IL-17 is associated with poor prognosis and promotes angiogenesis via stimulating VEGF production of cancer cells in colorectal carcinoma

Liu, Jiankun; Duan, Yu-zhong; Cheng, Xiaoming; Chen, Xi; Xie, Wei; Long, Haixia; Zhang, Lin; Zhu, Bo

doi:10.1016/j.bbrc.2011.03.021

Cited by 320 publications

(260 citation statements)

References 23 publications

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“…In prostate and ovarian cancers, increased numbers of Th17 cells in the tumor correlated with better patient outcome, demonstrating an anti-tumor role [28,29]. Conversely, in colorectal carcinoma, higher levels of serum IL-17 correlated to poor patient prognosis [54]. In our studies, no change in IL-17-expressing cells was observed after exposure to Survivin (Supplementary Figure 7), unlike our observed type 1 and type 2 T cell shift Fig.…”

Section: Discussioncontrasting

confidence: 63%

Tumor-Released Survivin Induces a Type-2 T Cell Response and Decreases Cytotoxic T Cell Function, in Vitro

Jutzy

Khan

Asuncion-Valenzuela

et al. 2012

Cancer Microenvironment

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Clinical studies of T cell profiles from cancer patients have shown a skewing toward a type-2 T cell response with decreased cytotoxic T cell function. However, the primary cause of this shift remains unknown. Here we show that tumor-released Survivin, an inhibitor of apoptosis (IAP) protein and tumor-specific antigen, is taken up by T cells and alters their response. The addition of Survivin to T cell cultures resulted in decreased T cell proliferation and reduced cytotoxic CD8 + T cell function. Additionally, type 1 cell numbers and IFN-γ and IL-2 production were significantly reduced, while IL-4 release and type 2 T cell numbers increased. In contrast, the function and numbers of Th17 and T regulatory cells were not affected. These studies show that tumor-released Survivin modulates T cells resulting in a phenotype similar to that observed in cancer patients with a polarity shift from a type 1 to a type 2 response.

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Section: Discussioncontrasting

confidence: 63%

Tumor-Released Survivin Induces a Type-2 T Cell Response and Decreases Cytotoxic T Cell Function, in Vitro

Jutzy

Khan

Asuncion-Valenzuela

et al. 2012

Cancer Microenvironment

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“…IL-17A and IL-17F, which are the main members of the IL-17 family, have the greatest homology (20) and share the same receptor and regulatory elements (21). IL-17A and IL-17F have been reported to be involved in vascular regeneration in some diseases (11,12,16,(22)(23)(24). In our study, we found that neutralization of IL-17A led to reduced vascularity in the lung of OVA-challenged mice, whereas IL-17F antagonism did not markedly influence the microvascular regeneration.…”

Section: Discussionmentioning

confidence: 99%

IL-17A, But Not IL-17F, Is Indispensable for Airway Vascular Remodeling Induced by Exaggerated Th17 Cell Responses in Prolonged Ovalbumin-Challenged Mice

Gao

et al. 2015

The Journal of Immunology

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We previously demonstrated an essential role of Th17 cells in excessive mucous secretion and airway smooth muscle proliferation in a prolonged OVA-challenged C57BL/6 mouse model. However, the impact of Th17 cells in vascular remodeling, another characteristic feature of airway remodeling in asthma, remains elusive. This issue was further investigated in this study. The time-course experiments showed that progressively increasing levels of Th17 cells and IL-17A (not IL-17F) in the lungs of prolonged allergen-challenged mice were positively correlated with microvessel density in peribronchial tissues. In addition, exaggerated airway vascular remodeling in this mouse model was exacerbated by airway administration of IL-17A or adoptive transfer of Th17 cells. This effect was dramatically alleviated by the administration of anti–IL-17A Ab, but not anti–IL-17F Ab. Boyden chamber assays indicated that IL-17A accelerates endothelial progenitor cell (EPC) migration. Furthermore, EPC accumulation in the airways of allergen-exposed mice after adoptive transfer of Th17 cells was eliminated by blockade of IL-17A. We found that IL-17A promoted tubule-like formation rather than proliferation of pulmonary microvascular endothelia cells (PMVECs) in vitro. In addition, IL-17A induced PMVEC tube formation via the PI3K/AKT1 pathway, and suppression of the PI3K pathway markedly reduced the formation of tubule-like structures. Collectively, our results indicate that Th17 cells contribute to the airway vascular remodeling in asthma by mediating EPC chemotaxis, as well as PMVEC tube formation, via IL-17A rather than IL-17F.

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“…Recent studies described the involvement of ILCs in tumour growth and progression (8)(9)(10)(11). In this paper, we summarize the role of ILCs in tumour genesis and anti-tumour immunity modulation.…”

Section: Innate Lymphoid Cellsmentioning

confidence: 98%

Innate Lymphoid Cells: Roles In Tumour Genesis And Progression

Jovanović

Gajovic

Radosavljević

et al. 2015

Serbian Journal of Experimental and Clinical Research

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IL-17 is associated with poor prognosis and promotes angiogenesis via stimulating VEGF production of cancer cells in colorectal carcinoma

Cited by 320 publications

References 23 publications

Tumor-Released Survivin Induces a Type-2 T Cell Response and Decreases Cytotoxic T Cell Function, in Vitro

Tumor-Released Survivin Induces a Type-2 T Cell Response and Decreases Cytotoxic T Cell Function, in Vitro

IL-17A, But Not IL-17F, Is Indispensable for Airway Vascular Remodeling Induced by Exaggerated Th17 Cell Responses in Prolonged Ovalbumin-Challenged Mice

Innate Lymphoid Cells: Roles In Tumour Genesis And Progression

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