T cell clones from a Sjögren’s syndrome salivary gland biopsy produce high levels of IL-10

Brookes, Sharon M.; Cohen, S. B. A.; Price, Elizabeth; Webb, Louise M. C.; Feldmann, Marc; Maini, R. N.; Venables, P. J. W.

doi:10.1046/j.1365-2249.1996.d01-623.x

Cited by 32 publications

(23 citation statements)

References 26 publications

(36 reference statements)

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“…One possible mechanism for autoimmune exocrinopathy is altered T helper differentiation and cytokine production (7). Interestingly, the pattern of cytokines we observe in PI3K-deficient CD4 ϩ T cells after Th2 polarization (increased IFN-␥ and IL-10, decreased IL-4) is similar to the unusual pattern observed in saliva and T cell clones from SS patients (21)(22)(23). IFN-␥ induces B cell activating factor of the TNF family (BAFF) and chemokine expression by salivary gland epithelial cells (24,25); this suggests that aberrant cytokine production may play a pivotal role in disease progression.…”

Section: Discussionsupporting

confidence: 82%

Sjögren's syndrome-like disease in mice with T cells lacking class 1A phosphoinositide-3-kinase

Oak

Deane

Kharas

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Sjögren's syndrome (SS) is an autoimmune disease that is characterized by infiltration of exocrine tissues, resulting in xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes). Here, we show that mice with T cell-specific loss of class IA phosphoinositide 3-kinase function develop organ-specific autoimmunity that resembles the human disease SS. Most mutant mice aged 3–8 months develop corneal opacity and eye lesions due to irritation and constant scratching. These mice display cardinal signs of primary SS such as marked lymphocytic infiltration of the lacrimal glands, antinuclear antibodies in the serum, and elevated titer of anti-SS-A antibody, in the absence of kidney pathology. Immunofluorescence studies show the presence of numerous CD4 + T cells with a smaller number of CD8 + T cells and B cells in the lacrimal glands. CD4 + T cells from these mice exhibit aberrant differentiation in vitro . These results indicate that aberrant T cells with impaired class IA phosphoinositide 3-kinase signaling can lead to organ-specific autoimmunity. In addition, the mouse model described here represents a tool to study the pathogenesis and treatment of SS.

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Section: Discussionsupporting

confidence: 82%

Sjögren's syndrome-like disease in mice with T cells lacking class 1A phosphoinositide-3-kinase

Oak

Deane

Kharas

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…These findings corroborate those of other studies in the literature, which also showed higher concentrations of inflammatory cytokines in the saliva of pSS patients. 10,34 Interestingly, Wu et al 35 reported that polymorphonuclear neutrophils exposed to the La antigen and anti-La autoantibodies present in autoimmune diseases such as pSS showed increased IL-8 production.…”

Section: Discussionmentioning

confidence: 99%

Effects of periodontal treatment on primary sjȫgren’s syndrome symptoms

et al. 2017

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“…CD30 expression and the pattern of cytokine production were then evaluated in clones generated by IL-2-expanded T cells from the joint. The experiments were performed with low concentrations of rIL-2 to avoid alterations in cytokine synthesis (47)(48)(49). Furthermore, because cytokine production may vary according to the different stage and/or activity of the disease and may be influenced by therapy (31, 46, 50 -52), our cloning experiments were performed in a patient with long-standing and in another subject with early, untreated, RA.…”

Section: Discussionmentioning

confidence: 99%

CD30+ T Cells in Rheumatoid Synovitis: Mechanisms of Recruitment and Functional Role

Gerli

Pitzalis

Bistoni

et al. 2000

The Journal of Immunology

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High serum levels of soluble CD30 (sCD30) have been reported to better predict the response to second line therapy in rheumatoid arthritis (RA). It is believed that sCD30 is released by CD30+ T cells present in the RA synovium. However, both the mechanism of recruitment to the joint and the functional role of this T cell subset in the pathogenesis of the disease remain unknown. This study confirmed higher levels of sCD30 in the serum and synovial fluid (SF) of RA patients compared with normal controls. However, analysis of mRNA and cell surface CD30 expression showed that CD30+ T cells are detectable in the SF, but not in the synovial membrane. In contrast, T cells expressing the CD30 transcript, but not the surface molecule, were found in the peripheral blood of both RA and normal controls. CD30 surface expression was up-regulated by adhesion and migration through endothelium in vitro and in a delayed-type hypersensitivity model in vivo. Although the great majority of fresh or cloned CD30+ T cells from SF produced both IFN-γ and IL-4, CD30 expression strictly correlated with IL-4 synthesis in synovial T cell clones. In addition, CD30+ T cell clones also produced high amounts of the anti-inflammatory cytokine IL-10. On this basis, we would like to propose that synovial CD30+ cells may play a role in the control of the inflammatory response. Serum sCD30 may reflect such cell activity and, therefore, explain the previously demonstrated correlation between high sCD30 serum levels and positive response to therapy.

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T cell clones from a Sjögren’s syndrome salivary gland biopsy produce high levels of IL-10

Cited by 32 publications

References 26 publications

Sjögren's syndrome-like disease in mice with T cells lacking class 1A phosphoinositide-3-kinase

Sjögren's syndrome-like disease in mice with T cells lacking class 1A phosphoinositide-3-kinase

Effects of periodontal treatment on primary sjȫgren’s syndrome symptoms

CD30+ T Cells in Rheumatoid Synovitis: Mechanisms of Recruitment and Functional Role

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