Different Features of Interleukin-37 and Interleukin-18 as Disease Activity Markers of Adult-onset Still’s Disease

Nam, Seoung Wan; Kang, Sang Mook; Lee, Jun Hyuk; Yoo, Dae Hyun

doi:10.21203/rs.3.rs-147805/v1

Cited by 3 publications

(2 citation statements)

References 32 publications

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“…100 Indeed, several studies have shown high levels of serum IL-18 in systemic forms of AoSD, so this cytokine has been proposed as a promising biomarker for the diagnosis of AoSD. [102][103][104][105]…”

Section: Interleukin-18 In Adult-onset Still Diseasementioning

confidence: 99%

“…IL‐18 is produced mainly by macrophages in an NLRP3 inflammasome‐dependent manner and further promotes immune cells to produce a large amount of proinflammatory cytokines, including IL‐6, IL‐8, IL‐17 and TNF‐α, thus contributing to the so‐called ‘cytokine storm’ in AoSD 100 . Indeed, several studies have shown high levels of serum IL‐18 in systemic forms of AoSD, so this cytokine has been proposed as a promising biomarker for the diagnosis of AoSD 102–105 …”

Section: Interleukin‐18 In Dermatological Diseasesmentioning

confidence: 99%

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Therapeutic potential of targeting interleukin‐1 family cytokines in chronic inflammatory skin diseases*

et al. 2022

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Summary The interleukin (IL)‐1 family of cytokines is a central regulator of a myriad of immunological responses. It comprises several cytokines, including those belonging to the IL‐1, IL‐36 and IL‐18 subfamilies, as well as IL‐33. The IL‐1 family primarily plays a role in orchestrating innate immune responses, but is also involved in adaptive immunity. Increased interest in the IL‐1 family occurred following the discovery that dysregulation of IL‐1 signalling underlies the pathogenesis of several monogenic autoinflammatory diseases, characterized by sterile inflammation involving the skin and other organs. This also provided increased understanding of the role of innate immunity and the IL‐1 family in polygenic autoinflammatory skin conditions, such as neutrophilic dermatoses, as well as in some of the most common chronic inflammatory skin diseases, such as psoriasis and hidradenitis suppurativa. Several therapeutic agents have been developed to inhibit the IL‐1 family members and their signalling pathways. These have shown therapeutic efficacy in several chronic inflammatory skin disorders. The aim of this review is to thoroughly describe the consequences of pathological dysregulation of the IL‐1, IL‐33, IL‐36 and IL‐18 pathways in dermatological conditions and to provide a forward‐looking update on therapeutic strategies targeting signalling by IL‐1 family cytokines.

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Section: Interleukin-18 In Adult-onset Still Diseasementioning

confidence: 99%

Section: Interleukin‐18 In Dermatological Diseasesmentioning

confidence: 99%

Therapeutic potential of targeting interleukin‐1 family cytokines in chronic inflammatory skin diseases*

et al. 2022

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Mast Cell Cytokines in Acute and Chronic Gingival Tissue Inflammation: Role of IL-33 and IL-37

Trimarchi

Lauritano

Ronconi

et al. 2022

IJMS

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Much evidence suggests autoimmunity in the etiopathogenesis of periodontal disease. In fact, in periodontitis, there is antibody production against collagen, DNA, and IgG, as well as increased IgA expression, T cell dysfunction, high expression of class II MHC molecules on the surface of gingival epithelial cells in inflamed tissues, activation of NK cells, and the generation of antibodies against the azurophil granules of polymorphonuclear leukocytes. In general, direct activation of autoreactive immune cells and production of TNF can activate neutrophils to release pro-inflammatory enzymes with tissue damage in the gingiva. Gingival inflammation and, in the most serious cases, periodontitis, are mainly due to the dysbiosis of the commensal oral microbiota that triggers the immune system. This inflammatory pathological state can affect the periodontal ligament, bone, and the entire gingival tissue. Oral tolerance can be abrogated by some cytokines produced by epithelial cells and activated immune cells, including mast cells (MCs). Periodontal cells and inflammatory–immune cells, including mast cells (MCs), produce cytokines and chemokines, mediating local inflammation of the gingival, along with destruction of the periodontal ligament and alveolar bone. Immune-cell activation and recruitment can be induced by inflammatory cytokines, such as IL-1, TNF, IL-33, and bacterial products, including lipopolysaccharide (LPS). IL-1 and IL-33 are pleiotropic cytokines from members of the IL-1 family, which mediate inflammation of MCs and contribute to many key features of periodontitis and other inflammatory disorders. IL-33 activates several immune cells, including lymphocytes, Th2 cells, and MCs in both innate and acquired immunological diseases. The classic therapies for periodontitis include non-surgical periodontal treatment, surgery, antibiotics, anti-inflammatory drugs, and surgery, which have been only partially effective. Recently, a natural cytokine, IL-37, a member of the IL-1 family and a suppressor of IL-1b, has received considerable attention for the treatment of inflammatory diseases. In this article, we report that IL-37 may be an important and effective therapeutic cytokine that may inhibit periodontal inflammation. The purpose of this paper is to study the relationship between MCs, IL-1, IL-33, and IL-37 inhibition in acute and chronic inflamed gingival tissue.

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Strategy and Challenges of Paraclinical Examinations in Adult-Onset Still’s Disease

Poursac

Odriozola

Truchetet

2022

JCM

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Adult-onset Still’s disease is a complex autoinflammatory disease with a multifactorial etiology. Its presentation is less stereotypical than that of a monogenic autoinflammatory disease and is actually relatively common with few specific signs. To avoid under- or over-prescription of complementary examinations, it is useful to advance in a structured manner, taking into consideration the actual added value of each supplemental examination. In this review, we detail the different complementary tests used in adult Still’s disease. We consider them from three different angles: positive diagnostic approach, the differential diagnosis, and the screening for complications of the disease. After discussing the various tests at our disposal, we look at the classical diagnostic strategy in order to propose a structured algorithm that can be used in clinical practice. We conclude with the prospects of new complementary examinations, which could in the future modify the management of patients.

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Different Features of Interleukin-37 and Interleukin-18 as Disease Activity Markers of Adult-onset Still’s Disease

Cited by 3 publications

References 32 publications

Therapeutic potential of targeting interleukin‐1 family cytokines in chronic inflammatory skin diseases*

Therapeutic potential of targeting interleukin‐1 family cytokines in chronic inflammatory skin diseases*

Mast Cell Cytokines in Acute and Chronic Gingival Tissue Inflammation: Role of IL-33 and IL-37

Strategy and Challenges of Paraclinical Examinations in Adult-Onset Still’s Disease

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