scholarly journals The role of liver sinusoidal cells in local hepatic immune surveillance

2016 ◽  
Vol 5 (12) ◽  
pp. e117 ◽  
Author(s):  
Dirk Wohlleber ◽  
Percy A Knolle
Keyword(s):  
Immune Surveillance ◽  
Sinusoidal Cells ◽  
Liver Sinusoidal Cells

Transfer of MHC-class-I molecules among liver sinusoidal cells facilitates hepatic immune surveillance

2014 ◽  
Vol 61 (3) ◽  
pp. 600-608 ◽  
Author(s):  
Katrin Schölzel ◽  
Frank A. Schildberg ◽  
Meike Welz ◽  
Carolin Börner ◽  
Sergej Geiger ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Immune Surveillance ◽  
Class I ◽  
Sinusoidal Cells ◽  
Liver Sinusoidal Cells ◽  
Mhc Class I Molecules

scholarly journals LIVER SINUSOIDAL CELLS

1972 ◽  
Vol 54 (1) ◽  
pp. 107-119 ◽  
Author(s):  
D. Montgomery Bissell ◽  
Lydia Hammaker ◽  
Rudi Schmid
Keyword(s):  
Cell Population ◽  
Cellular Localization ◽  
Isolated Cells ◽  
Sulfur Colloid ◽  
Sinusoidal Cells ◽  
Heat Treated ◽  
Sinusoidal Cell ◽  
Liver Sinusoidal Cells

Sequestration and degradation of red blood cells (RBC) are believed to occur in part in the liver, but the magnitude and cellular localization of this process remain uncertain. This problem was studied in rats by investigating isolated parenchymal and sinusoidal cell populations of the liver. After digesting the perfused liver with pronase, hepatic sinusoidal cells were isolated free of RBC and debris. Of the isolated cells, 90% were phagocytic, as judged by their uptake of colloidal 198Au or of aggregated albumin-131I administered in vivo After administration of spherocytic (heat-treated) RBC, however, only about one quarter of the isolated cells were found to contain phagocytized RBC. This apparently distinct population of RBC-phagocytizing cells is designated as "erythrophagocytic (EP)" cells. The EP cell population was further characterized functionally by its specific phagocytosis of colloidal carbon and of 99mtechnetium-sulfur colloid and histochemically by its peroxidase activity. The role of the EP population in the catabolism of RBC-hemoglobin was studied in isolated hepatic sinusoidal cells by assay of microsomal heme oxygenase (MHO), which is the inducible enzyme system that converts heme to bilirubin. The MHO activity of individual sinusoidal isolates was related directly to their content of EP cells Assay of the MHO activity of the whole spleen and of the total EP cell population of the liver suggested that these two tissues may be of comparable importance in their ability to degrade RBC-hemoglobin.

scholarly journals The Role of Liver Sinusoidal Cells in Hepatocyte-Directed Gene Transfer

2010 ◽  
Vol 176 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Frank Jacobs ◽  
Eddie Wisse ◽  
Bart De Geest
Keyword(s):  
Gene Transfer ◽  
Sinusoidal Cells ◽  
Liver Sinusoidal Cells

Growth control of primary culture hepatocytes by nonparenchymal liver cells. Role of interferon produced by liver sinusoidal cells.

1994 ◽  
Vol 61 (2) ◽  
pp. 120-128 ◽  
Author(s):  
Ayako Mabuchi ◽  
Eiji Watari ◽  
Masakazu Ikeda ◽  
Yoshihiko Watanabe ◽  
Kozo Yokomuro
Keyword(s):  
Primary Culture ◽  
Growth Control ◽  
Liver Cells ◽  
Sinusoidal Cells ◽  
Liver Sinusoidal Cells

ROLE OF THE STROMAL CELLULAR COMPONENT IN COMPENSATORY PROCESSES IN DIFFUSE LIVER DAMAGE

2018 ◽  
pp. 32-37 ◽  
Author(s):  
Z. A. Shafigullina ◽  
S. Yu. Medvedeva ◽  
I. G. Danilova
Keyword(s):  
Toxic Hepatitis ◽  
Intraperitoneal Administration ◽  
Sharp Decrease ◽  
Cellular Component ◽  
Ki 67 ◽  
Sinusoidal Cells ◽  
Toxic Damage ◽  
Stromal Component ◽  
Regeneration Processes

The aim of the study was to assess the role of the cellular component of the stroma in liver regeneration after its toxic damage. The experimental model of toxic hepatitis caused by intraperitoneal administration of tetrachloromethane (CCl4) showed that regeneration processes in the liver on the 3rd day are manifested in an increase in binuclear hepatocytes, Ki-67 + cells and hepatocytes dividing by mitosis. The reaction of the stromal component is expressed in an increase in the number of CD45 +, mast and sinusoidal cells (SC). On the 7th day of the development of toxic hepatitis the hepatocyte alteration increases, that is accompanied by a sharp decrease in the mitotic index and the number of Ki-67 + cells. In the stromal component there is a decrease in the number of sinusoidal cells, CD45 + and a significant increase in mast cells with a high secretion granule content.

Deciphering the Role of microRNAs in Regulation of Immune Surveillance, Self-Tolerance and Allograft Transplant Outcome

2018 ◽  
Vol 13 (5) ◽  
pp. 336-344
Author(s):  
Cherry S. Leung ◽  
Song Lu ◽  
Jiatao Li ◽  
William KK Wu ◽  
Kathy O. Lui
Keyword(s):  
Immune Surveillance ◽  
Transplant Outcome ◽  
Self Tolerance

scholarly journals Impact of Temozolomide on Immune Response during Malignant Glioma Chemotherapy

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Sadhak Sengupta ◽  
Jaclyn Marrinan ◽  
Caroline Frishman ◽  
Prakash Sampath
Keyword(s):  
Immune Response ◽  
Malignant Glioma ◽  
Dna Methyltransferase ◽  
Opportunistic Infections ◽  
Immune Surveillance ◽  
Drug Resistant ◽  
Methylguanine Dna Methyltransferase ◽  
Drug Resistant Mutation ◽  
Resistant Mutation

Malignant glioma, or glioblastoma, is the most common and lethal form of brain tumor with a median survival time of 15 months. The established therapeutic regimen includes a tripartite therapy of surgical resection followed by radiation and temozolomide (TMZ) chemotherapy, concurrently with radiation and then as an adjuvant. TMZ, a DNA alkylating agent, is the most successful antiglioma drug and has added several months to the life expectancy of malignant glioma patients. However, TMZ is also responsible for inducing lymphopenia and myelosuppression in malignant glioma patients undergoing chemotherapy. Although TMZ-induced lymphopenia has been attributed to facilitate antitumor vaccination studies by inducing passive immune response, in general lymphopenic conditions have been associated with poor immune surveillance leading to opportunistic infections in glioma patients, as well as disrupting active antiglioma immune response by depleting both T and NK cells. Deletion of O6-methylguanine-DNA-methyltransferase (MGMT) activity, a DNA repair enzyme, by temozolomide has been determined to be the cause of lymphopenia. Drug-resistant mutation of the MGMT protein has been shown to render chemoprotection against TMZ. The immune modulating role of TMZ during glioma chemotherapy and possible mechanisms to establish a strong TMZ-resistant immune response have been discussed.

scholarly journals A2B Adenosine Receptor and Cancer

2019 ◽  
Vol 20 (20) ◽  
pp. 5139 ◽  
Author(s):  
Zhan-Guo Gao ◽  
Kenneth A. Jacobson
Keyword(s):  
G Proteins ◽  
Anticancer Agents ◽  
Immune Suppression ◽  
Adenosine Receptors ◽  
Immune Surveillance ◽  
G Protein Coupled Receptors ◽  
Normal Tissues ◽  
Cancer Tissues ◽  
G Protein Coupled

There are four subtypes of adenosine receptors (ARs), named A1, A2A, A2B and A3, all of which are G protein-coupled receptors (GPCRs). Locally produced adenosine is a suppressant in anti-tumor immune surveillance. The A2BAR, coupled to both Gαs and Gαi G proteins, is one of the several GPCRs that are expressed in a significantly higher level in certain cancer tissues, in comparison to adjacent normal tissues. There is growing evidence that the A2BAR plays an important role in tumor cell proliferation, angiogenesis, metastasis, and immune suppression. Thus, A2BAR antagonists are novel, potentially attractive anticancer agents. Several antagonists targeting A2BAR are currently in clinical trials for various types of cancers. In this review, we first describe the signaling, agonists, and antagonists of the A2BAR. We further discuss the role of the A2BAR in the progression of various cancers, and the rationale of using A2BAR antagonists in cancer therapy.

scholarly journals LANA and hnRNP A1 Regulate the Translation of LANA mRNA through G-Quadruplexes

2019 ◽  
Vol 94 (3) ◽  
Author(s):  
Prerna Dabral ◽  
Jay Babu ◽  
Andrew Zareie ◽  
Subhash C. Verma
Keyword(s):  
Viral Genome ◽  
Immune Surveillance ◽  
Class I ◽  
Nuclear Antigen ◽  
Host Immune System ◽  
Immune Recognition ◽  
Hnrnp A1 ◽  
Multifunctional Protein ◽  
G Quadruplex

ABSTRACT During the latent phase, Kaposi’s sarcoma-associated herpes virus (KSHV) maintains itself inside the host by escaping the host immune surveillance mechanism through restricted protein expression. Latency-associated nuclear antigen (LANA), the most abundantly expressed protein, is essential for viral persistence, as it plays important roles in latent viral DNA replication and efficient segregation of the viral genome to the daughter cells following cell division. KSHV evades immune detection by maintaining the levels of LANA protein below a threshold required for detection by the host immune system but sufficient to maintain the viral genome. LANA achieves this by controlling its expression through regulation of its promoters and by inhibiting its presentation through interaction with the proteins of class I and class II major histocompatibility complex (MHC) pathways. In this study, we identified a mechanism of LANA expression and restricted immune recognition through formation of G-quadruplexes in LANA mRNA. We show that the formation of these stable structures in LANA mRNA inhibits its translation to control antigen presentation, which was supported by treatment of cells with TMPyP4, a G-quadruplex-stabilizing ligand. We identified heterogenous ribonucleoprotein A1 (hnRNP A1) as a G-quadruplex-unwinding helicase, which unfolds these stable secondary structures to regulate LANA translation. IMPORTANCE LANA, the most abundantly expressed protein during latency, is a multifunctional protein which is absolutely required for the persistence of KSHV in the host cell. Even though the functions of LANA in aiding pathogenesis of the virus have been extensively studied, the mechanism of how LANA escapes host’s immune surveillance is not fully understood. This study sheds light on the autoregulatory role of LANA to modulate its expression and immune evasion through formation of G-quadruplexes in its mRNA. We used G-quadruplex-stabilizing ligand to define the inhibition in LANA expression and presentation on the cell surface through MHC class I. We defined the autoregulatory role of LANA and identified a cellular RNA helicase, hnRNP A1, regulating the translation of LANA mRNA. This interaction of hnRNP A1 with LANA mRNA could be exploited for controlling KSHV latency.

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