| treatment of resistant a/j mice with methylprednisolone (mp) results in loss of resistance to murine hepatitis strain 3 (mhv-3) and induction of macrophage procoagulant activity (pca). | balb/cj mice die of fulminant hepatitis within 7 days of exposure to murine hepatitis virus strain 3 (mhv-3) whereas a/j mice are fully resistant to the lethal effects of mhv-3 infection. previous studies have implicated macrophage activation with production of a unique macrophage prothrombinase (pca) and lymphocyte cytokine secretion in the pathogenesis of mhv-3 susceptibility and have demonstrated that immunosuppression induces susceptibility in resistant mice. this study was undertaken to det ... | 1995 | 8830551 |
| pattern of disease after murine hepatitis virus strain 3 infection correlates with macrophage activation and not viral replication. | murine hepatitis virus strain (mhv-3) produces a strain-dependent pattern of disease which has been used as a model for fulminant viral hepatitis. this study was undertaken to examine whether there was a correlation between macrophage activation and susceptibility or resistance to mhv-3 infection. peritoneal macrophages were isolated from resistant a/j and susceptible balb/cj mice and, following stimulation with mhv-3 or lipopolysaccharide (lps), analyzed for transcription of mrna and production ... | 1995 | 7636967 |
| cyclosporine a fails to alter innate host resistance to murine hepatitis virus strain 3 infection in a/j mice. | | 1987 | 3029911 |
| resistance to murine hepatitis virus strain 3 (mhv-3) infection in a/j mice is not affected by cyclosporin a (csa). | | 1987 | 2829562 |
| activation of the immune coagulation system by murine hepatitis virus strain 3. | viral infections result in alterations in hemostasis and coagulation. it has previously been shown that susceptibility to murine hepatitis virus strain 3 (mhv-3), a coronavirus, correlates directly with the spontaneous, t lymphocyte-instructed expression of a procoagulant monokine that exhibits prothrombin-cleaving activity (procoagulant activity [pca]). a biologic role for pca in the pathogenesis of mhv-3 infection is suggested by results of in vivo microscopic observations made during acute mh ... | 1989 | 2546245 |
| mechanism of protective effect of prostaglandin e in murine hepatitis virus strain 3 infection: effects on macrophage production of tumour necrosis factor, procoagulant activity and leukotriene b4. | | 1990 | 1966446 |
| effect of eicosanoids on induction of procoagulant activity by murine hepatitis virus strain 3 in vitro. | the development of hepatitis secondary to murine hepatitis virus strain 3 (mhv-3) infection correlates with the induction of macrophage procoagulant activity (pca). 16,16 dimethyl prostaglandin e2 (dmpge2) has previously been shown to inhibit the development of disease in this model and in parallel, inhibit induction of pca, a macrophage effector molecule which has previously been shown to correlate with resistance/susceptibility to mhv-3 infection. these studies were undertaken to determine if ... | 1991 | 1666190 |
| expression of the fgl2 and its protein product (prothrombinase) in tissues during murine hepatitis virus strain-3 (mhv-3) infection. | murine hepatitis virus strain 3 (mhv-3) produces fulminant hepatitis with 80-90% mortality in balb/cj mice. previous studies in our laboratory have shown that peritoneal macrophages from mhv-3 infected mice produce a procoagulant (pca) which has the ability to cleave prothrombin to thrombin (prothrombinase) encoded by the gene fgl2 located on chromosome 5. pca accounts for sinusoidal thrombosis and hepatic necrosis and the necrosis and mortality can be prevented by treatment of animals with a mo ... | 1998 | 9782336 |
| resistance of naive mice to murine hepatitis virus strain 3 requires development of a th1, but not a th2, response, whereas pre-existing antibody partially protects against primary infection. | murine hepatitis virus strain 3 (mhv-3) produces a host-strain-dependent spectrum of disease. the development of liver necrosis has been shown to be related to production of a unique macrophage procoagulant activity (pca), encoded by the gene fgl-2, in susceptible mice. these studies were designed to examine the influence of th1/th2 cells on resistance/susceptibility and production of macrophage procoagulant activity (pca) in resistant (a/j) and susceptible (balb/cj) strains of mice following in ... | 1998 | 9782309 |
| loss of resistance to murine hepatitis virus strain 3 infection after treatment with corticosteroids is associated with induction of macrophage procoagulant activity. | activation of the immune coagulation system has been implicated in the pathogenesis of liver injury following infection of inbred mice with murine hepatitis virus strain 3 (mhv-3). following mhv-3 infection, macrophages isolated from mhv-3-susceptible and -semisusceptible inbred strains of mice express increased procoagulant activity (pca), whereas macrophages from resistant strains express no increase in pca over basal levels. the pca induced by mhv-3 is a prothrombinase, encoded by the gene fg ... | 1996 | 8676449 |
| a 2',5'-oligoadenylate analogue inhibits murine hepatitis virus strain 3 (mhv-3) replication in vitro but does not reduce mhv-3-related mortality or induction of procoagulant activity in susceptible mice. | exposure of inbred mice to murine hepatitis virus strain 3 (mhv-3) causes a strain dependent spectrum of disease symptoms which correlates with induction of procoagulant activity (pca) by macrophages. previous studies have demonstrated a role for interferons in resistance to mhv-3 infection. these cytokines have both antiviral and immunoregulatory effects which may be crucial for mhv-3 resistance. one of their antiviral effects is the ability to induce 2',5'-oligoadenylate (2-5a) synthetase lead ... | 1995 | 7844557 |
| protein interferon-stimulated gene 15 conjugation delays but does not overcome coronavirus proliferation in a model of fulminant hepatitis. | coronaviruses express a deubiquitinating protein, the papain-like protease-2 (plp2), that removes both ubiquitin and the ubiquitin-like interferon (ifn)-stimulated gene 15 (isg15) protein from target proteins. isg15 has antiviral activity against a number of viruses; therefore, we examined the effect of isg15 conjugation (isgylation) in a model of acute viral hepatitis induced by the murine hepatitis virus strain 3 (mhv-3) coronavirus. mice deficient in the isg15 deconjugating enzyme, ubiquitin- ... | 2014 | 24648452 |
| the nlrp3 inflammasome and il-1β accelerate immunologically mediated pathology in experimental viral fulminant hepatitis. | viral fulminant hepatitis (fh) is a severe disease with high mortality resulting from excessive inflammation in the infected liver. clinical interventions have been inefficient due to the lack of knowledge for inflammatory pathogenesis in the virus-infected liver. we show that wild-type mice infected with murine hepatitis virus strain-3 (mhv-3), a model for viral fh, manifest with severe disease and high mortality in association with a significant elevation in il-1β expression in the serum and l ... | 2015 | 26367131 |
| effect of alterations in early signal transduction events on the induction of procoagulant activity by murine hepatitis virus strain 3 in vitro. | the induction of macrophage procoagulant activity (pca) has been shown to correlate with the development of fulminant hepatic necrosis after infection with murine hepatitis virus strain 3 (mhv-3). however, comparatively little is known about the early events in cells after viral infection leading to pca expression. accordingly, we investigated the early cellular events in the induction of macrophage pca by mhv-3. mhv-3 stimulation of macrophages did not result in a detectable increase in intrace ... | 1995 | 7730802 |
| resistance of naive mice to murine hepatitis virus strain 3 requires development of a th1, but not a th2, response, whereas pre-existing antibody partially protects against primary infection. | murine hepatitis virus strain 3 (mhv-3) produces a strain-dependent spectrum of disease. the development of liver necrosis has been shown to be related to production of a unique macrophage procoagulant activity (pca), encoded by the gene fgl-2, in susceptible mice. these studies were designed to examine the influence of th1/th2 cells on resistance/susceptibility and production of macrophage pca in resistant (a/j) and susceptible (balb/cj) strains of mice following infection with mhv-3. immunizat ... | 1996 | 8617959 |
| a th1 cell line (3e9.1) from resistant a/j mice inhibits induction of macrophage procoagulant activity in vitro and protects against mhv-3 mortality in vivo. | induction of immune coagulants has been implicated in the pathogenesis of murine hepatitis virus strain 3 (mhv-3)-induced fulminant hepatic necrosis. previous work from our laboratory has shown that the induction of procoagulant activity (pca) correlates with the resistance/susceptibility to disease in inbred and recombinant inbred (ri) strains of mice. macrophages from susceptible, but not resistant, strains of mice expressed increased levels of pca in response to mhv-3 stimulation. t lymphocyt ... | 1994 | 7835959 |
| monoclonal antibody analysis of a unique macrophage procoagulant activity induced by murine hepatitis virus strain 3 infection. | a panel of 24 igg2ak monoclonal antibodies was produced against murine hepatitis virus strain 3 (mhv-3)-induced procoagulant activity (pca) from murine macrophages. the antibodies were specific and did not react in an enzyme-linked immunosorbent assay with purified mhv-3; lipopolysaccharide-induced pca; crude mouse, human, or rabbit tissue factor, or unstimulated murine macrophages. sixteen of 24 monoclonal antibodies inhibited functional pca expression in a one-stage clotting assay. more detail ... | 1991 | 1846363 |
| cellular and metabolic requirements for induction of macrophage procoagulant activity by murine hepatitis virus strain 3 in vitro. | the cellular basis for the variation in induction of monocyte procoagulant activity (pca) by murine hepatitis virus strain 3 (mhv-3) was examined using a set of recombinant inbred strains of mice derived from the resistant (a/j) and susceptible c57b1/6j (b) progenitors. induction of pca by mhv-3 required live virus and host protein and rna synthesis. absolute restriction for induction of pca was observed at the level of the macrophage. peritoneal macrophages from resistant parental a/j and ri st ... | 1991 | 1701794 |
| monoclonal antiprothrombinase (3d4.3) prevents mortality from murine hepatitis virus (mhv-3) infection. | the induction of monocyte/macrophage procoagulant activity (pca) has been implicated in the pathogenesis of murine hepatitis virus strain 3 (mhv-3) infection and disease. previously, we have shown that induction of pca by mhv-3 correlated with resistance/susceptibility to infection in different mouse strains. in this study, all balb/cj mice that were infected with 10(3) plaque-forming units of mhv-3 developed severe liver disease and died within 96-120 h. examination of the livers of these anima ... | 1992 | 1324969 |
| increased killing of liver nk cells by fas/fas ligand and nkg2d/nkg2d ligand contributes to hepatocyte necrosis in virus-induced liver failure. | the role of liver nk cells in virus-induced severe viral hepatitis and, subsequently, hepatic failure is not well defined. in this study, we investigated the role of liver nk cells in the development of hepatocyte necrosis in fulminant hepatic failure (fhf) and acute-on-chronic liver failure (aclf) because of viral infection. a mouse model of fhf induced by murine hepatitis virus strain 3 (mhv-3) was used to study the role of liver nk cells. samples from patients with hepatitis b virus-related a ... | 2010 | 19949088 |
| induction of macrophage procoagulant activity by murine hepatitis virus strain 3: role of tyrosine phosphorylation. | the induction of a unique macrophage procoagulant molecule by murine hepatitis virus strain 3 correlates with the severity of viral hepatitis. the role of tyrosine phosphorylation in the signalling pathway leading to procoagulant expression was studied. murine hepatitis virus strain 3 initiated a rapid increase in phosphotyrosine accumulation. tyrosine kinase inhibition precluded this increase and abrogated expression of the virus-induced procoagulant mouse fibrinogen-like protein (musfiblp) gen ... | 1995 | 7543590 |
| 16, 16 dimethyl prostaglandin e2 prevents the development of fulminant hepatitis and blocks the induction of monocyte/macrophage procoagulant activity after murine hepatitis virus strain 3 infection. | 16, 16 dimethyl prostaglandin e2 (dmpge2), a known cytoprotective agent, was examined for its ability to alter the course of fulminant hepatitis in an experimental model of fulminant viral hepatitis, murine hepatitis murine hepatitis type 3 (mhv-3). fully susceptible balb/cj mice, infected with 100 50% lethal doses (ld50) of mhv-3 developed histologic and biochemical evidence of fulminant hepatitis, as evidenced by massive hepatic necrosis with hypoglycemia, metabolic acidosis, and a markedly el ... | 1987 | 3624490 |
| [hfgl2/fibroleukin expression in liver and peripheral blood mononuclear cells (pbmc) and its correlation with disease severity]. | viral hepatitis remains a major public health problem and the most common type of liver disease worldwide. there are an increasing number of patients with chronic hepatitis b who develop acute hepatitis on chronic condition (aoc) and die of acute hepatic failure both as a result of lack of understanding of the pathogenesis of the disease and lack of effective treatment. the hallmark of aoc is the extreme rapidity of the necromicroinflammatory process resulting in widespread or total hepatocellul ... | 2004 | 15268797 |
| targeted delivery of ribavirin improves outcome of murine viral fulminant hepatitis via enhanced anti-viral activity. | side effects of interferon-ribavirin combination therapy limit the sustained viral response achievable in hepatitis c virus (hcv) patients. coupling ribavirin to macromolecular carriers that target the drug to the liver would reduce systemic complications. the aim of this study was to evaluate the efficacy of a hemoglobin-ribavirin conjugate (hrc 203) in murine hepatitis virus strain 3 (mhv-3) induced viral hepatitis. hrc 203 had greater anti-viral activity on both isolated hepatocytes and macro ... | 2006 | 16496340 |
| the fgl2/fibroleukin prothrombinase contributes to immunologically mediated thrombosis in experimental and human viral hepatitis. | fibrin deposition and thrombosis within the microvasculature is now appreciated to play a pivotal role in the hepatocellular injury observed in experimental and human viral hepatitis. importantly, the pathways by which fibrin generation is elicited in viral hepatitis may be mechanistically distinct from the classical pathways of coagulation induced by mechanical trauma or bacterial lipopolysaccharide (lps). in the setting of murine hepatitis virus strain-3 (mhv-3) infection, a member of the coro ... | 2003 | 12840059 |
| murine hepatitis virus strain 3 induces the macrophage prothrombinase fgl-2 through p38 mitogen-activated protein kinase activation. | the clinical syndrome of acute liver failure produced by fulminant viral hepatitis can be reproduced in mice by infection with murine hepatitis virus strain 3 (mhv-3). although it is clear that mhv-3-induced hepatitis depends upon macrophage activation and the expression of a specific prothrombinase, fgl-2, the signaling pathways involved in virally stimulated cell activation are unclear. since we had previously found that mhv-3 induces the tyrosine phosphorylation of cellular proteins, we inves ... | 1998 | 9822700 |
| resistance to murine hepatitis virus strain 3 is dependent on production of nitric oxide. | the strain-specific spectrum of liver disease following murine hepatitis virus type 3 (mhv-3) infection is dependent on inflammatory mediators released by macrophages. production of nitric oxide (no) by macrophages has been implicated in resistance to a number of viruses, including ectromelia virus, vaccinia virus, and herpes simplex virus type 1. this study was undertaken to define the role of no in mhv-3 infection. gamma interferon-induced production of no inhibited growth of mhv-3 in a murine ... | 1998 | 9696801 |
| fulminant hepatic failure in murine hepatitis virus strain 3 infection: tissue-specific expression of a novel fgl2 prothrombinase. | activation of the immune coagulation system has been implicated in the pathogenesis of fulminant liver failure caused by murine hepatitis virus strain 3 (mhv-3). the recent discovery of the fgl2 gene, which encodes for mhv-3-induced prothrombinase (fgl2 prothrombinase), allows for fundamental studies to determine the molecular basis for fulminant liver failure. transcription of the fgl2 gene and translation of the protein it encodes were examined in the liver and other organs of susceptible mice ... | 1997 | 9371581 |
| association between nitric oxide synthesis and vaccination-acquired resistance to murine hepatitis virus by spf mice. | murine hepatitis virus strain 3 (mhv-3) produces a strain-dependent pattern of disease, with a/j and balb/c mice being considered models of resistance and susceptibility, respectively. a role for nitric oxide in controlling infection remains debatable; thus, we monitored nitric oxide levels in blood and liver of immunized and nonimmunized spf mice during infection by electron paramagnetic resonance. in parallel, liver histology, virus titers, and plasma alanine aminotransferase (alt) activity we ... | 2006 | 17045921 |
| expression of b and t lymphocyte attenuator (btla) in macrophages contributes to the fulminant hepatitis caused by murine hepatitis virus strain-3. | fulminant viral hepatitis (fh) remains a serious clinical problem for which the underlying pathogenesis remains unclear. the b and t lymphocyte attenuator (btla) is an immunoglobulin-domain-containing protein that has the capacity to maintain peripheral tolerance and limit immunopathological damage during immune responses. however, its precise role in fh has yet to be investigated. | 2013 | 22637698 |
| ribavirin inhibits viral-induced macrophage production of tnf, il-1, the procoagulant fgl2 prothrombinase and preserves th1 cytokine production but inhibits th2 cytokine response. | ribavirin, a synthetic guanosine analogue, possesses a broad spectrum of activity against dna and rna viruses. it has been previously shown to attenuate the course of fulminant hepatitis in mice produced by murine hepatitis virus strain 3. we therefore studied the effects of ribavirin on murine hepatitis virus strain 3 replication, macrophage production of proinflammatory mediators including tnf, il-1, and the procoagulant activity (pca), fgl2 prothrombinase; and th1/th2 cytokine production. alt ... | 1998 | 9531310 |
| cd69+nk cells contribute to the murine hepatitis virus strain 3-induced murine hepatitis. | the role of hepatic cd69+ natural killer (nk) cells in virus-induced severe liver injury and subsequent hepatic failure is not well defined. in this study, a mouse model of fulminant liver failure (fhf) induced by murine hepatitis virus strain 3 (mhv-3) was used to study the role of hepatic cd69+nk cells in the development of fhf. the cd69 expression in nk cells in the liver, spleen, bone marrow and peripheral blood was detected by using flow cytometry. the correlation between the cd69 level in ... | 2013 | 23904369 |
| a disparate subset of double-negative t cells contributes to the outcome of murine fulminant viral hepatitis via effector molecule fibrinogen-like protein 2. | the underlying immune-mediated mechanisms involved in virus-induced severe hepatitis have not been well elucidated. in this study, we investigated the role of cd3(+)cd4(-)cd8(-) double-negative t (dn t) cells in the pathogenesis of fulminant viral hepatitis (fvh) induced by murine hepatitis virus strain 3 (mhv-3). after mhv-3 infection, the proportions of dn t cells increased significantly in balb/cj mice, and splenic dn t cells expressing high levels of cd69 were recruited by mhv-3-infected hep ... | 2016 | 26482053 |
| c5a/c5ar pathway is essential for the pathogenesis of murine viral fulminant hepatitis by way of potentiating fgl2/fibroleukin expression. | viral fulminant hepatitis (fh) remains a serious clinical problem with very high mortality. lacking understanding of fh pathogenesis has in essence hindered efficient clinical treatment. inferring from a correlation observed between the genetic differences in the complement component 5 (c5) and the susceptibility of mouse strains to murine hepatitis virus strain-3 (mhv-3) infections, we propose that excessive complement activation plays a critical role in the development of fh. we show that mhv- ... | 2014 | 24604562 |
| tumor necrosis factor α (tnf-α) receptor-i is required for tnf-α-mediated fulminant virus hepatitis caused by murine hepatitis virus strain-3 infection. | tnf-α plays an essential role in the pathogenesis of fulminant virus hepatitis (fh) caused by infection with murine hepatitis virus strain-3 (mhv-3). however, the specific tnf-α receptors (tnfr) involved in this disease and how they mediate this effect are uncertain. here, we showed that the expression of tnfr1 and tnfr2 in the liver and spleen was triggered by mhv-3. however, only tnfr1(-/-) mice were resistant to mhv-3 mediated fh, as displayed by a dramatic decrease in tissue necrosis and cel ... | 2014 | 24286726 |
| cd4-cd8-t cells contribute to the persistence of viral hepatitis by striking a delicate balance in immune modulation. | viral hepatitis remains the most common cause of liver disease and a major public health problem. here, we focus on the role of cd4 cd8 double negative t (dn t) cells involved in the mechanisms of viral persistence in hepatitis. c3h/hej mice infected with murine hepatitis virus strain 3 (mhv-3) were used to display chronic viral hepatitis. dn t cells dramatically increased in mhv-3 infected mice. adoptive transfer of dn t cells from mhv-3 infected mice led to a significant increase in mice survi ... | 2012 | 23261832 |
| liver tcrγδ(+) cd3(+) cd4(-) cd8(-) t cells contribute to murine hepatitis virus strain 3-induced hepatic injury through a tnf-α-dependent pathway. | the mechanisms of each subset of immune cells contributing to the pathogenesis of viral hepatitis remain incompletely understood. in this study, we examined the role of liver cd4(-) cd8(-) (double negative, dn) t cells during murine hepatitis virus strain 3 (mhv-3)-induced hepatitis in c3h/hej mice. we demonstrate that predominant population of dn t cells in the liver of healthy or mhv-3-infected mice express tcrγδ(+). the proportion of tcrγδ(+) dn t cells in liver cd3(+) t cells was markedly in ... | 2012 | 22750070 |
| [the functions of liver natural killer cells in murine fulminant hepatitis induced by murine hepatitis virus strain 3]. | to investigate the role of liver natural killer cells (nk cells) in murine hepatitis virus strain 3 (mhv-3) induced murine fulminant hepatitis. | 2008 | 18822205 |
| the novel cd4+cd25+ regulatory t cell effector molecule fibrinogen-like protein 2 contributes to the outcome of murine fulminant viral hepatitis. | fulminant viral hepatitis (fh) remains an important clinical problem in which the underlying pathogenesis is not well understood. here, we present insight into the immunological mechanisms involved in fh caused by murine hepatitis virus strain 3 (mhv-3), indicating a critical role for cd4(+)cd25(+) regulatory t cells (tregs) and production of the novel treg effector molecule fgl2. before infection with mhv-3, susceptible balb/cj mice had increased numbers of tregs and expression of fgl2 messenge ... | 2009 | 19085958 |
| dual interference with novel genes mfgl2 and mtnfr1 ameliorates murine hepatitis virus type 3-induced fulminant hepatitis in balb/cj mice. | our studies and those of many others have implicated hepatocyte necrosis and apoptosis mediated by fibrinogen-like protein-2 (fgl2) prothrombinase and tumor necrosis factor receptor (tnfr) in the development of fulminant viral hepatitis, a disease with a mortality rate greater than 80% in cases lacking immediate organ transplantation. this study was designed to explore the efficacy of dual short hairpin rna (shrna) interference with fgl2 and tnfr1 in the treatment of murine hepatitis virus strai ... | 2010 | 20218879 |
| programmed death (pd)-1-deficient mice are extremely sensitive to murine hepatitis virus strain-3 (mhv-3) infection. | the inhibitory receptor programmed death-1 (pd-1) has the capacity to maintain peripheral tolerance and limit immunopathological damage; however, its precise role in fulminant viral hepatitis (fh) has yet to be described. here, we investigated the functional mechanisms of pd-1 as related to fh pathogenesis induced by the murine hepatitis virus strain-3 (mhv-3). high levels of pd-1-positive cd4(+), cd8(+) t cells, nk cells and macrophages were observed in liver, spleen, lymph node and thymus tiss ... | 2011 | 21750671 |
| il-33 protects murine viral fulminant hepatitis by targeting coagulation hallmark protein fgl2/fibroleukin expression. | fulminant hepatitis (fh) is characterized by rapid liver failure and high mortality. the pathogenesis of viral fh includes virus-induced immune activation, inflammation, and subsequent hepatic apoptosis and necrosis. however, the mechanisms that underlie fh progression are unclear. il-33 is a member of the il-1-related cytokines, considered to be an "alarmin" that participates in various diseases, but its precise role in the coagulation of fh is not very clear. in our study, we found that il-33 ... | 2017 | 28494352 |
| vsig4 inhibits proinflammatory macrophage activation by reprogramming mitochondrial pyruvate metabolism. | exacerbation of macrophage-mediated inflammation contributes to pathogenesis of various inflammatory diseases, but the immunometabolic programs underlying regulation of macrophage activation are unclear. here we show that v-set immunoglobulin-domain-containing 4 (vsig4), a b7 family-related protein that is expressed by resting macrophages, inhibits macrophage activation in response to lipopolysaccharide. vsig4-/-mice are susceptible to high-fat diet-caused obesity and murine hepatitis virus stra ... | 2017 | 29109438 |
| clara cell 10 kda protein alleviates murine hepatitis virus strain 3-induced fulminant hepatitis by inhibiting fibrinogen-like protein 2 expression. | background: fulminant hepatitis (fh) is a serious threat to human life, accompanied by massive and rapid necroinflammation. kupffer cells, the major immune cell population involved in innate immune responses, are considered to be central for fh. fibrinogen-like protein 2 (fgl2) is a pro-coagulant protein that is substantially induced in macrophages upon viral infection, and fgl2 depletion represses murine hepatitis virus strain 3 (mhv-3) infection. clara cell 10 kda (cc10) protein is a secretory ... | 2018 | 30619295 |
| kctd9 deficiency impairs natural killer cell development and effector function. | we previously showed that potassium channel tetramerization domain containing 9 (kctd9) is aberrantly expressed in natural killer (nk) cells in patients with hepatitis b virus-associated acute-on-chronic liver failure and mice with experimental fulminant hepatitis. however, the mechanism underlying the regulation of nk cell function and fulminant hepatitis progression by kctd9 is unknown. here, we investigated the role of kctd9 in regulation of early development, maturation, and function of nk c ... | 2019 | 31024568 |
| γδ t cells contribute to the outcome of murine fulminant viral hepatitis via effector cytokines tnf-α and ifn-γ. | the mechanisms involved in virus-induced severe hepatitis have not been fully elucidated. in this study, we investigated the role of gamma delta t cell receptors (γδ) t cells in the pathogenesis of fulminant viral hepatitis (fvh) induced by murine hepatitis virus strain 3 (mhv-3). the model of fvh was established by intraperitoneal injection of mhv-3 into balb/cj mice. the survival days of mice, and the serum levels of alanine aminotransferase (alt) and aspartate aminotransferase (ast) were exam ... | 2018 | 30128874 |
| c5ar, tnf-α, and fgl2 contribute to coagulation and complement activation in virus-induced fulminant hepatitis. | viral fulminant hepatitis (fh) is a disease with a high mortality rate. activation of the complement system correlates with the development of fh. however, the key factors mediating complement activation in fh remain elusive. | 2015 | 25200905 |