IL-38 serum levels in patients with Behcet’s disease and the relationship with clinical features

Zarrabi, Maryam; Gholijani, Nasser; Shenavandeh, Saeedeh; Aflaki, Elham; Amirghofran, Zahra

doi:10.1684/ecn.2019.0430

Cited by 17 publications

(3 citation statements)

References 42 publications

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“…This conclusion, however, is at odds with previous studies that claim inflammatory diseases like RA [29] and SLE [30] are marked by a high expression of the cytokine IL-38. Patients with Behçet's disease had lower serum IL-38 concentrations, according to Maryam et al [31]. It is possible that variations in the pathophysiology of various diseases contribute to the variances in IL-38 concentrations in AIH and other autoimmune diseases.…”

Section: Discussionmentioning

confidence: 93%

Serum Level and Genetic Polymorphism of IL-38 and IL-40 in Autoimmune Thyroid Disease

Abed

Abdulmalek

Yaaqoob

et al. 2023

Iraqi Journal of Science

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Autoimmune thyroid disease mainly includes Graves’ disease (GD) and autoimmune hypothyroidism (AIH), which is caused by individual genetics, autoimmune dysfunction, and a variety of external environmental factors. Interleukin IL-38 and IL- 40 are involved in a wide range of autoimmune diseases, but little is known about IL-38 and IL-40 expression in autoimmune thyroid disease. This research included 82 female patients with Graves' disease (GD), 78 females with autoimmune hypothyroidism (AIH), and 85 female healthy controls (HC). An enzyme linked immunosorbent assay and sequencing of IL-38 and IL-40 were used to evaluate serum levels and gene polymorphism, respectively. Results showed that significantly lower level of serum IL-38 levels in the GD and AIH groups in comparison with HC group (both p 0.0001). While there were highly significant differences in the GD and AIH groups than in the HC population (both p 0.0001). There was a significant variability in genotype and allele frequencies in the promoter region of IL-38 and IL-40 genes between patients with thyroid disease and healthy controls. The IL-38 homozygote genotype GG exhibits a substantial correlation with GD (P=0.000). While the CC genotype of IL-40 was shown to have a significant correlation with AIH. The findings suggest that serum concentrations of IL-38 and IL-40 are potential novel diagnostic biomarkers in patients with GD and AIH, and that the homozygotes GG and CC of IL-38 and IL-40, respectively, serve as a potential predisposing factor on GD and AIH development in the Iraqi population.

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Section: Discussionmentioning

confidence: 93%

Serum Level and Genetic Polymorphism of IL-38 and IL-40 in Autoimmune Thyroid Disease

Abed

Abdulmalek

Yaaqoob

et al. 2023

Iraqi Journal of Science

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“…8 Nevertheless, many studies have reported that IL-38 has an unpredictable inflammatory role in infections 9,10 and autoimmune diseases. [11][12][13] IL-38-mediated LPS stimulation increased cytokine production. 14,15 Some studies have revealed that IL-38 has multiple functions depending on its forms: full-length (amino acid 1-152) or truncated forms (amino acid 20-152).…”

Section: Introductionmentioning

confidence: 93%

“…IL‐38 is a recently discovered inflammatory factor of the IL‐1 family and was deemed to be an IL‐1 receptor antagonist (IL‐1Ra) because of its 41% homology with IL‐1Ra 8 . Nevertheless, many studies have reported that IL‐38 has an unpredictable inflammatory role in infections 9,10 and autoimmune diseases 11–13 . IL‐38‐mediated LPS stimulation increased cytokine production 14,15 .…”

Section: Introductionmentioning

confidence: 99%

Whether full‐length IL‐38 acts as a promoter or inhibitor in activating rheumatoid arthritis fibroblast‐like synoviocytes depends on IL‐1β

Ding,

Shao,

Liu

et al. 2024

Int J of Rheum Dis

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AimIL‐38 is a recently discovered inflammatory factor that belongs to the IL‐1 family and has full‐length and truncated forms. Clinical findings demonstrated that serum IL‐38 levels in people with infectious and autoimmune diseases are significantly different from those in healthy people, but the form remains unclear. We are keenly interested in learning more about the regulatory role of full‐length IL‐38 in rheumatoid arthritis (RA), a classic autoimmune disease.MethodsRA‐fibroblast‐like synoviocytes (RA‐FLS) were isolated from six RA patients and stimulated with full‐length IL‐38 to observe IL‐6 and IL‐8 secretion. Then, the migration and invasion functions of FLS were assessed. Next, the protein expressions of the MAPK, NF‐κB, and JAK pathways were evaluated. In addition, we examined the effect of full‐length IL‐38 on FLS functions in the presence of IL‐1β. The function of FLS affected by full‐length IL‐38 was also examined after blocking IL‐1 and IL‐36 receptors.ResultsThe functions of FLS were activated after the cells were stimulated with full‐length IL‐38. IL‐6 and IL‐8 levels increased with an increase in the full‐length IL‐38 concentration, and full‐length IL‐38 induced the acceleration of FLS migration and invasion functions. In addition, the levels of proteins in the MAPK signaling pathway increased after stimulation with full‐length IL‐38 and depended on its concentration. However, when the FLS were stimulated by IL‐38 and IL‐1β simultaneously, all experiments generated opposite results. Full‐length IL‐38 inhibited FLS function in the presence of IL‐1β. IL‐1R and IL‐36R blockers terminated all effects of full‐length IL‐38 on RA‐FLS.ConclusionFull‐length IL‐38 activates FLS functions and acts as a promoter in RA, whereas it inhibits FLS functions and acts as an inhibitor of RA in the presence of IL‐1β. The function of full‐length IL‐38 can be blocked by IL‐1Ra and IL‐36Ra.

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Adamantiades–Behçet Disease

Zouboulis

2024

Rook's Textbook of Dermatology

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Adamantiades–Behçet disease (ABD) is a rare, multisystem inflammatory disease of unknown aetiology, classified as a systemic vasculitis and as a neutrophilic dermatosis involving all types and sizes of blood vessels. A genetically determined background with environmental triggering factor(s) are probably involved. A chronic, relapsing, progressive course of oral aphthous ulcers, genital ulcers, skin lesions (papulopustules, erythema nodosum) and iridocyclitis/posterior uveitis is characteristic. ABD is occasionally accompanied by arthritis and vascular, neurological and gastrointestinal manifestations. ABD has a worldwide occurrence with varying prevalence, being endemic in eastern and central Asian and the eastern Mediterranean countries. Characteristic histopathological features of ABD are vasculitis and thrombosis. ABD is not considered contagious. There is no specific mode of Mendelian transmission in ABD. The disease has potentially poor prognosis (especially in males with systemic presenting signs). HLA‐B51 and ERAP‐1 seem to be associated with a more severe prognosis. Immunological mechanisms are considered to play a major role in the pathogenesis of ABD. The disease has currently been classified among the autoinflammatory disorders. The endothelium seems to be the primary target. Diagnosis of ABD is based on clinical signs. The Revised International Criteria for Behçet's Disease provides the most accurate diagnosis. Ophthalmic and neurological sequelae are leading causes of morbidity, followed by severe vascular and gastrointestinal manifestations. Their effects on morbidity may be cumulative. The clinical course of ABD is variable. A multidisciplinary approach in the management of ABD patients is mandatory. The choice of treatment depends on the site and severity of the clinical manifestations of the disease.

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IL-38 serum levels in patients with Behcet’s disease and the relationship with clinical features

Cited by 17 publications

References 42 publications

Serum Level and Genetic Polymorphism of IL-38 and IL-40 in Autoimmune Thyroid Disease

Serum Level and Genetic Polymorphism of IL-38 and IL-40 in Autoimmune Thyroid Disease

Whether full‐length IL‐38 acts as a promoter or inhibitor in activating rheumatoid arthritis fibroblast‐like synoviocytes depends on IL‐1β

Adamantiades–Behçet Disease

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