scholarly journals The Role of TRAIL/DRs in the Modulation of Immune Cells and Responses

Cancers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1469 ◽  
Author(s):  
Duygu Sag ◽  
Zeynep Ozge Ayyildiz ◽  
Sinem Gunalp ◽  
Gerhard Wingender
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Necrosis Factor ◽  
Immune Responses ◽  
Tumor Cells ◽  
Immune Cells ◽  
Tumor Necrosis ◽  
Death Receptors ◽  
Induction Of Apoptosis ◽  
Necrosis Factor

Expression of TRAIL (tumor necrosis factor–related apoptosis–inducing ligand) by immune cells can lead to the induction of apoptosis in tumor cells. However, it becomes increasingly clear that the interaction of TRAIL and its death receptors (DRs) can also directly impact immune cells and influence immune responses. Here, we review what is known about the role of TRAIL/DRs in immune cells and immune responses in general and in the tumor microenvironment in particular.

scholarly journals The Role of Tumor Necrosis Factor in Manipulating the Immunological Response of Tumor Microenvironment

2021 ◽  
Vol 12 ◽  
Author(s):  
Dipranjan Laha ◽  
Robert Grant ◽  
Prachi Mishra ◽  
Naris Nilubol
Keyword(s):  
Drug Delivery ◽  
Extracellular Matrix ◽  
Tumor Microenvironment ◽  
Tumor Necrosis Factor ◽  
Tumor Cells ◽  
Immune Cells ◽  
Tumor Necrosis ◽  
Cancer Drug ◽  
Tnf Α ◽  
Necrosis Factor

The tumor microenvironment (TME) is an intricate system within solid neoplasms. In this review, we aim to provide an updated insight into the TME with a focus on the effects of tumor necrosis factor-α (TNF-α) on its various components and the use of TNF-α to improve the efficiency of drug delivery. The TME comprises the supporting structure of the tumor, such as its extracellular matrix and vasculature. In addition to cancer cells and cancer stem cells, the TME contains various other cell types, including pericytes, tumor-associated fibroblasts, smooth muscle cells, and immune cells. These cells produce signaling molecules such as growth factors, cytokines, hormones, and extracellular matrix proteins. This review summarizes the intricate balance between pro-oncogenic and tumor-suppressive functions that various non-tumor cells within the TME exert. We focused on the interaction between tumor cells and immune cells in the TME that plays an essential role in regulating the immune response, tumorigenesis, invasion, and metastasis. The multifunctional cytokine, TNF-α, plays essential roles in diverse cellular events within the TME. The uses of TNF-α in cancer treatment and to facilitate cancer drug delivery are discussed. The effects of TNF-α on tumor neovasculature and tumor interstitial fluid pressure that improve treatment efficacy are summarized.

scholarly journals Inactive Rhomboid Protein 2 Mediates Intestinal Inflammation by Releasing Tumor Necrosis Factor–α

2019 ◽  
Vol 26 (2) ◽  
pp. 242-253
Author(s):  
Jee Hyun Kim ◽  
Sung Wook Hwang ◽  
Jaemoon Koh ◽  
Jaeyoung Chun ◽  
Changhyun Lee ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Immune Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Inflammation ◽  
Converting Enzyme ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Inactive rhomboid 2 (iRhom2) is an essential molecule required for the maturation of tumor necrosis factor–α–converting enzyme in immune cells, which regulates TNF-α release. The aim of this study was to investigate the role of iRhom2 in intestinal inflammation.

scholarly journals Yersinia pestis YopJ Suppresses Tumor Necrosis Factor Alpha Induction and Contributes to Apoptosis of Immune Cells in the Lymph Node but Is Not Required for Virulence in a Rat Model of Bubonic Plague

2006 ◽  
Vol 74 (9) ◽  
pp. 5126-5131 ◽  
Author(s):  
Nadine Lemaître ◽  
Florent Sebbane ◽  
Daniel Long ◽  
B. Joseph Hinnebusch
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Rat Model ◽  
Immune Cells ◽  
Tumor Necrosis ◽  
Bubonic Plague ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The virulence of the pathogenic Yersinia species depends on a plasmid-encoded type III secretion system that transfers six Yop effector proteins into host cells. One of these proteins, YopJ, has been shown to disrupt host cell signaling pathways involved in proinflammatory cytokine production and to induce macrophage apoptosis in vitro. YopJ-dependent apoptosis in mesenteric lymph nodes has also been demonstrated in a mouse model of Yersinia pseudotuberculosis infection. These results suggest that YopJ attenuates the host innate and adaptive immune response during infection, but the role of YopJ during bubonic plague has not been completely established. We evaluated the role of Yersinia pestis YopJ in a rat model of bubonic plague following intradermal infection with a fully virulent Y. pestis strain and an isogenic yopJ mutant. Deletion of yopJ resulted in a twofold decrease in the number of apoptotic immune cells in the bubo and a threefold increase in serum tumor necrosis factor alpha levels but did not result in decreased virulence, systemic spread, or colonization levels in the spleen and blood. Our results indicate that YopJ is not essential for bubonic plague pathogenesis, even after peripheral inoculation of low doses of Y. pestis. Instead, the effects of YopJ appear to overlap and augment the immunomodulatory effects of other Y. pestis virulence factors.

A possible role of sphingosine in induction of apoptosis by tumor necrosis factor-α, in human neutrophils

FEBS Letters ◽  
1994 ◽  
Vol 355 (3) ◽  
pp. 267-270 ◽  
Author(s):  
Hideki Ohta ◽  
Yutaka Yatomi ◽  
Elizabeth A. Sweeney ◽  
Sen-itiroh Hakomori ◽  
Yasuyuki Igarashi
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Human Neutrophils ◽  
Induction Of Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals The Role of Chemoattractant Receptors in Shaping the Tumor Microenvironment

2014 ◽  
Vol 2014 ◽  
pp. 1-33 ◽  
Author(s):  
Jiamin Zhou ◽  
Yi Xiang ◽  
Teizo Yoshimura ◽  
Keqiang Chen ◽  
Wanghua Gong ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Immune Responses ◽  
Tumor Cells ◽  
Immune Cells ◽  
Malignant Tumors ◽  
G Protein Coupled Receptors ◽  
Host Cells ◽  
The Past ◽  
G Protein Coupled

Chemoattractant receptors are a family of seven transmembrane G protein coupled receptors (GPCRs) initially found to mediate the chemotaxis and activation of immune cells. During the past decades, the functions of these GPCRs have been discovered to not only regulate leukocyte trafficking and promote immune responses, but also play important roles in homeostasis, development, angiogenesis, and tumor progression. Accumulating evidence indicates that chemoattractant GPCRs and their ligands promote the progression of malignant tumors based on their capacity to orchestrate the infiltration of the tumor microenvironment by immune cells, endothelial cells, fibroblasts, and mesenchymal cells. This facilitates the interaction of tumor cells with host cells, tumor cells with tumor cells, and host cells with host cells to provide a basis for the expansion of established tumors and development of distant metastasis. In addition, many malignant tumors of the nonhematopoietic origin express multiple chemoattractant GPCRs that increase the invasiveness and metastasis of tumor cells. Therefore, GPCRs and their ligands constitute targets for the development of novel antitumor therapeutics.

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