scholarly journals Macrophage therapy for murine liver fibrosis recruits host effector cells improving fibrosis, regeneration, and function

Hepatology ◽  
2011 ◽  
Vol 53 (6) ◽  
pp. 2003-2015 ◽  
Author(s):  
James A. Thomas ◽  
Caroline Pope ◽  
Davina Wojtacha ◽  
Andrew J. Robson ◽  
Timothy T. Gordon-Walker ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Effector Cells ◽  
Murine Liver ◽  
And Function

MRI Measures of Murine Liver Fibrosis

2021 ◽  
Author(s):  
Diana M. Lindquist ◽  
Elizabeth M. Fugate ◽  
Jiang Wang ◽  
Akanksha Sharma ◽  
Chandrashekhar R. Gandhi ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Murine Liver

Recipient immune-competent T lymphocytes can survive intensive conditioning for bone marrow transplantation

Blood ◽  
1986 ◽  
Vol 68 (4) ◽  
pp. 954-956 ◽  
Author(s):  
A Butturini ◽  
RC Seeger ◽  
RP Gale
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
T Lymphocytes ◽  
Graft Rejection ◽  
Marrow Transplantation ◽  
Interleukin 2 ◽  
Marrow Transplant ◽  
Effector Cells ◽  
And Function

Abstract Bone marrow transplantation is usually preceded by intensive chemotherapy and radiation therapy designed to completely eliminate recipient immune-competent cells that might reject the donor bone marrow. We show that seven of 14 bone marrow transplant recipients who received intensive conditioning retained circulating T lymphocytes that proliferate after incubation with interleukin 2 and phytohemagglutinin and function as effector cells in an in vitro model of graft rejection. These T cells may mediate graft rejection.

Immunodeficiency Disorders

Hematology ◽  
2003 ◽  
Vol 2003 (1) ◽  
pp. 314-330 ◽  
Author(s):  
Max D. Cooper ◽  
Lewis L. Lanier ◽  
Mary Ellen Conley ◽  
Jennifer M. Puck
Keyword(s):  
B Cells ◽  
B Cell ◽  
Host Defense ◽  
Diagnosis And Treatment ◽  
T And B Cells ◽  
Phagocytic Cells ◽  
Effector Cells ◽  
Immunodeficiency Diseases ◽  
Cellular And Humoral Immunity ◽  
And Function

Abstract Hematological complications occur frequently in patients with both primary and secondary immunodeficiency disorders. Anemia, thrombocytopenia or leukopenias may bring these individuals to the attention of hematologists. Conversely, evidence suggesting a lymphoproliferative disorder may be the cause for referral. This session will provide an update on the diagnosis and treatment of immunodeficiency diseases ranging from isolated defects in antibody production to the severe combined immunodeficiencies (SCID). Immunodeficiency diseases have traditionally been defined as defects in the development and function of T and B cells, the primary effector cells of specific cellular and humoral immunity. However, it has become increasingly evident that innate immune mechanisms contribute greatly to host defense, either through acting alone or by enhancing specific T and B cell responses. In Section I, Dr. Lewis Lanier reviews the burgeoning information on the extensive families of activating and inhibitory immunoreceptors that are expressed on NK cells, dendritic cells, T and B cells, and phagocytic cells. He provides an overview on the biological functions of these receptors in host defense. In Section II, Dr. Mary Ellen Conley defines the spectrum of antibody deficiency disorders, the most frequently occurring types of primary immunodeficiencies. She covers the different defects in B-cell development and function that lead to antibody deficiencies, and includes diagnosis and therapy of these disorders. In Section III, Dr. Jennifer Puck discusses the diagnosis and treatment of the different types of SCID. She describes the genetic basis for SCID, and the benefits, pitfalls, and complications of gene therapy and bone marrow transplantation in SCID patients.

scholarly journals SOCS1 Is a Suppressor of Liver Fibrosis and Hepatitis-induced Carcinogenesis

2004 ◽  
Vol 199 (12) ◽  
pp. 1701-1707 ◽  
Author(s):  
Takafumi Yoshida ◽  
Hisanobu Ogata ◽  
Masaki Kamio ◽  
Akiko Joo ◽  
Hiroshi Shiraishi ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hepatic Injury ◽  
Negative Regulator ◽  
Cytokine Signaling ◽  
Strongly Correlated ◽  
Wild Type ◽  
Gene Methylation ◽  
Severe Liver ◽  
Hepatocellular Carcinomas ◽  
Murine Liver

Hepatocellular carcinomas (HCCs) mainly develop from liver cirrhosis and severe liver fibrosis that are established with long-lasting inflammation of the liver. Silencing of the suppressor of the cytokine signaling-1 (SOCS1) gene, a negative regulator of cytokine signaling, by DNA methylation has been implicated in development or progress of HCC. However, how SOCS1 contributes to HCC is unknown. We examined SOCS1 gene methylation in >200 patients with chronic liver disease and found that the severity of liver fibrosis is strongly correlated with SOCS1 gene methylation. In murine liver fibrosis models using dimethylnitrosamine, mice with haploinsufficiency of the SOCS1 gene (SOCS1−/+ mice) developed more severe liver fibrosis than did wild-type littermates (SOCS1+/+ mice). Moreover, carcinogen-induced HCC development was also enhanced by heterozygous deletion of the SOCS1 gene. These findings suggest that SOCS1 contributes to protection against hepatic injury and fibrosis, and may also protect against hepatocarcinogenesis.

Activator protein 1 transcription factor fos-related antigen 1 (fra-1) is dispensable for murine liver fibrosis, but modulates xenobiotic metabolism

Hepatology ◽  
2013 ◽  
Vol 59 (1) ◽  
pp. 261-273 ◽  
Author(s):  
Sebastian C. Hasenfuss ◽  
Latifa Bakiri ◽  
Martin K. Thomsen ◽  
Rainer Hamacher ◽  
Erwin F. Wagner
Keyword(s):  
Transcription Factor ◽  
Liver Fibrosis ◽  
Xenobiotic Metabolism ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
Murine Liver

scholarly journals 11Beta-hydroxysteroid dehydrogenase-1 deficiency or inhibition enhances hepatic myofibroblast activation in murine liver fibrosis

Hepatology ◽  
2018 ◽  
Vol 67 (6) ◽  
pp. 2167-2181 ◽  
Author(s):  
Xiantong Zou ◽  
Prakash Ramachandran ◽  
Timothy J. Kendall ◽  
Antonella Pellicoro ◽  
Elena Dora ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Hydroxysteroid Dehydrogenase ◽  
Murine Liver

scholarly journals Serine Protease HtrA2/Omi Deficiency Impairs Mitochondrial Homeostasis and Promotes Hepatic Fibrogenesis via Activation of Hepatic Stellate Cells

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1119 ◽  
Author(s):  
Hur ◽  
Kang ◽  
Kim ◽  
Lee ◽  
Kim ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Serine Protease ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Mitochondrial Morphology ◽  
Mice Model ◽  
Hepatic Fibrogenesis ◽  
Mitochondrial Homeostasis ◽  
And Function ◽  
Intracellular Energy

The loss of mitochondrial function impairs intracellular energy production and potentially results in chronic liver disease. Increasing evidence suggests that mitochondrial dysfunction in hepatocytes contributes to the activation of hepatic stellate cells (HSCs), thereby resulting in hepatic fibrogenesis. High-temperature requirement protein A2 (HtrA2/Omi), a mitochondrial serine protease with various functions, is responsible for quality control in mitochondrial homeostasis. However, little information is available regarding its role in mitochondrial damage during the development of liver fibrosis. This study examined whether HtrA2/Omi regulates mitochondrial homeostasis in hepatocyte during the development of hepatic fibrogenesis. In this study, we demonstrated that HtrA2/Omi expression considerably decreased in liver tissues from the CCl4-induced liver fibrotic mice model and from patients with liver cirrhosis. Knockdown of HtrA2/Omi in hepatocytes induced the accumulation of damaged mitochondria and provoked mitochondrial reactive oxygen species (mtROS) stress. We further show that the damaged mtDNA isolated from HtrA2/Omi-deficient hepatocytes as a form of damage-associated molecular patterns can induce HSCs activation. Moreover, we found that motor neuron degeneration 2-mutant mice harboring the missense mutation Ser276Cys in the protease domain of HtrA2/Omi displayed altered mitochondrial morphology and function, which increased oxidative stress and promoted liver fibrosis. Conversely, the overexpression of HtrA2/Omi via hydrodynamics-based gene transfer led to the antifibrotic effects in CCl4-induced liver fibrosis mice model through decreasing collagen accumulation and enhancing anti-oxidative activity by modulating mitochondrial homeostasis in the liver. These results suggest that suppressing HtrA2/Omi expression promotes hepatic fibrogenesis via modulating mtROS generation, and these novel mechanistic insights involving the regulation of mitochondrial homeostasis by HtrA2/Omi may be of importance for developing new therapeutic strategies for hepatic fibrosis.

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