Human rhinoviruses induce IL‐35‐producing Treg <i>via</i> induction of B7‐H1 (CD274) and sialoadhesin (CD169) on DC

Seyerl, Maria; Kirchberger, Stefanie; Majdic, Otto; Seipelt, Joachim; Jindra, Christoph; Schrauf, Catharina; Stöckl, Johannes

doi:10.1002/eji.200939527

Cited by 82 publications

(54 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Taking into account IL-35 is expressed in human regulatory T cells (Tregs) (Pflanz et al, 2006), it is deemed to characteristics of Treg cells. Previous study found IL-35 inhibit advancement of inflammatory diseases by suppressing the activity of effector T cells such as Th2 and Th17 (Collison et al, 2007;Collison et al, 2010;Kochetkova et al, 2010;Seyerl et al, 2010;Huang et al, 2011;Whitehead et al, 2012).…”

Section: Introductionmentioning

confidence: 94%

IL-35 Over-expression is Associated with Genesis of Gastric Cancer

Fan

Zhai²,

Wang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Overexpression of interleukin (IL)-35 has been found in a variety of malignancies, but the expression status in gastric cancer has yet to be elucidated clearly. In the present study, positive expression of EBI3 and p35 was 63.3% and 70.0% of cases, respectively. EBI3 expression was strongly related with larger tumor size and invasion depth (P <0.05). Similarly, expression of p35 was also correlated with larger tumor size (P <0.05). These results indicate that IL-35 might be involved in growth of gastric cancer. Interestingly, EBI3 and p35 expressions were positive correlated with Ki-67 expression. Moreover, EBI3 immunoreactivity was associated with Bcl-2 staining. Our data suggest IL-35 is correlated with genesis of gastric cancer by regulating growth and apoptosis.

show abstract

Section: Introductionmentioning

confidence: 94%

IL-35 Over-expression is Associated with Genesis of Gastric Cancer

Fan

Zhai²,

Wang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

show abstract

“…IL-35 expression has been thought to be specific to Tregs, because EBI3 is a downstream target of Foxp3 (35). However, according to recent reports, EBI3 is also expressed in other cell types, including intestinal epithelium and aortic smooth muscle cells (36,37).…”

Section: Discussionmentioning

confidence: 99%

EBI3 Downregulation Contributes to Type I Collagen Overexpression in Scleroderma Skin

Kudo

Wang

Jinnin

et al. 2015

The Journal of Immunology

View full text Add to dashboard Cite

IL-12 family cytokines are implicated in the pathogenesis of various autoimmune diseases, but their role in the regulation of extracellular matrix expression and its contribution to the phenotype of systemic sclerosis (SSc) remain to be elucidated. Among the IL-12 family members, IL-35 decreases type I collagen expression in cultured dermal fibroblasts. IL-35 consists of p35 and EBI3 subunits, and EBI3 alone could downregulate the protein and mRNA expression of type I or type III collagen in the presence or absence of TGF-β costimulation. We found that collagen mRNA stability was reduced by EBI3 via the induction of miR-4500. The IL-35 levels in the sera or on the surface of T cells were not altered in SSc patients, while EBI3 expression was decreased in the keratinocytes of the epidermis and regulatory T cells of the dermis in SSc skin compared with normal skin, which may induce collagen synthesis in SSc dermal fibroblasts. We also found that gp130, the EBI3 receptor, was expressed in both normal and SSc fibroblasts. Moreover, we revealed that EBI3 supplementation by injection into the skin improves mice skin fibrosis. Decreased EBI3 in SSc skin may contribute to an increase in collagen accumulation and skin fibrosis. Clarifying the mechanism regulating the extracellular matrix expression by EBI3 in SSc skin may lead to better understanding of this disease and new therapeutic strategies using ointment or microinjection of the subunit.

show abstract

“…IL-35-mediated tumor immunosuppression IL-35 is a heterodimeric cytokine belonging to the IL-12 family, consisting of the Epstein-Barr virus-induced gene-3 and IL-12p35 subunits. IL-35 is highly expressed by mouse FOXP3 + Treg cells (Collison et al, 2007) and stimulated human Treg cells (Chaturvedi et al, 2011;Seyerl et al, 2011). There are contradictory reports regarding the role of IL-35.…”

Section: Cd28mentioning

confidence: 99%

Failure of immunological cells to eradicate tumor and cancer cells: an overview

Sharma¹,

Talukdar²,

Malik³

et al. 2014

Turk J Biol

View full text Add to dashboard Cite

Inflammation can be broadly understood as a successive immune response of an organism's immune system towards nonnative or foreign antigens. This is a protective mechanism of the immune system, mediated by diverse immunological cells, to ensure homeostasis of an individual. Once activated, these immunological cells release a number of cytokines, chemokines, reactive oxygen species, reactive nitrogen species, histamines, prostaglandins, and other materials leading to inflammation. Tumor cells express altered proteins due to mutations of their genes, DNA modifications such as histone modification, DNA methylation, or other mechanisms of altered protein expression. The body's immunological cells actively recognize these altered proteins, now acting as tumor antigens, and eliminate the tumor cell; this is popularly known as tumor immunosurveillance. However, in unmanaged or inexorable circumstances, tumor cells escape from immunosurveillance mechanisms. This ultimately leads to the cascading events of cancer development and progression. T regulatory cells, tumor-associated macrophages, and myeloid-derived suppressor cells are pronounced cells involved in immunosuppression. These cells not only dodge the immune system's surveillance but also significantly increase the survival, proliferation, and metastasis rates of tumor cells. They hinder T cytotoxic activation by secreting inhibitory cytokines (which inhibit the antitumor activity of natural killer cells) along with dendritic cells and disrupt presentation of antigens, ultimately leading to cancer development. On their own, these cells have emerged as promising therapeutic targets in cancer immunotherapy. This review highlights some of the mechanisms by which these cells escape immunosurveillance and mediate immune suppression.

show abstract

Human rhinoviruses induce IL‐35‐producing Treg via induction of B7‐H1 (CD274) and sialoadhesin (CD169) on DC

Cited by 82 publications

References 37 publications

IL-35 Over-expression is Associated with Genesis of Gastric Cancer

IL-35 Over-expression is Associated with Genesis of Gastric Cancer

EBI3 Downregulation Contributes to Type I Collagen Overexpression in Scleroderma Skin

Failure of immunological cells to eradicate tumor and cancer cells: an overview

Contact Info

Product

Resources

About