critical enzymes involved in the degradation of ECM. Olmesartan is an inhibitor of the angiotensin II receptor developed for the treatment of hypertension, and recent studies show that it exerts anti-inflammatory effects in arthritis. The present study aimed to investigate the mechanism of the protective effect of Olmesartan on cartilage ECM degradation. Interleukin-29 (IL-29) is a novel inflammatory mediator involved in the inflammation and degradation of cartilage in OA, and human T/C-28a2 cells treated with it were the inflammatory model in vitro . We found that the degradation of type 2 collagens and aggrecans was induced by IL-29, accompanied by the upregulation of MMPs and ADAMTSs, but the presence of Olmesartan significantly ameliorated these increases. In addition, Olmesartan abolished IL-29- induced oxidative stress and elevated the expression level of TNF receptor-associated factor 6 (TRAF-6). Mechanistically, we showed that Olmesartan suppressed IL-29- caused inhibitor kappa B α (IκBα) expression and nuclear translocation of nuclear factor kappa-B (NF-κB) p65, indicating it suppressed the activation of the NF-κB pathway. Collectively, our data reveal that Olmesartan exerted a protective function on IL-29- induced type 2 collagen degradation in human chondrocytes.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: The protective effects of Olmesartan against interleukin-29 (IL-29)-induced type 2 collagen degradation in human chondrocytes

Liu

et al. 2022

Bioengineered

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“…35 Moreover, there is evidence that IL-29 also affects cell-mediated immunity, as it acts on monocytes, macrophages, dendritic cells, neutrophils and mast cells to modulate their secretory function. 36 For example, IL-29 stimulates monocytes to excrete IL-6, IL-10 and IL-8, 37 which is strongly associated with GD. 38 It has also been described in GD that intrathyroidal dendritic cells correlate positively with the serum TRAb concentration 39 and macrophages migrate into the thyroid.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, B lymphocytes (producing TRAb) are responsive to IL‐29 because they are able to enhance TLR7‐mediated B cell activation, which affects the function of both naive and memory B cells 35 . Moreover, there is evidence that IL‐29 also affects cell‐mediated immunity, as it acts on monocytes, macrophages, dendritic cells, neutrophils and mast cells to modulate their secretory function 36 . For example, IL‐29 stimulates monocytes to excrete IL‐6, IL‐10 and IL‐8, 37 which is strongly associated with GD 38 .…”

Section: Discussionmentioning

confidence: 99%

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Evaluation of interleukin‐29 in autoimmune and inflammatory thyroid diseases

Falkowski

Szczepanek‐Parulska

Krygier

et al. 2021

Clinical Endocrinology

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Interleukins play an important role in the development of autoimmune disorders. Interleukin-29, abbreviated IL-29, is also called interferon lambda 1, abbreviated IFN-λ1. This protein is quite a new member of the recently discovered interferon lambda (IFN-λ) family. IL-29 is known to play a strong antiviral role. 1 However, dendritic cells and macrophages produce IL-29 during a wide range of autoimmune disorders without any underlying viral infection during pathogenesis. 2 Elevated IL-29 concentrations were found in diseases with autoimmune aetiology, such as Sjögren's syndrome, rheumatoid arthritis, systemic sclerosis, systemic lupus erythematosus and psoriasis. [3][4][5][6][7] The concentration of IL-29 was also evaluated in atopic dermatitis and asthma, where elevated levels were detected. 8,9 Moreover, concentrations of IL-29 were

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“…IL-17A, alone or synergistically with TNF- α , induces the release of proinflammatory molecules from keratinocytes and enhances aberrant proliferation of keratinocytes leading to epidermal hyperplasia. Increased production of IL-26 and IL-29 by Th17 stimulate further release of proinflammatory mediators which recruit Th1 cells into psoriatic skin lesions [ 37 , 38 ]. Increased production of IL-17 results in increased secretion of IL-19, IL-22, and IL-36 which also contribute to the development of epidermal hyperplasia [ 39 , 40 ].…”

Section: Introductionmentioning

confidence: 99%

Psoriasis between Autoimmunity and Oxidative Stress: Changes Induced by Different Therapeutic Approaches

Medovic

Jakovljević

Živković

et al. 2022

Oxidative Medicine and Cellular Longevity

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Psoriasis is defined as chronic, immune-mediated disease. Regardless of the development of new therapeutic approaches, the precise etiology of psoriasis remains unknown and speculative. The aim of this review was to systematize the results of previous research on the role of oxidative stress and aberrant immune response in the pathogenesis of psoriasis, as well as the impact of certain therapeutic modalities on the oxidative status in patients with psoriasis. Complex immune pathways of both the innate and adaptive immune systems appear to be major pathomechanisms in the development of psoriasis. Oxidative stress represents another important contributor to the pathophysiology of disease, and the redox imbalance in psoriasis has been reported in skin cells and, systemically, in plasma and blood cells, and more recently, also in saliva. Current immune model of psoriasis begins with activation of immune system in susceptible person by some environmental factor and loss of immune tolerance to psoriasis autoantigens. Increased production of IL-17 appears to be the most prominent role in psoriasis pathogenesis, while IL-23 is recognized as master regulator in psoriasis having a specific role in cross bridging the production of IL-17 by innate and acquired immunity. Other proinflammatory cytokines, including IFN-γ, TNF-α, IL-1β, IL-6, IL-22, IL-26, IL-29, or IL-36, have also been reported to play important roles in the development of psoriasis. Oxidative stress can promote inflammation through several signaling pathways. The most noticeable and most powerful antioxidative effects exert various biologics compared to more convenient therapeutic modalities, such as methotrexate or phototherapy. The complex interaction of redox, immune, and inflammatory signaling pathways should be focused on further researches tackling the pathophysiology of psoriasis, while antioxidative supplementation could be the solution in some refractory cases of the disease.

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Insights into IL‐29: Emerging role in inflammatory autoimmune diseases

Cited by 21 publications

References 45 publications

RETRACTED ARTICLE: The protective effects of Olmesartan against interleukin-29 (IL-29)-induced type 2 collagen degradation in human chondrocytes

RETRACTED ARTICLE: The protective effects of Olmesartan against interleukin-29 (IL-29)-induced type 2 collagen degradation in human chondrocytes

Evaluation of interleukin‐29 in autoimmune and inflammatory thyroid diseases

Psoriasis between Autoimmunity and Oxidative Stress: Changes Induced by Different Therapeutic Approaches

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