scholarly journals The Treg/Th17 Paradigm in Lung Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Min-Chao Duan ◽  
Xiao-Ning Zhong ◽  
Guang-Nan Liu ◽  
Jin-Ru Wei
Keyword(s):  
Lung Cancer ◽  
Immune Responses ◽  
Th17 Cells ◽  
Close Relation ◽  
Cancer Pathogenesis ◽  
Th2 Cell ◽  
Cancer Immunity ◽  
Self Tolerance ◽  
Tumor Growth And Metastasis ◽  
Cell Balance

Pathogenic mechanisms underlying the development of lung cancer are very complex and not yet entirely clarified. T lymphocytes and their immune-regulatory cytokines play a pivotal role in controlling tumor growth and metastasis. Following activation by unique cytokines, CD4+ T helper cells differentiate into Th1, Th2, Th17, and regulatory T cells (Tregs). Traditionally, research in lung cancer immunity has focused almost exclusively on Th1/Th2 cell balance. Recently, Th17 cells and Tregs represent an intriguing issue to be addressed in lung cancer pathogenesis. Tregs play an important role in the preservation of self-tolerance and modulation of overall immune responses against tumor cells. Th17 cells directly or via other proinflammatory cytokines modulate antitumor immune responses. Notably, there is a close relation between Tregs and Th17 cells. However, the possible interaction between these subsets in lung cancer remains to be elucidated. In this setting, targeting Treg/Th17 balance for therapeutic purposes may represent a useful tool for lung cancer treatment in the future. The purpose of this review is to discuss recent findings of the role of these novel populations in lung cancer immunity and to highlight the pleiotropic effects of these subsets on the development and regulation of lung cancer.

scholarly journals Th17 cells are associated with the Th1/Th2-cell balance during Echinococcus multilocularis infection

2014 ◽  
Vol 10 (1) ◽  
pp. 236-240 ◽  
Author(s):  
XIUMIN MA ◽  
LIANG WANG ◽  
HUI ZHAO ◽  
NANNAN PANG ◽  
FENGBO ZHANG ◽  
...  
Keyword(s):  
Echinococcus Multilocularis ◽  
Th17 Cells ◽  
Th2 Cell ◽  
Cell Balance

scholarly journals ERK5 modulates IL-6 secretion and contributes to tumor-induced immune suppression

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Kristina Riegel ◽  
Hajime Yurugi ◽  
Janine Schlöder ◽  
Helmut Jonuleit ◽  
Manuel Kaulich ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune Responses ◽  
Tumor Cells ◽  
Immune Suppression ◽  
Th17 Cells ◽  
Surface Expression ◽  
Mitogen Activated Protein Kinase ◽  
Cancer Associated Fibroblasts ◽  
Activation Markers ◽  
Mitogen Activated Protein

AbstractTumors exhibit a variety of strategies to dampen antitumor immune responses. With an aim to identify factors that are secreted from tumor cells, we performed an unbiased mass spectrometry-based secretome analysis in lung cancer cells. Interleukin-6 (IL-6) has been identified as a prominent factor secreted by tumor cells and cancer-associated fibroblasts isolated from cancer patients. Incubation of dendritic cell (DC) cultures with tumor cell supernatants inhibited the production of IL-12p70 in DCs but not the surface expression of other activation markers which is reversed by treatment with IL-6 antibody. Defects in IL-12p70 production in the DCs inhibited the differentiation of Th1 but not Th2 and Th17 cells from naïve CD4+ T cells. We also demonstrate that the classical mitogen-activated protein kinase, ERK5/MAPK7, is required for IL-6 production in tumor cells. Inhibition of ERK5 activity or depletion of ERK5 prevented IL-6 production in tumor cells, which could be exploited for enhancing antitumor immune responses.

Galectin-9 ameliorates anti-GBM glomerulonephritis by inhibiting Th1 and Th17 immune responses in mice

2014 ◽  
Vol 306 (8) ◽  
pp. F822-F832 ◽  
Author(s):  
Qian Zhang ◽  
Hong Luan ◽  
Le Wang ◽  
Fan He ◽  
Huan Zhou ◽  
...  
Keyword(s):  
Immune Responses ◽  
Th17 Cells ◽  
Protective Role ◽  
Blood Levels ◽  
Th2 Cell ◽  
Cell Mediated Immune Response ◽  
Ifn Γ ◽  
Th2 Immunity ◽  
Renal Tubular

Antiglomerular basement membrane glomerulonephritis (anti-GBM GN) is a Th1- and Th17-predominant autoimmune disease. Galectin-9 (Gal-9), identified as the ligand of Tim-3, functions in diverse biological processes and leads to the apoptosis of CD4+Tim-3+ T cells. It is still unclear how Gal-9 regulates the functions of Th1 and Th17 cells and prevents renal injury in anti-GBM GN. In this study, Gal-9 was administered to anti-GBM GN mice for 7 days. We found that Gal-9 retarded the increase of Scr, ameliorated renal tubular injury, and reduced the formation of crescents. The infiltration of Th1 and Th17 cells into the spleen and kidneys significantly decreased in Gal-9-treated nephritic mice. The reduced infiltration of Th1 and Th17 cells might be associated with the downregulation of CCL-20, CXCL-9, and CXCL-10 mRNAs in the kidney. In parallel, the blood levels of IFN-γ and IL-17A declined in Gal-9-treated nephritic mice at days 21 and 28. In addition, an enhanced Th2 cell-mediated immune response was observed in the kidneys of nephritic mice after a 7-day injection of Gal-9. In conclusion, the protective role of Gal-9 in anti-GBM GN is associated with the inhibition of Th1 and Th17 cell-mediated immune responses and enhanced Th2 immunity in the kidney.

scholarly journals MicroRNA-520a discourages lung cancer pathogenesis and progression involving the downregulation of RRM2 and Wnt signaling deficits

2020 ◽  
Author(s):  
Yi Xie ◽  
Congyu Xue ◽  
Shuai Guo ◽  
Lei Yang
Keyword(s):  
Lung Cancer ◽  
Survival Rate ◽  
Wnt Signaling ◽  
Cell Lines ◽  
Cancer Progression ◽  
Altered Expression ◽  
Cancer Pathogenesis ◽  
Tumor Growth And Metastasis

Abstract Background Increasingly evidence has noted the critical functions of microRNAs (miRNAs) in disease control including cancer progression. This paper aimed to explore the functions of miR-520a in lung cancer (LC) and the downstream molecules implicated. Methods Aberrantly expressed miRNAs in LC tissues were screened out by miRNA microarrays. miR-520a expression in LC tissues and cell lines was determined, and the correlation between miR-520a level and survival rate of patients was analyzed. Altered expression of miR-520a was introduced to evaluate its function in LC cell malignant behaviors. The target mRNA and the potential signaling pathway mediated by miR-520a were figured out. Xenograft tumors were induced in mice to test the role of miR-520a in tumorigenesis in vivo. Results Poor expression of miR-520a was found in LC tissues and cell lines. A higher miR-520a level indicated a better survival rate in LC patients. Overexpression of miR-520a led to declines in cell viability, proliferation, migration, invasion and resistance to apoptosis. The target mRNAs of miR-520a were enriched on the Wnt signaling. miR-520a inactivated the Wnt pathway. miR-520a could bind to RRM2 and downregulate RRM2 expression in LC cells. Overexpression of RRM2 promoted the malignant behaviors of cancer cells, but this promotion was inhibited by miR-520a. Overexpression of miR-520a also inhibited the tumor growth and metastasis in nude mice. Conclusion The present study provided evidence that miR-520a could inhibit LC progression through RRM2 down-regulation and Wnt signaling deficit. This paper may offer novel ideas concerning LC treatment.

Molecular Profiles for Lung Cancer Pathogenesis and Detection in U.S. Veterans

2014 ◽  
Author(s):  
Steven M. Dubinett ◽  
Pierre Massion ◽  
Ignacio Wistuba ◽  
Avrum Spira
Keyword(s):  
Lung Cancer ◽  
Cancer Pathogenesis ◽  
Molecular Profiles

scholarly journals NF-κB in Cancer Immunity: Friend or Foe?

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 355
Author(s):  
Guilhem Lalle ◽  
Julie Twardowski ◽  
Yenkel Grinberg-Bleyer
Keyword(s):  
Immune Responses ◽  
Therapeutic Potential ◽  
Cell Types ◽  
Transcriptional Activators ◽  
New Class ◽  
Complex Interactions ◽  
Cancer Immunity ◽  
Distinct Cell ◽  
Cancer Initiation ◽  
Cancer Outcome

The emergence of immunotherapies has definitely proven the tight relationship between malignant and immune cells, its impact on cancer outcome and its therapeutic potential. In this context, it is undoubtedly critical to decipher the transcriptional regulation of these complex interactions. Following early observations demonstrating the roles of NF-κB in cancer initiation and progression, a series of studies converge to establish NF-κB as a master regulator of immune responses to cancer. Importantly, NF-κB is a family of transcriptional activators and repressors that can act at different stages of cancer immunity. In this review, we provide an overview of the selective cell-intrinsic contributions of NF-κB to the distinct cell types that compose the tumor immune environment. We also propose a new view of NF-κB targeting drugs as a new class of immunotherapies for cancer.

scholarly journals Progress in research on the role of fibrinogen in lung cancer

2020 ◽  
Vol 15 (1) ◽  
pp. 326-330
Author(s):  
Xing Liu ◽  
Bin Shi
Keyword(s):  
Lung Cancer ◽  
Coagulation Factor ◽  
Coagulation System ◽  
Plasma Coagulation ◽  
Hepatic Cells ◽  
Tumor Growth And Metastasis ◽  
Cancer Côlon ◽  
The Relationship ◽  
Multiple Interactions

AbstractLung cancer is one of the most prevalent malignancies worldwide. Local recurrence and distant metastasis remain the major causes of treatment failure. It has been recognized that the process of tumor growth and metastasis involves multiple interactions between tumor and host. Various biomarkers have been used for predicting tumor recurrence, metastasis, and prognosis in patients with lung cancer. However, these biomarkers are still controversial and require further validation. The relationship between malignancy and coagulation system disorders has been explored for more than a century. Fibrinogen is the most abundant plasma coagulation factor synthesized mainly by hepatic cells. Increased plasma fibrinogen levels were observed in various carcinomas such as gastric cancer, colon cancer, and pancreatic cancer. Recent studies have also investigated the role of fibrinogen in patients with lung cancer. This review aimed to address the role of fibrinogen in lung cancer.

scholarly journals Role of lung and gut microbiota on lung cancer pathogenesis

2021 ◽  
Author(s):  
Yue Zhao ◽  
Yuxia Liu ◽  
Shuang Li ◽  
Zhaoyun Peng ◽  
Xiantao Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Gut Microbiota ◽  
Cancer Progression ◽  
Gut Microbiome ◽  
Intestinal Flora ◽  
Inflammatory Factors ◽  
Cancer Pathogenesis ◽  
Research Findings ◽  
Relationship Of

Abstract Background Lung cancer is the leading cause of cancer-related deaths worldwide (Ferlay et al., Int J Cancer 136:E359–386, 2015). In addition, lung cancer is associated with the highest mortality among all cancer types (Wu et al., Exp Ther Med 16:3004–3010, 2018). Previous studies report that microbiota play an important role in lung cancer. Notably, changes in lung and gut microbiota, are associated with progression of lung cancer. Several studies report that lung and gut microbiome promote lung cancer initiation and development by modulating metabolic pathways, inhibiting the function of immune cells, and producing pro-inflammatory factors. In addition, some factors such as microbiota dysbiosis, affect production of bacteriotoxins, genotoxicity and virulence effect, therefore, they play a key role in cancer progression. These findings imply that lung and gut microbiome are potential markers and targets for lung cancer. However, the role of microbiota in development and progression of lung cancer has not been fully explored. Purpose The aim of this study was to systemically review recent research findings on relationship of lung and gut microbiota with lung cancer. In addition, we explored gut–lung axis and potential mechanisms of lung and gut microbiota in modulating lung cancer progression. Conclusion Pulmonary and intestinal flora influence the occurrence, development, treatment and prognosis of lung cancer, and will provide novel strategies for prevention, diagnosis, and treatment of lung cancer.

Review: Contact Hypersensitivity: The Mechanism of Immune Responses and T Cell Balance

2002 ◽  
Vol 22 (4) ◽  
pp. 407-412 ◽  
Author(s):  
Hideaki Watanabe ◽  
Mark Unger ◽  
Brandon Tuvel ◽  
Binghe Wang ◽  
Daniel N. Sauder
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Contact Hypersensitivity ◽  
Cell Balance

scholarly journals Systemic Platelet-activating Factor Receptor Activation Augments Experimental Lung Tumor Growth and Metastasis

2014 ◽  
Vol 7 ◽  
pp. CGM.S14501 ◽  
Author(s):  
Patrick C. Hackler ◽  
Sarah Reuss ◽  
Raymond L. Konger ◽  
Jeffrey B. Travers ◽  
Ravi P. Sahu
Keyword(s):  
Lung Cancer ◽  
Tumor Growth ◽  
Cancer Progression ◽  
Lung Tumor ◽  
Platelet Activating Factor ◽  
Receptor Activation ◽  
Dependent Manner ◽  
Melanoma Tumor ◽  
Tumor Growth And Metastasis ◽  
The Impact

Pro-oxidative stressors including cigarette smoke (CS) generate novel lipids with platelet-activated factor-receptor (PAF-R) agonistic activity mediate systemic immunosuppression, one of the most recognized events in promoting carcinogenesis. Our previous studies have established that these oxidized-PAF-R-agonists augment murine B16F10 melanoma tumor growth in a PAF-R-dependent manner because of its effects on host immunity. As CS generates PAF-R agonists, the current studies sought to determine the impact of PAF-R agonists on lung cancer growth and metastasis. Using the murine Lewis Lung Carcinoma (LLC1) model, we demonstrate that treatment of C57BL/6 mice with a PAF-R agonist augments tumor growth and lung metastasis in a PAF-R-dependent manner as these findings were not seen in PAF-R-deficient mice. Importantly, this effect was because of host rather than tumor cells PAF-R dependent as LLC1 cells do not express functional PAF-R. These findings indicate that experimental lung cancer progression can be modulated by the PAF system.

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