Sjögren's syndrome

Delaleu, Nicolas; Jönsson, Roland; Koller, Markus

doi:10.1111/j.1600-0722.2004.00183.x

Cited by 142 publications

(107 citation statements)

References 140 publications

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“…In the present study, we asked whether the Th17/IL-23 system, involving both of the cytokines IL-23 and IL-17, is important in the development of Sjögren's syndrome (SS), an autoimmune disease characterized primarily by destruction of acinar tissue within the salivary and lacrimal glands (14)(15)(16)(17)(18)(19)(20)(21)(22)(23). Using an animal model of SS, we were able to investigate the temporal appearance of both IL-17-and IL-23-positive cells in the targeted glandular tissues, as well as the correlation between these cell populations and the presence of lymphocytic foci.…”

Section: Conclusion These Results Suggest That the Th17/ Il-23 Systementioning

confidence: 99%

Salivary gland tissue expression of interleukin‐23 and interleukin‐17 in Sjögren's syndrome: Findings in humans and mice

Nguyen

et al. 2008

Arthritis & Rheumatism

264

228

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Objective. Recently, the Th1/Th2 paradigm has been expanded by the discovery of Th17 cells, a subset of CD4؉ memory T cells characterized by their unique ability to secrete interleukin-17 (IL-17) family cytokines. Importantly, Th17 cells appear to be intimately involved in autoimmunity. We undertook the present study to investigate whether the Th17/IL-23 system is up-regulated in Sjögren's syndrome (SS).Methods. Sera, saliva, and salivary glands from C57BL/6.NOD-Aec1Aec2 mice (a model for primary SS), as well as sera, saliva, and salivary gland biopsy specimens obtained from patients with primary SS, were evaluated for IL-17 and IL-23 expression by immunohistochemistry, real-time polymerase chain reaction, and the Luminex system.Results. Immunohistochemical stainings of submandibular glands from C57BL/6.NOD-Aec1Aec2 mice and of salivary gland biopsy specimens from SS patients revealed strong positive staining for both IL-17 and IL-23 within lymphocytic foci and diffuse staining on epithelial tissues. Temporal expression of IL-17 and IL-23 in submandibular glands of C57BL/6.NODAec1Aec2 mice correlated with expression of retinoic acid-related orphan receptor ␥t, the Th17 cell master control gene. While IL-17 could not be detected in saliva from 4-20-week-old C57BL/6.NOD-Aec1Aec2 mice, this cytokine was present in the blood of mice up to age 16 weeks. This contrasted with sera and saliva from SS patients, in which IL-17 and IL-6 were present at varying levels.Conclusion. These results suggest that the Th17/ IL-23 system is up-regulated in C57BL/6.NOD-Aec1Aec2 mice and SS patients at the time of disease. A correlation between up-regulated IL-17/IL-23 expression and specific clinical manifestations of SS has yet to be identified.

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Section: Conclusion These Results Suggest That the Th17/ Il-23 Systementioning

confidence: 99%

Salivary gland tissue expression of interleukin‐23 and interleukin‐17 in Sjögren's syndrome: Findings in humans and mice

Nguyen

et al. 2008

Arthritis & Rheumatism

264

228

View full text Add to dashboard Cite

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“…Onset of clinical symptoms of SjS is highly dependent on the activity of B lymphocytes, including the well-documented hyperreactivity of B cells, extreme hypergammaglobulinemia, production of numerous autoantibodies, and eventually glandular dysfunction (1,2,(5)(6)(7)(8)(9)(10)(11)(12). One mechanism known to control survival, activation, and proliferation of B cells is through cross-linking of their Ag receptors (BCR) and their coreceptors, especially CD19 and CD21.…”

Section: S Jögren's Syndrome (Sjs)mentioning

confidence: 99%

Development of Sjögren’s Syndrome in Nonobese Diabetic-Derived Autoimmune-Prone C57BL/6.NOD-Aec1Aec2 Mice Is Dependent on Complement Component-3

Nguyen

Kim

Cornelius

et al. 2007

The Journal of Immunology

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The role of complement in the etiology of Sjögren’s syndrome (SjS), a human autoimmune disease manifested primarily by salivary and lacrimal gland dysfunction resulting in dry mouth/dry eye syndrome, remains ill-defined. In the present study, we examined the role of complement component-3 (C3) using a newly constructed C3-gene knockout mouse, C57BL/6.NOD-Aec1Aec2.C3−/−. Inactivation of C3 in the parental C57BL/6.NOD-Aec1Aec2 strain, a model of primary SjS, resulted in a diminished or total absence of both preclinical and clinical manifestations during development and onset of disease, including reduced acinar cell apoptosis, reduced levels of caspase-3, lack of leukocyte infiltration of submandibular glands, reduced synthesis of disease-associated autoantibodies, maintenance of normal glandular architecture, and retention of normal saliva secretion. In addition, C57BL/6-NOD.Aec1Aec2.C3−/− mice did not exhibit increased numbers of marginal zone B cells, a feature of SjS-prone C57BL/6-NOD.Aec1Aec2 mice. Interestingly, C57BL/6-NOD.Aec1Aec2.C3−/− mice retained some early pathological manifestations, including activation of serine kinases with proteolytic activity for parotid secretory protein. This improvement in the clinical manifestations of SjS-like disease in C57BL/6.NOD-Aec1Aec2.C3−/− mice, apparently a direct consequence of C3 deficiency, supports a much more important role for complement in the adaptive autoimmune response than previously recognized, possibly implicating an essential role for innate immunity.

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“…[1][2][3] Dependendo dos critérios de classificação apresenta uma prevalên-cia na população adulta entre 0,5 a 3%, considerando-se como uma das patologias auto-imunes mais comuns. 4 Como consequência da xerostomia/hipossialia, a susceptibilidade a doenças orais encontra-se aumentada e a utilização de prótese removível poderá estar condicionada. [5][6][7][8] Por conseguinte, a saúde oral pode revelar-se como um fator influenciador da qualidade de vida destes doentes.…”

Section: Introductionunclassified