Aberrant frequency of TNFR2+ Treg and related cytokines in patients with CIN and cervical cancer

Zhang, Teng; Jiao, Jun; Jiao, Xinlin; Zhao, Lu; Tian, Xinli; Zhang, Qing; Ma, Daoxin; Cui, Baoxia

doi:10.18632/oncotarget.23581

Cited by 19 publications

(15 citation statements)

References 39 publications

(36 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Treg cells expressing TNFR2 is the maximally suppressive subgroup of Treg in humans. TNFR2 + Treg contributed to cervical cancer development (36) but had no prognostic value in RCC in our study. In humans, CD45RO + are thought to be memory T cells.…”

Section: Discussioncontrasting

confidence: 58%

Prognostic Value of the Neo-Immunoscore in Renal Cell Carcinoma

et al. 2019

View full text Add to dashboard Cite

Objective: This study evaluated the prognostic value of the newly-built Immunoscore (neo-Immunoscore) in patients with renal cell carcinoma (RCC). Methods: Eighty-two patients with RCC were enrolled in this study. Their 3- and 5-year survival rates and overall survival (OS) were evaluated. The clinicopathologic data of the 82 patients were collected and analyzed. CD3, CD4, CD8, CD45RO, Foxp3, tumor necrosis factor receptor type II (TNFR2), programmed death ligand-1 (PD-L1), CD68, programmed death-1 (PD-1), cytokeratin (CK), and indoleamine 2,3-dioxygenase (IDO) were separated into two panels and stained using multiplex fluorescent immunohistochemistry methods. An immunologic prediction model of RCC patients, the neo-Immunoscore (neo-IS), was constructed using a Cox regression model. For the prognostic prediction of RCC, the neo-IS with the immunoscore (IS) proposed by the Society for Immunotherapy of Cancer (SITC) were compared by receiver operator characteristic (ROC) curve analysis. Survivals between the neo-IS low and neo-IS high groups were analyzed using the Kaplan–Meier method. Multivariate Cox regression survival analysis was applied to analyze independent indicators. Results: The Cox regression model allowed the establishment of a neo-IS based on three features: CD , CD4 + Foxp3 + CD45RO , and CD8 + PD- . Compared to that of the IS proposed by the SITC, the neo-IS obtained a better prediction. The 3- and 5-year survival rates in neo-IS high RCC patients were significantly higher than those in neo-IS low RCC patients (94.7 vs. 77.4%, P = 0.035 and 94.7 vs. 64.5%, P = 0.002, respectively). The OS in the neo-IS low group was significantly shorter than that in the neo-IS high group (73 vs. 97 months, P = 0.000). In comparisons of the neo-IS with clinical pathological factors, we found that the risk stratification and neo-IS were independent factors for the prognosis of patients with RCC. Moreover, the OS rate of neo-IS high RCC patients with low- and intermediate- risk was higher than that of neo-IS low patients. Conclusion: The newly-constructed IS model more precisely predicted the survival of patients with RCC and may supplement the prognostic value of risk stratification.

show abstract

Section: Discussioncontrasting

confidence: 58%

Prognostic Value of the Neo-Immunoscore in Renal Cell Carcinoma

et al. 2019

View full text Add to dashboard Cite

show abstract

“…TNFR2 also participates in enhancing apoptosis, by activating B cells and plays a crucial role in other pro-inflammatory responses, including proliferation of T cells [2]. Since Chen and his research group discovered TNFR2 for the first time in 2008, many reports have followed up on the potential impacts of TNFR2 expression on cancer cells [25][26][27][28]. As we mentioned before, these studies confirmed that TNFR2 was implicated in proliferation, metastasis and immune evasion of cancer cells by activating immunosuppressive cells.…”

Section: Implication Of Tnfr2 In Cancer Developmentsupporting

confidence: 52%

Synergistic Effects of Nanomedicine Targeting TNFR2 and DNA Demethylation Inhibitor—An Opportunity for Cancer Treatment

Al-Hatamleh

Boer

et al. 2019

Cells

View full text Add to dashboard Cite

Tumor necrosis factor receptor 2 (TNFR2) is expressed on some tumor cells, such as myeloma, Hodgkin lymphoma, colon cancer and ovarian cancer, as well as immunosuppressive cells. There is increasingly evidence that TNFR2 expression in cancer microenvironment has significant implications in cancer progression, metastasis and immune evasion. Although nanomedicine has been extensively studied as a carrier of cancer immunotherapeutic agents, no study to date has investigated TNFR2-targeting nanomedicine in cancer treatment. From an epigenetic perspective, previous studies indicate that DNA demethylation might be responsible for high expressions of TNFR2 in cancer models. This perspective review discusses a novel therapeutic strategy based on nanomedicine that has the capacity to target TNFR2 along with inhibition of DNA demethylation. This approach may maximize the anti-cancer potential of nanomedicine-based immunotherapy and, consequently, markedly improve the outcomes of the management of patients with malignancy.Cells 2020, 9, 33 2 of 16 and tumor cells [6][7][8]. In contrast, TNFR2 expression was only reported on tumor cells and suppressive immune cells, suggesting that TNFR2 directly promotes cancer development [9]. Furthermore, the latest preclinical and clinical studies confirmed the implication of TNF-TNFR2 signaling in cancer proliferation and the suppression of immune response [10,11]. Consequently, blockade of TNF-TNFR2 axis could be a promising option for cancer treatment (Figure 1).On the other hand, nanotechnology provided several platforms in the field of immunotherapy and made significant advances towards safe and efficient targeting systems with positive clinical outcomes and minimal side effects; this is the so-called field of nanomedicine [12]. Despite the emerging trends of using nanoparticles in immunotherapy, no studies have investigated any type of nanocarriers to target TNFR2 on cancer cells. However, based on some previous novel reports about the effects of nanoparticles on immune homeostasis [13], especially using nanoparticles to promote TNFR2 + Foxp3 + regulatory T cells (Tregs) in inflammatory models [14,15], we have suggested in our recent perspective review the possibility of blocking TNF-TNFR2 axis via nanoparticles [16].

show abstract

“…TNFRSF1B usually accelerates the malignant transformation and growth of tumor cells, rather than inducing cell death through apoptosis (52). Similar to tumor cells, TNFRSF1B protects immunosuppressive regulatory T (T reg ) cells and myeloid-derived suppressor cells (MDSC) from the death-inducing TNF and thus enhances the proliferation and function of those tumor-promoting cells (53). To make matters worse, TNFRSF1B worsens the programmed death of phagocytic macrophages responsible for clearing of tumor cells.…”

Section: Discussionmentioning

confidence: 99%