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Kazuhide Yamamoto

Publications and source records attributed to Kazuhide Yamamoto.

At least 19 recordsLinked to original sources
PubMed2006

Gene expression profiling in biliary epithelial cells of primary biliary cirrhosis using laser capture microdissection and cDNA microarray.

UNLABELLED: Primary biliary cirrhosis (PBC) is a chronic, cholestatic liver disease characterized by progressive destruction of interlobular bile ducts that leads to biliary cirrhosis. To elucidate the etiology of PBC, the gene expression profile in biliary epithelial cells (BECs) was analyzed. Liver specimens of 5 PBC, 3 chronic hepatitis C (CHC), and 3 normal subjects were obtained. BECs were selectively collected by laser capture microdissection (LCM), RNA were obtained by extraction and amplification with T7 RNA polymerase, and a cDNA microarray analysis was performed. The following genes exhibited increased expression in BEC of PBC, as compared with CHC or normal subjects: human leukocyte antigen DQ alpha 1 (HLA-DQA-1), carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), and vascular cell adhesion molecule 1 (VCAM-1). The immunohistochemistry for HLA-DQA-1, CEACAM1, TRAIL, and VCAM-1 confirmed these results. Furthermore, two-way cluster analysis showed that the gene expression profiling in BEC of PBC were categorized into a separate cluster, distinct from CHC or normal subjects. CONCLUSIONS: The gene expression profiling in BEC of PBC differed from those of CHC and normal subjects, and the genes concerning local immune response, such as HLA-DQA-1, CEACAM1, TRAIL, and VCAM-1, exhibited increased expression, indicating that they were involved in the development of bile duct injury.

Adult↗
PubMed2005

Association of virus infected-T cell in severe hepatitis caused by primary Epstein-Barr virus infection.

BACKGROUND: Infectious mononucleosis owing to primary Epstein-Barr virus (EBV) infection sometimes causes hepatitis, which is usually self-limiting with mildly elevated transaminases, but can rarely develop into severe hepatitis with jaundice. OBJECTIVE: To clarify the pathogenesis of severe hepatitis by primary EBV infection. METHODS: We experienced four cases of severe hepatitis with jaundice caused by primary EBV infection. These cases were analyzed virologically and histologically, and compared with infectious mononucleosis patients without jaundice. RESULTS AND DISCUSSION: Using real-time PCR, more EBV-DNA was detected in peripheral blood from patients with severe hepatitis, as compared to those without jaundice. Furthermore, CD3+, CD4+ or CD8+ cells contained more EBV DNA than did other cell populations, indicating that in severe hepatitis, T cells harbor most of the EBV. By contrast, mainly B cells were infected in infectious mononucleosis patients without jaundice. The liver was biopsied in three of the four cases. An in situ hybridization study showed that EBV infected lymphocytes, not hepatocytes. In addition, in one patient, it was confirmed that the infected lymphocytes were CD8+ T cells. These results suggest that a large EBV burden and T cell infection may play major roles in the mechanism of severe hepatitis caused by primary EB virus infection.

Adolescent↗
PubMed2005

Are bile duct lesions of primary biliary cirrhosis distinguishable from those of autoimmune hepatitis and chronic viral hepatitis? Interobserver histological agreement on trimmed bile ducts.

BACKGROUND: Primary biliary cirrhosis (PBC) is histopathologically characterized by chronic nonsuppurative destructive cholangitis and ductopenia of interlobular bile ducts. Bile duct injury is also often encountered in chronic viral hepatitis (CVH) and in autoimmune hepatitis (AIH). METHODS: In this study, we performed interobserver agreement analysis on 90 injured bile ducts from liver specimens of PBC (17 cases), CVH (26 cases), and AIH (18 cases), with 30 bile ducts chosen from each disease group. Digital images of bile ducts with minimal periductal elements were recorded in CD-ROM format and sent to 14 observers (six special hepatopathologists, four local hepatopathologists, and four general pathologists). We analyzed the following issues: (1) diagnostic accuracy of PBC, based only on bile duct lesions; (2) classification of bile duct lesions in AIH cases as destructive cholangitis equivalent to PBC-associated injury, or not. RESULTS: The diagnostic accuracy of PBC cases with severe bile duct injuries was very high (over 80%), although the accuracy in cases with only mild bile duct injuries was low (50% or less). For AIH, each observer classified 9 of the 30 bile ducts, on average, as destructive cholangitis. CONCLUSIONS: This study revealed that 66.9% of PBC cases could be diagnosed based on trimmed bile ducts alone. Bile duct injury similar to that in PBC could be encountered in AIH.

Bile Ducts↗
PubMed2005

Stool decay-accelerating factor as a marker for monitoring the disease activity during leukocyte apheresis therapy in patients with refractory ulcerative colitis.

BACKGROUND AND AIMS: We have shown previously that concentrations of stool decay-accelerating factor (DAF; CD55), a complement regulatory protein, in patients with ulcerative colitis (UC) are increased in relation to the severity of the colonic mucosal inflammation. In the present study, we evaluated the usefulness of stool DAF as a marker for monitoring disease activity in patients with steroid-resistant active UC being treated with leukocyte apheresis performed with a centrifugal cell separator. METHODS: Twenty-one patients with active and steroid-resistant UC were treated with leukocyte apheresis once a week for 4 weeks, and stool DAF concentrations were determined weekly by immunoassay. RESULTS: After treatment, 11 (52%) of the 21 UC patients went into remission. Stool DAF concentrations decreased promptly and steadily in the responsive group. The difference reached statistical significance as soon as after the second apheresis session (P < 0.003), compared with values before the therapy and corresponding values in the non-responsive group (P = 0.024). The reduction in stool DAF concentrations after the second apheresis session was significantly greater in the responsive group (median 90%, range 22-90%) than in the non-responsive group (median -13%, range -307-94%) (P = 0.008). Hematological tests, that is, white blood cell (WBC) count and C-reactive protein, declined significantly during the apheresis therapy, but not in relation to therapeutic response. CONCLUSION: Stool DAF concentration is a useful marker in the clinical response of UC patients to treatment with leukocyte apheresis.

Adolescent↗
PubMed2004

Caspase induction by IgA antimitochondrial antibody: IgA-mediated biliary injury in primary biliary cirrhosis.

Anti-mitochondrial antibodies (AMAs) have long been recognized as a serological hallmark of primary biliary cirrhosis (PBC). Although high titers of immunoglobulin (Ig)A AMAs are found in bile, saliva, and urine of patients, a pathogenic role for this antibody has remained elusive. Functional studies of this IgA in general have been impeded by low quantities of antibody and the inability to recover antigen-specific IgA in dimeric form. Using a newly defined synthetic group A. Streptococcus derived peptide, we purified large quantities of dimeric and monomeric IgA from patient sera. The purified IgA was incubated with Madine-Darby canine kidney (MDCK) cells transfected with the human polymeric Ig receptor (pIgR) and the cells studied by flow cytometric analysis for binding of carboxyfluorescein conjugated VAD-fmk peptide to activated caspase enzymes. A total of 87% of PBC patients that were anti-PDC-E2 positive had serum IgA that increased caspase activation in MDCK-pIgR+ cells compared to serum-derived IgA from controls with a maximum reaction 48 hours after addition of IgA. The titer of anti-PDC-E2 IgA among the PBC patients strongly correlated with caspase activation (cc = 0.88). Pre-absorption of the IgA using recombinant 2-oxo-acid dehydrogenase complex significantly diminished this activation. IgG from the same PBC patients did not induce caspase activation. These data suggest that during transcytosis through pIgR-positive cells, exposure to PDC-E2-specific dimeric IgA results in the initiation of caspase activation. In conclusion, we propose that due to an even greater concentration of dimeric IgA in biliary and mucosal secretions, constant transcytosis would render the exposed cells more susceptible to apoptosis resulting in subsequent bile duct damage.

Animals↗
PubMed2004

Increased serum concentrations and surface expression on peripheral white blood cells of decay-accelerating factor (CD55) in patients with active ulcerative colitis.

Inflammatory stimuli induce expression and release of decay-accelerating factor (DAF), a complement-regulatory protein present on peripheral-blood cells. Therefore, in ulcerative colitis (UC), an inflammatory colonic disease in which activated leukocytes are involved, DAF may be released from leukocytes into the circulation. In this study we compared serum DAF concentrations and surface DAF expression on peripheral-blood cells in patients with UC with disease activity. Peripheral-blood samples were obtained from 60 patients with UC (30 with active and 30 with inactive disease) and 19 healthy volunteers. Serum DAF concentrations were determined by means of immunoassay, and surface DAF expression on blood cells was examined with the use of flow cytometry. Serum DAF concentrations in patients with active disease (mean 48.6 ng/mL) were significantly higher than those in patients whose disease was in remission (33.3 ng/mL; P =.0003) and those in healthy controls (32.3 ng/mL; P =.0007). Surface DAF expression on neutrophils, CD14+ monocytes, and subsets of lymphocytes in patients with active UC was significantly increased compared with that in patients with UC in remission and in healthy controls. The increased serum DAF concentrations and surface DAF expression on leukocyte fractions in patients with active disease fell to significantly lower levels when the disease had gone into remission after medical therapy. Serum DAF concentrations are increased in UC patients in relation to disease activity. The likely source of increased DAF concentrations is peripheral-blood leukocytes that have been activated as part of the UC disease process.

Adult↗
PubMed2004

Difference in Ulex europaeus agglutinin I-binding activity of decay-accelerating factor detected in the stools of patients with colorectal cancer and ulcerative colitis.

Expression of decay-accelerating factor (DAF, CD55), a complement-regulatory glycoprotein, is enhanced in colorectal-cancer (CC) cells and colonic epithelium in ulcerative colitis (UC), and stools from these patients contain increased amounts of DAF. Carbohydrate chains of glycoproteins are often altered during malignant transformation or inflammation. In this study, we investigated whether DAF molecules in patients with CC and those with UC differ with respect to oligosaccharide side chains. We analyzed DAF in stools and homogenates of colonic-tissue specimens obtained from patients with CC or UC using solid-phase enzyme-linked assay and Western blotting for reactivity with the lectins Ulex europaeus agglutinin I (UEA-I), wheat-germ agglutinin, peanut agglutinin, and concanavalin A. UEA-I bound to DAF in stools from patients with UC but not in that from the stools of CC patients, as demonstrated on the solid-phase enzyme-linked assay (P <.05, Mann-Whitney U test) and Western blotting. Binding of UEA-I was specifically inhibited by the addition of fucose. The difference in UEA-I reactivity with DAF was observed also in colonic-tissue homogenates from patients with UC and those with CC. DAF expressed in the mucosa and excreted into the stools of UC patients is different from that expressed in CC with regard to UEA-I reactivity. Future studies should be directed toward determining whether a qualitatively unique isoform of DAF is present, of which sugar chains are specific to CC in UC patients.

Adenocarcinoma↗
PubMed2004

Enhanced expression of decay-accelerating factor, a complement-regulatory protein, in the specialized intestinal metaplasia of Barrett's esophagus.

Intestinal-type epithelium in Barrett's esophagus, so-called specialized intestinal metaplasia (SIM), is a risk factor for the development of esophageal adenocarcinoma. Surface expression of decay-accelerating factor (DAF), a complement-regulatory protein, is markedly enhanced in intestinal metaplasia of the gastric mucosa. We therefore examined DAF expression in areas of SIM in Barrett's esophagus in an attempt to determine whether DAF is a biomarker of SIM. We obtained 53 endoscopic biopsy specimens from the esophageal columnar mucosae of 45 patients. We immunohistochemically examined the distribution of DAF and 2 other complement-regulatory proteins: homologous restriction factor-20 and membrane cofactor protein. We also examined the expression of DAF messenger RNA in SIM with the use of laser-capture microdissection and reverse transcription-polymerase chain reaction. Of the 53 specimens, 10 were found histologically to involve areas of SIM, 41 were SIM-negative epithelium, and 2 comprised areas of SIM and SIM-negative epithelium. DAF staining was negligible in 35 of 43 specimens of the SIM-negative columnar epithelium, but DAF was strongly stained on the apical surface in all 12 SIM-positive specimens (P <.0001). In the 2 biopsy specimens in which both SIM and SIM-negative columnar epithelium were present, DAF staining was confined to the area of SIM. The expression of DAF messenger RNA was detected significantly more often in SIM than in SIM-negative columnar epithelium (P =.022). We conclude that DAF may be a surface marker for SIM and therefore useful in the identification of areas of the mucosa at risk for the development of adenocarcinoma in Barrett's esophagus.

Adult↗
PubMed2004

Helicobacter pylori eradication improves pre-existing reflux esophagitis in patients with duodenal ulcer disease.

BACKGROUND & AIMS: There has been significant controversy over the relationship between Helicobacter pylori infection and reflux esophagitis. We investigated the effects of eradicating H. pylori on the reflux esophagitis found in patients with peptic ulcers. METHODS: Prospective posteradication evaluations were conducted yearly in 162 H. pylori-positive patients who had reflux esophagitis together with peptic ulcer disease (4 women and 158 men, mean age = 49.1 yr). The Los Angeles classification of the patients' esophagitis was: grade A, 90; grade B, 63; and grade C, 9. The follow-up evaluations began 1 to 2 months after completion of the eradication treatment (mean time of follow-up = 22 mo), and consisted of endoscopy and an interview focusing on heartburn. RESULTS: Six patients were withdrawn from the study because of adverse drug reactions or a failure to regularly keep their appointments. After eradication therapy, we observed endoscopically that reflux esophagitis had improved in 87 (55.8%) of the 156 patients. The improvement rate was significantly higher in patients cured of infection (60.8%) than in those with persistent H. pylori infection (38.9%) (P = 0.04). Body mass index (odds ratio = 0.86, 95% confidence interval [CI] = 0.76-0.97), cure of infection (3.68, 95% CI = 1.56-8.69), the absence of a hiatal hernia (3.90, 95% CI = 1.83-8.28), and an ulcer located in the duodenum (2.75, 95% CI = 1.33-5.70) were identified as significant independent factors for the improvement of reflux esophagitis. CONCLUSIONS: In patients with reflux esophagitis associated with duodenal ulcer, a significant improvement in pre-existing reflux esophagitis was noted after H. pylori eradication.

Adolescent↗
PubMed2004

Research on potential radiation risks in areas with nuclear power plants in Japan: leukaemia and malignant lymphoma mortality between 1972 and 1997 in 100 selected municipalities.

The results of a geographical correlation study using Poisson regression analysis are reported for leukaemia and malignant lymphoma mortality between 1972 and 1997 in 100 selected Japanese municipalities with or without a nuclear power plant (NPP). The data did not support social concerns of an increased risk of malignant lymphoma in the vicinity of Japanese NPPs. However, some estimates of overall excess relative risk (ERR; relative risk minus one) were statistically significantly positive for leukaemia mortality in 20 NPP municipalities compared with mortality in the remaining 80 control areas, taking into account a minimum two-year latency following the start of commercial operation. One estimate was 0.228 (95% CI: 0.074-0.404) from a simple area adjustment using the mortality in all Japan as the external baseline rate. This superficial increase is not due to leukaemia among young people, aged less than 25 years at death. The ERR estimate for ages at death of 50-74 years was confounded to be positive for leukaemia and distorted to be negative for malignant lymphoma. For leukaemia, a positive ERR estimate was seen, especially for females and during specific periods. Confounding of the ERR estimate for two causes was also seen in some NPP areas including a high adult T-cell leukaemia (ATL) area. Temporal area variations associated with ATL misclassification and a temporal increasing trend of leukaemia mortality in the elderly caused the confounding effects. Our findings do not support the hypothesis of a leukaemogenic impact of NPPs in Japan.

Adult↗
PubMed2004

Complement regulatory proteins in normal human esophagus and esophageal squamous cell carcinoma.

BACKGROUND: Altered expression of three complement regulatory proteins, decay-accelerating factor (CD55), membrane cofactor protein (CD46) and homologous restriction factor 20 (CD59) has been identified in human gastrointestinal malignancies, but their expression in esophageal cancer has not been described. Therefore the purpose of the present paper was to study the distribution of these proteins in human normal and malignant esophageal mucosa. METHODS AND RESULTS: In the normal esophageal mucosa, CD55 predominantly stained on the cell membrane of squamous epithelium in the superficial and prickle cell layers, whereas CD46 most intensely stained on the cell membrane in the basal and parabasal cell layers. In contrast to this reciprocal expression of CD55 and CD46, CD59 was broadly distributed on the cell membrane in all layers. In the esophageal squamous cell carcinoma, CD55 staining was intense in the stroma but was negligible in the cancer cells. In contrast, CD46 and CD59 stained almost uniformly on the tumor cell membrane. There was a significant difference in the intensity of the staining of CD55 and CD46 among cells in various layers of normal esophageal mucosa and esophageal carcinoma cells, but not in the staining of CD59. Similar expression patterns of the three complement regulatory proteins in carcinoma cells and in normal epithelium in the basal and parabasal cell layers were observed. CONCLUSIONS: These observations on the expression of the three complement regulatory proteins would help understanding of the host immune responses involving the complement system against esophageal squamous cell carcinoma.

Antigens, CD↗
PubMed2003

A scoring system for primary biliary cirrhosis and its application for variant forms of autoimmune liver disease.

BACKGROUND: Although primary biliary cirrhosis (PBC) and autoimmune hepatitis (AIH) are two independent autoimmune liver diseases, it is sometimes difficult to characterize the variant forms of autoimmune liver disease. A PBC scoring system, in combination with the AIH scoring system may be helpful to characterize such patients. METHODS: A PBC scoring system was introduced that selected 14 categories characteristic of PBC. One hundred and thirty-four patients with PBC, 31 patients with autoimmune cholangitis (AIC), 22 patients with overlap syndrome, and 48 patients with AIH were included in the study. The AIC patients fulfilled the PBC criteria but were negative for anti-mitochondrial antibody and positive for anti-nuclear antibody. Overlap syndrome patients fulfilled both the PBC and AIH criteria. RESULTS: The total scores (means +/- SD) for the PBC, AIC, overlap syndrome, and AIH patients were 23.3 +/- 4.7, 9.3 +/- 4.4, 18.0 +/- 5.9, and 3.6 +/- 3.3, respectively. When definite and probable PBC patients were defined as those with a total score of over 17 and 9-17, respectively, all except for 1 patient could be classified as definite or probable PBC. Four of the 48 AIH patients were classified as probable PBC. PBC scores for the variant autoimmune liver diseases showed a wide deviation. Plotting both PBC and AIH scores in a rectangular coordinate enabled us to locate each patient with variant forms according to the deviation from classical PBC or AIH. CONCLUSIONS: The PBC scoring system might be useful in characterizing the features of variant forms of autoimmune liver disease.

Autoimmune Diseases↗
PubMed2003

Release of decay-accelerating factor into stools of patients with colorectal cancer by means of cleavage at the site of glycosylphosphatidylinositol anchor.

The expression of decay-accelerating factor (DAF), a cell-membrane-complement regulator, is enhanced in colorectal cancer, and DAF is detected in the stools of patients with colorectal cancer. In this study, to elucidate mechanisms whereby DAF is released into the colonic lumen, we analyzed and compared the properties of DAF in stools and colorectal-cancer tissues. Stool specimens taken before surgery and tissue samples from surgically resected colorectal cancers were obtained from 21 patients. We analyzed DAF in stool and tissue specimens using immunoblotting, ultracentrifugation, and phase separation with Triton X-114. We analyzed the expression profile of DAF mRNA in cancer tissues using reverse transcription-polymerase chain reaction to determine whether DAF transcripts for a secretory form of DAF were present. With the use of immunoblotting, stool DAF was detected as a broad band with a molecular weight of around 70,000 kDa that migrated slightly more slowly than cancer-tissue DAF. About 90% of stool DAF was present as a soluble form that remained in the 100,000 g supernatant after ultracentrifugation. On phase separation with Triton X-114, the soluble stool DAF was partitioned mainly into the aqueous phase, indicating its hydrophilic nature and lack of the fatty-acid glycosylphosphatidylinositol anchor component. In colorectal cancer tissues, reverse transcription-polymerase chain reaction experiments revealed a nonspliced DAF messenger RNA that encodes a secretory form of DAF in just 2 of the 21 specimens examined. These data suggest that DAF is released from colorectal cancer cells by way of cleavage of membrane-bound DAF at the site of the glycosylphosphatidylinositol anchor.

Adult↗
PubMed2003

Clinicopathological features of acute-onset autoimmune hepatitis.

The clinicopathological features of nine acute-onset autoimmune hepatitis (AIH) patients were compared with those of 29 classical AIH patients. The clinical features of acute-onset AIH showed significantly higher serum ALT levels, lower serum IgG levels and AIH score than those of classical AIH, although the type of auto-antibodies, age and gender were not different between the two groups. Pathological features showed that the stages of acute-onset AIH varied from stage 1 to stage 4 and were less advanced compared with those of classical AIH. One patient showed submassive hepatic necrosis. Both centrilobular necrosis and interface hepatitis were observed in 7 and 8 of 9, respectively. Three stage 1 patients with centrilobular necrosis and one patient with submassive hepatic necrosis were suggestive of acute presentation, while patients with stages 2 and 4 fibrosis were suggestive of acute exacerbation of chronic disease. An immunohistochemical study demonstrated that CD8 T cells were predominant at both interface hepatitis and centrilobular necrosis, while CD79alpha-positive B lineage cells were predominant at interface hepatitis. These results suggest that acute-onset AIH includes both acute presentation and acute exacerbation of chronic disease and that centrilobular necrosis might be a prevailing pathological feature.

Journal Article↗
PubMed2003

A monoclonal antibody to rat asialoglycoprotein receptor that recognizes an epitope specific to its major subunit.

We previously developed three mouse monoclonal antibodies (MoAbs) identifying the domain-specific plasma membrane proteins of rat hepatocytes. Based on the results of immunohistochemical and immunoblot analysis, one of them, clone 8D7, likely recognizes the rat asialoglycoprotein receptor (ASGPR), which consists of three polypeptide subunits: rat hepatic lectin (RHL)-1, RHL-2 and RHL-3. In this study, we examined the reactivity of MoAb 8D7 with these subunits in order to identify specifically the protein it recognizes. RHL-1 and RHL-2/3 were expressed in COS-1 mammalian kidney cells transfected with cloned cDNAs. Reactivity of MoAb 8D7 with these proteins was examined by flow cytometry, immunoblotting, and an immunofluorescence staining. By flow cytometry, MoAb 8D7 reacted with cell surface proteins on the COS-1 cells transfected with RHL-1 cDNA but not with RHL-2/3 cDNA. By immunoblotting, the antibody recognized proteins (molecular weights 45 and 96 kDa) in RHL-1-expressing cells but not in the RHL-2/3 cDNA-transfected cells. Immunoreactive staining with MoAb 8D7 was observed on the cell surface and in the cytoplasm of RHL-1-transfected COS-1 cells but not in cells expressing RHL-2/3. These findings indicate that MoAb 8D7 recognizes a subunit-specific epitope on RHL-1 of rat ASGPR.

Journal Article↗
PubMed2003

HBcAg-specific CD8 T cells play an important role in virus suppression, and acute flare-up is associated with the expansion of activated memory T cells.

We analyzed the prevalence and longitudinal fluctuation of hepatitis B virus (HBV)-specific CD8 T cells in chronic HBV infection using an HLA-A2-HBc18-27 tetramer. Thirty-five HLA-A2-positive patients with chronic HBV infection were divided into 17 HBe antigen (HBeAg)-positive and 18 anti-HBe antibody (anti-HBe)-positive patients. Five HLA-A2-positive normal subjects, five HLA-A2-negative patients with chronic HBV infection, and two HLA-A2-positive patients with acute HBV infection were included as controls. HBc18-27-specific CD8 T cells (c18-27-CD8Ts) were detected at a significantly higher prevalence in patients with anti-HBe (6/18) than in those with HBeAg (1/17), and their frequency reached 0.28% of the total CD8 T cells. The prevalence was significantly higher in patients with HBV DNA below 4.0 log genome equivalents (LGE)/ml (5/12) than in those with HBV DNA above 4.0 LGE/ml (2/23). The frequency of c18-27-CD8Ts was consistently higher in liver-infiltrating lymphocytes, ranging from 0.18 to 1.28%, than in autologous peripheral blood lymphocytes. Longitudinal analysis of patients with acute flare-up demonstrated that the elevation of alanine aminotransferase (ALT) was intimately associated with the expansion of c18-27-CD8Ts. Phenotypic analysis revealed that most c18-27-CD8Ts during acute flare-up expressed HLA-DR and CCR5, while those during low-ALT periods showed low expression. Furthermore, most liver-infiltrating c18-27-CD8Ts were positive for HLA-DR and CCR5, suggesting selective recruitment of activated c18-27-CD8Ts into the liver. In conclusion. HBV-specific CD8 T cells play an important role in the suppression of virus replication, and acute flare-up is associated with the expansion and activation of HBV-specific memory cells.

Adult↗