Analysis of host versus tumor interaction in cancer patients: opposing role of transforming growth factor-β1 and interleukin-6 in the development of in situ tumor immunity

Tsai, Jy Ping; Chen, Hsin–Wei; Cheng, Ming Fang; Liu, Hsiung Kun; Lee, Yi Ping; Hsieh, Chia Ling; Luh, Kwen Tay; Wu, Chew Wun; Hsu, Li‐Han; Chao, Tsu Yi; Wang, Wen Hua; Chang, Chung Ming; Ting, Chou‐Chik

doi:10.1016/j.imbio.2005.07.004

Cited by 19 publications

(21 citation statements)

References 21 publications

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“…As shown in Fig. 5A In a previous study, we found that high levels of TGF-b and IL-6 were present in the malignant effusions from cancer patients (22).…”

Section: Cd4 + T Cells Inhibit Tc17 Cell Developmentmentioning

confidence: 58%

“…In a previous study, we detected very high levels of TGF-b and IL-6 in the malignant effusions of cancer patients (22). In addition, it has been demonstrated that tumor-activated monocytes promote the expansion of Tc17 cells (43).…”

Section: Discussionmentioning

confidence: 85%

“…These IL-17-secreting CD8 + T cells are now termed Tc17 cells. Recently, we found that there were high levels of TGF-b, IL-6, and PGE 2 in the malignant effusions of cancer patients (22). TGFb and IL-6 are the key factors in the development of the Th17 (23)(24)(25) and Tc17 (18-21) cell lineages.…”

mentioning

confidence: 99%

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CD4+ T Cells Disarm or Delete Cytotoxic T Lymphocytes under IL-17–Polarizing Conditions

Tsai

Lee

Hsu

et al. 2012

The Journal of Immunology

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Previous studies have shown that TGF-β acts cooperatively with IL-6 to elicit a high frequency of IL-17–secreting CD4+ T cells (termed Th17) and an elevated CD8+IL-17+ T cell population (termed Tc17). These CD8+ cells fail to behave like most cytotoxic T lymphocytes that express IFN-γ and granzyme B, but they exhibit a noncytotoxic phenotype. Although a significant increase in the number of these Tc17 cells was found in tumors, their role and interaction with other cell types remain unclear. In this study, we demonstrate that the presence of CD4+CD25− T cells, but not the CD4+CD25+ (regulatory T [Treg]) cell population, significantly reduced the elicitation of Tc17 cells, possibly as a result of the induction of apoptotic signals. Importantly, these signals may be derived from soluble mediators, and the addition of anti–IL-2 restored the reduction of Tc17 cells in the presence of CD4+CD25− T cells. Finally, the elicited Tc17 and Treg cells exhibited a close association in patients with head and neck cancer, indicating that the surrounding Treg cells might maintain the survival of the Tc17 cells. Taken together, these results reveal an intriguing mechanism in which Tc17 cells are controlled by a finely tuned collaboration between the different types of CD4+ T cells in distinct tumor microenvironments.

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“…As shown in Fig. 5A In a previous study, we found that high levels of TGF-b and IL-6 were present in the malignant effusions from cancer patients (22).…”

Section: Cd4 + T Cells Inhibit Tc17 Cell Developmentmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 85%

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CD4+ T Cells Disarm or Delete Cytotoxic T Lymphocytes under IL-17–Polarizing Conditions

Tsai

Lee

Hsu

et al. 2012

The Journal of Immunology

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“…Ikebe et al (34) found that lipopolysaccharide can promote the invasion and progression of pancreatic cancer through the TLR4 signaling pathway. Other pathways, such as the 'Fc ε RI signaling pathway' and the 'T cell receptor signaling pathway' also play important roles in the immunological features of tumors (35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Screening for transcription factors and their regulatory small molecules involved in regulating the functions of CL1-5 cancer cells under the effects of macrophage-conditioned medium

Xue

Gao

et al. 2013

Oncology Reports

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Abstract. Many reports have inferred that macrophages can interact with tumor cells in the tumor microenvironment (TME) in a vicious cycle of tumor development; however, the changes in gene expression in tumor cells under the effects of macrophages are still largely unknown. The present study was carried out to illustrate the changes in the gene expression profile in lung cancer cells under the effects of macrophageconditioned medium. Gene expression profile data were derived from the GEO database GSE9315. The GSM234968 sample was derived from a highly invasive human pulmonary adenocarcinoma cell line, CL1-5, and was treated with conditioned medium (supernatant of a culture solution of human monocyte THP-1). The GSM234967 sample that was not treated with the conditioned medium was used as a control. GO and KEGG enrichment analyses were carried out using DAVID software, and visualization networks were constructed using Cytoscape software. The results showed that 40 differentially expressed genes were annotated. Five differentially expressed transcription factors were identified, EIF2B4, EIF2B5, JUNB, GNG11 and HMGB2, which were all related to 'stress' and 'responses'. The gene cluster of JUNB was mainly enriched in cancer-related pathways, 'Wnt signaling pathway' and 'MAPK signaling pathway'. Finally, 10 small molecules, thioridazine, resveratrol, astemizole, ciclopirox, calmidazolium, etoposide, anisomycin, pyrvinium, azacyclonol and terfenadine, which may act on transcription factors, were identified using the CMap database. In conclusion, we identified transcription factors playing key roles in tumor cells under the effects of macrophages in order to provide new clues for blocking this vicious cycle of tumor development.

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“…Ovarian cancer cell lines and primary ovarian cancer cell cultures seem to produce tumor-promoting cytokines like interleukin 6 (IL-6) and IL-8 (5,6). The interaction between tumor and immune system and the production of cytokines by the tumor itself can result in different local and systemic levels of cytokines in cancer patients (7). Previous studies showed that most cytokines are not independent prognostic markers, and individual cytokines are not specific enough for screening purposes (3,8,9).…”

mentioning

confidence: 99%

Serum Cytokine Profiling as a Diagnostic and Prognostic Tool in Ovarian Cancer: A Potential Role for Interleukin 7

Lambeck¹,

Crijns²,

Leffers³

et al. 2007

Clinical Cancer Research

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Purpose: To evaluate if serum cytokine levels could be used as diagnostic or prognostic markers in ovarian cancer. Experimental Design: A cytokine bead array was done to simultaneously analyze 14 cytokines in the sera of 187 ovarian cancer patients with complete clinicopathologic data and follow-up, 45 patients with benign ovarian tumors, and 50 healthy controls. Serum levels of the well-known serum tumor marker CA-125 were routinely measured in all patients. Results: Serum levels of CA-125, interleukin 6 (IL-6), IL-7, and IL-10 were elevated in ovarian cancer patients compared with patients with benign ovarian tumors. Analyzing the cytokines in combination with CA-125 showed that a combination of IL-7 and CA-125 serum levels could accurately predict 69% of the ovarian cancer patients, without falsely classifying patients with benign pelvic mass. The cytokines IL-6, IL-7, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), and IP-10 and CA-125 were associated with disease-free and overall survival in univariate analysis. In multivariate analysis, IL-7 and IP-10 were independent predictors of overall survival, although after inclusion of the clininopathologic parameters, only stage and residual disease remained as independent predictors of survival. Conclusions: IL-7 levels were found to be strongly associated with ovarian cancer and could be used in combination with CA-125 to distinguish between malignant and benign ovarian tumors.

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Analysis of host versus tumor interaction in cancer patients: opposing role of transforming growth factor-β1 and interleukin-6 in the development of in situ tumor immunity

Cited by 19 publications

References 21 publications

CD4+ T Cells Disarm or Delete Cytotoxic T Lymphocytes under IL-17–Polarizing Conditions

CD4+ T Cells Disarm or Delete Cytotoxic T Lymphocytes under IL-17–Polarizing Conditions

Screening for transcription factors and their regulatory small molecules involved in regulating the functions of CL1-5 cancer cells under the effects of macrophage-conditioned medium

Serum Cytokine Profiling as a Diagnostic and Prognostic Tool in Ovarian Cancer: A Potential Role for Interleukin 7

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