Interleukin 1beta and tumour necrosis factor alpha secreting cells are increased in the peripheral blood of patients with primary Sjogren's syndrome

Willeke, P.; Schotte, Heiko; Schlüter, B.; Erren, Michael; Becker, H; Dyong, A; Mickholz, E.; Domschke, Wolfram; Gaubitz, M.

doi:10.1136/ard.62.4.359

Cited by 40 publications

(31 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The decline in the chemoattractants was also coincided with the decrease of other cytokines, specifically GM-CSF, IL-3, TNF-α, and IFN-γ in female SjS s mice and only GM-CSF and IFN-γ in male SjS s mice. We and others have shown that IFN-γ and TNF-α can mediate epithelial cell apoptosis373839. Therefore, we sought to determine whether a decrease in these inflammatory cytokines by knocking out IL-17 would have an effect on gland cell death.…”

Section: Resultsmentioning

confidence: 99%

Sexual dimorphic function of IL-17 in salivary gland dysfunction of the C57BL/6.NOD-Aec1Aec2 model of Sjögren’s syndrome

Voigt

Esfandiary

Wanchoo

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Interleukin (IL)-17 is one of the critical inflammatory cytokines that plays a direct role in development of Sjögren’s syndrome (SjS), a systemic autoimmune disease characterized by a progressive chronic attack against the exocrine glands. The expression levels of IL-17 are correlated with a number of essential clinical parameters such as focus score and disease duration in human patients. Significantly immunological differences of Th17 cells were detected at the onset of clinical disease in female SjS mice compared to males. To further define the role of IL-17 in SjS and elucidate its involvement in the sexual dimorphism, we examined the systemic effect of IL-17 by genetically ablating Il-17 in the C57BL/6.NOD-Aec1Aec2, spontaneous SjS murine model. The results indicate that IL-17 is a potent inflammatory molecule in the induction of chemoattractants, cytokines, and glandular apoptosis in males and females. Elimination of IL-17 reduced sialadenitis more drastically in females than males. IL-17 is highly involved in modulating Th2 cytokines and altering autoantibody profiles which has a greater impact on changing plasma cells and germinal center B cell populations in females than males. The result supports a much more important role for IL-17 and demonstrates the sexual dimorphic function of IL-17 in SjS.

show abstract

Section: Resultsmentioning

confidence: 99%

Sexual dimorphic function of IL-17 in salivary gland dysfunction of the C57BL/6.NOD-Aec1Aec2 model of Sjögren’s syndrome

Voigt

Esfandiary

Wanchoo

et al. 2016

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Between the major proinflammatory cytokines found to be important in SS there is TNF-a. TNF-a, in combination with IFN-c, sensitizes epithelial salivary gland SS cells to apoptosis (Kamachi et al 2002;Kulkarni et al 2006), plays a role in the presentation of autoantigens as the nuclear antigens Ro, La, and alpha fodrin, recognized by autoantibodies in many SS patients (McArthur et al 2002) and high levels of TNF-a and TNF-a secreting cells have been found in peripheral blood and in lymphocytic infiltrates in salivary gland biopsies from patients with SS (Willeke et al 2003). In addition, TNF-a and its receptors are present in biopsies of healthy controls but are expressed at higher levels in SS patients (Koski et al 2001).…”

Section: Discussionmentioning

confidence: 95%

Expression of pro-inflammatory TACE-TNF-α-amphiregulin axis in Sjögren’s syndrome salivary glands

Sisto

Lisi

Lofrumento

et al. 2010

Histochem Cell Biol

View full text Add to dashboard Cite

The tumor-necrosis-factor-converting-enzyme (TACE)-TNF-α-Amphiregulin (AREG) axis plays an important pathogenic role in inflammatory and autoimmune disorders. However, the pathological roles of these proteins in the chronic autoimmune disease Sjögren's syndrome (SS) remain to be elucidated. It is known that the TACE-AREG axis is clearly part of a larger cascade of signals that starts with the activation of Furin, responsible for maturation of TACE that, in turn, determines the production of active TNF-α, directly involved in the up-regulation of AREG expression. This study showed that Furin, TACE, TNF-α, and AREG proteins, detected in acinar and ductal cells of human salivary glands from SS patients, increased remarkably in comparison with biopsies of labial salivary glands from healthy controls. The changes in Furin, TACE, TNF- α, and AREG proteins' level detected in salivary glands biopsies of SS patients could be responsible for pro-inflammatory cytokines overexpression characterizing Sjögren's syndrome.

show abstract

“…Our results are somehow different from those previously reported (Table 3). 6,16,21,[33][34][35][36][37] As stated by Hall et al 37 differences in assay methods, population origin and their health status, reagents, sample size, and monocyte numbers might all contribute to the differences observed among studies (Table 3). Our functional study was carried out in healthy homozygous individuals, who had not suffered from infection disease and were free of medication.…”

Section: Discussionmentioning

confidence: 97%

“…15 In addition, the number of IL-1b-secreting PBMC is significantly higher in pSS patients (mainly in those with recurrent parotid swelling) than in healthy controls. 16 Systemic lupus erythematosus (SLE) is characterized by the production of pathogenic autoantibodies, B-cell hyperactivation, and defective clearance of immune complexes, affecting several organs. Although the role of IL-1b in SLE has not been fully examined, there is evidence suggesting that IL-1 is crucial for the synthesis of IgG autoantibodies in these patients.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

Correa

Castiblanco

et al. 2004

Genes Immun

View full text Add to dashboard Cite

Interleukin-1 beta (IL-1b) exerts a range of inflammatory and immunomodulatory activities that are important in host defense and autoimmune response. The IL-1b gene, located on chromosome 2 (2q13), is polymorphic. The influence of its polymorphism on 355 patients with autoimmune rheumatic diseases was examined. To this effect, 172 patients with rheumatoid arthritis (RA), 114 with systemic lupus erythematosus (SLE), and 69 with primary Sjö gren's syndrome (pSS) were studied. The control group consisted of 392 matched healthy individuals. Genotyping of IL-1b single-nucleotide polymorphisms (SNPs) at positions À511 (C/T) and þ 3953 (C/T) was performed by the polymerase chain reaction-restriction fragment length polymorphism technique. In addition, levels of IL-1b were measured by immunoassay in supernatants of lipopolysaccharide (LPS)-stimulated and nonstimulated peripheral blood monocytes (PBM) obtained from 19 homozygous individuals for the three most common IL-1b likely haplotypes, all belonging to the control group. Allele þ 3953T was protective for SLE (odds ratio (OR) ¼ 0.57, 95% confidence intervals (CI) ¼ 0.34-0.88, P ¼ 0.01) as was the haplotype À511C þ 3953T (OR ¼ 0.43, 95%CI ¼ 0.25-0.74, pc ¼ 0.006). The latter was associated with a lower LPS-stimulated-PBM IL-1b secretion. Results suggest that IL-1b polymorphism influences the susceptibility to acquire SLE in our population. The protective association might be explained by the observed inhibitory effect of IL-1b þ 3953T allele on the secretion of IL-1b under inflammatory circumstances.

show abstract

Interleukin 1beta and tumour necrosis factor alpha secreting cells are increased in the peripheral blood of patients with primary Sjogren's syndrome

Cited by 40 publications

References 9 publications

Sexual dimorphic function of IL-17 in salivary gland dysfunction of the C57BL/6.NOD-Aec1Aec2 model of Sjögren’s syndrome

Sexual dimorphic function of IL-17 in salivary gland dysfunction of the C57BL/6.NOD-Aec1Aec2 model of Sjögren’s syndrome

Expression of pro-inflammatory TACE-TNF-α-amphiregulin axis in Sjögren’s syndrome salivary glands

Interleukin-1β polymorphisms in Colombian patients with autoimmune rheumatic diseases

Contact Info

Product

Resources

About