It is possible that telomerase mutations would impair the regenerative reserves of hepatocytes in the context of chronic liver damage. Accordingly, an increased frequency of telomerase mutations could be associated with cirrhosis induced by chronic liver diseases. Here, we sequenced the TERT and TERC genes in a cohort of 1,121 individuals, 521 patients with liver cirrhosis and 600 controls. The analysis revealed a significantly increased frequency of telomerase mutations in cirrhosis patients (14 heterozygous, two homozygous allelic variants in 521 individuals; allele frequency 0.017) compared to controls (three heterozygous sequencing

variants in 600 individuals; 0.003, P value 0.0007; Relative risk [RR] 1.859; 95% confidence interval [CI] 1.552-2.227). Cirrhosis-associated telomerase selleck screening library mutations showed functional defects and were associated with the evolution of disease complications. Together, these data provide the first demonstration of a broad involvement of telomerase mutations in the evolution and Vismodegib progression of cirrhosis in response to chronic liver injury. The finding could impact on the future development of molecular therapies and surveillance programs in patient with chronic liver disease. DKC, dyskeratosis congenita; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; PCR, polymerase

chain reaction; TERC, telomerase RNA component; TERT, telomerase reverse transcriptase; TRAP, telomere repeat amplification protocol; TRF telomere restriction fragment. A total of 1,121 individuals were recruited for the current study. Among them, 521 patients were diagnosed MCE with liver cirrhosis; 600 controls were either healthy individuals (n = 473) or patients with chronic HCV infection

who did not develop cirrhosis during follow-up (average time of follow-up: 21 years, n = 127). We included the group of hepatitis C carriers who did not progress towards liver cirrhosis because this cohort provides an important control indicating that telomerase mutations do associate with the development of cirrhosis and not with the occurrence of chronic liver disease per se. Subjects were recruited from (1) the Liver Unit, Hôpital Jean Verdier in Bondy Cedex, France, (2) the Department of Gastroenterology, Hepatology and Endocrinology of Hannover Medical School in Hannover, Germany, (3) the Henriettenstiftung Hannover, Germany, (4) the Institute for Clinical Transfusion Medicine and Immunogenetics, DRK Blood Donor Service Baden-Württemberg-Hesse, University of Ulm, and (5) the Peking Union Medical College Hospital, Chinese Academy of Medical Sciences. The study was approved by the local Institutional Review Boards and written informed consent was obtained from all subjects. The study was designed in accordance with the principles of the Declaration of Helsinki and patient data were evaluated anonymously.

It is possible that telomerase mutations would impair the regenerative reserves of hepatocytes in the context of chronic liver damage. Accordingly, an increased frequency of telomerase mutations could be associated with cirrhosis induced by chronic liver diseases. Here, we sequenced the TERT and TERC genes in a cohort of 1,121 individuals, 521 patients with liver cirrhosis and 600 controls. The analysis revealed a significantly increased frequency of telomerase mutations in cirrhosis patients (14 heterozygous, two homozygous allelic variants in 521 individuals; allele frequency 0.017) compared to controls (three heterozygous sequencing

variants in 600 individuals; 0.003, P value 0.0007; Relative risk [RR] 1.859; 95% confidence interval [CI] 1.552-2.227). Cirrhosis-associated telomerase GDC-0068 clinical trial mutations showed functional defects and were associated with the evolution of disease complications. Together, these data provide the first demonstration of a broad involvement of telomerase mutations in the evolution and Palbociclib molecular weight progression of cirrhosis in response to chronic liver injury. The finding could impact on the future development of molecular therapies and surveillance programs in patient with chronic liver disease. DKC, dyskeratosis congenita; HBV, hepatitis B virus; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; PCR, polymerase

chain reaction; TERC, telomerase RNA component; TERT, telomerase reverse transcriptase; TRAP, telomere repeat amplification protocol; TRF telomere restriction fragment. A total of 1,121 individuals were recruited for the current study. Among them, 521 patients were diagnosed MCE with liver cirrhosis; 600 controls were either healthy individuals (n = 473) or patients with chronic HCV infection

who did not develop cirrhosis during follow-up (average time of follow-up: 21 years, n = 127). We included the group of hepatitis C carriers who did not progress towards liver cirrhosis because this cohort provides an important control indicating that telomerase mutations do associate with the development of cirrhosis and not with the occurrence of chronic liver disease per se. Subjects were recruited from (1) the Liver Unit, Hôpital Jean Verdier in Bondy Cedex, France, (2) the Department of Gastroenterology, Hepatology and Endocrinology of Hannover Medical School in Hannover, Germany, (3) the Henriettenstiftung Hannover, Germany, (4) the Institute for Clinical Transfusion Medicine and Immunogenetics, DRK Blood Donor Service Baden-Württemberg-Hesse, University of Ulm, and (5) the Peking Union Medical College Hospital, Chinese Academy of Medical Sciences. The study was approved by the local Institutional Review Boards and written informed consent was obtained from all subjects. The study was designed in accordance with the principles of the Declaration of Helsinki and patient data were evaluated anonymously.

0.34 A recent JAK inhibitor hospital-based

study in Sri Lanka reported an incidence of UC of 0.6935 and CD of 0.09. In the West, the incidence of CD has overtaken that of UC in a number of studies.8–12 Traditionally in low incidence areas UC emerges first followed by CD, but over time the incidence of CD ultimately matches, and may eventually overtake, the incidence of UC.2,44 A recent review from China compared the crude incidence for CD and UC in the Chinese medical literature over two time periods: 1989 to 2003 and 2004 to 2007. In both periods, there were more cases of UC, but a relative increase in CD was seen, with the UC to CD ratio dropping from 41 to 15 over time.45 Similarly, a study from South Korea has reported a higher incidence of UC than CD, but the rise in incidence of CD between 1986 and 2005 was more rapid than that of UC, with the ratio of the incidence of UC to CD dropping from 6.8 to 2.3 between 1986 learn more and 2005.13 A recent pediatric study from Korea demonstrated that a rising incidence of IBD diagnosis was more marked for CD, with a new patient CD : UC ratio of 3.4 : 1.46 Overall,

incidence rates of IBD in Asia are still low compared to recent figures from Western countries such as North America, Canada, New Zealand and Australia, where incidence rates for CD and UC range from 14.6 to 17.4 and 7.6 to 14.3, respectively.9–12 Prevalence.  A rise in the prevalence of UC in Japan from 7.85 to 63.6 per 100 000 population has been reported across three different studies between 1984 to 2005.14,16,28 Data from the national register have demonstrated the CD prevalence rise from 2.9 to 13.5 between 1986 and 1998.15 A separate study from Japan documented CD prevalence to be 21.2 in 2005.16 In Hong Kong the prevalence of UC appears to have almost tripled from 2.3 to 6.3 over the period 1997 to 2006.25 There are very few reports of prevalence of CD in Hong Kong or China. One review, which extrapolated

the crude prevalence rate based on 55 years of research in China (which included the Chinese literature), calculated the prevalence of CD to be 2.29;27 this figure has increased from the estimate of 1.3 in a hospital based study in 1994.23 There has been a substantial rise in UC prevalence in Korea from 7.6 in MCE公司 1997 to 30.9 in 2005.13,47 In 2005 CD prevalence was reported to be 11.2.13 A selective report in 19-year-old males having a health assessment for military service in Korea identified a striking increase of more than threefold over the period 2006 to 200948 Although no diagnostic criteria were reported, the latter report supports a likely major increase in IBD prevalence in this country over the last one or two decades. In studies from Singapore, UC and CD prevalence has risen from 6.0 to 8.6,31,32and from,1.3 to 7.2,31–33 respectively.

The total allele frequency of telomerase mutations in cirrhosis patients was 0.017, compared to 0.003 in healthy controls or hepatitis C patients without fibrosis progression (P = 0.0007). Furthermore, subgroup analysis (number of identified mutations in healthy controls compared to

the cirrhosis group: P = 0.0021, number of mutations in chronic liver disease patients without cirrhosis compared to the cirrhosis group: P = 0.0349) find more reconfirmed that the identified telomerase mutations are associated with cirrhosis but do not occur in healthy controls or patients with indolent HCV infection. To our knowledge, these data

represent the first association of telomerase mutations with the evolution and progression of cirrhosis in response to chronic liver injury. The ethnic group in our study consisted mainly of whites (70.1%). It remains to be analyzed whether telomerase mutations occur with similar frequency in other ethnic groups. The study shows that EPZ-6438 order cirrhosis-associated TERT mutations exhibit an impaired function compared to wildtype TERT. Cirrhosis-associated telomerase mutations result in reduced telomerase activity, impaired telomere maintenance, and reduced growth rates of fibroblasts and lymphocytes. Moreover,

a reduction in telomere length was seen in peripheral blood and immortalized lymphocytes of mutation carriers compared to controls. We did not see any significant difference in the percentage of γH2Ax-positive hepatocytes between liver cirrhosis patients with and without telomerase mutations. This, however, does not argue against an involvement of telomerase mutations in cirrhosis. Previous studies have demonstrated that telomere shortening and senescence are general signs of cirrhosis induced by different etiologies.13, 14 We propose that telomerase mutations can lead to accelerated telomere shortening, thus shortening the time to progression of chronic liver disease toward 上海皓元 cirrhosis. In addition, telomerase mutations may have extratelomeric effects influencing disease progression. Recent studies have revealed telomere length-independent effects of TERT in regulating the transcriptional function of the Wnt-signaling pathway and stem cell activity in mice.32 It remains to be seen whether cirrhosis-associated TERT mutations show defects in these noncanonical TERT-pathways and whether TERT mutations affect the latency of cirrhosis development in patients with chronic liver disease.

RGC-32 silencing inhibits the expression of Zeb1 and Snail in TGF-β-induced EMT. Conclusion: RGC-32 might be a new metastasis promoting factor for pancreatic cancer and it mediates TGF-β-induced

EMT via MAPK signaling pathways and transcription factors Zeb1 and Snail. Key Word(s): 1. RGC-32; 2. Pancreatic cancer; 3. TGF-β; 4. EMT; Presenting Author: YUFEN ZHOU Additional Authors: LIYA HUANG, LINGXIAO XU, FAN ZHANG, FANG GUO, WEIYAN YAO, YAOZONG YUAN Corresponding Author: YAOZONG YUAN Affiliations: Ruijin Hospital, Shanghai Jiaotong University School of Medicine; Department of Gastroenterology, General Hospital of Ningxia Medical University. Objective: Pancreatic cancer is the eleventh malignant tumor and the fourth leading cause of cancer-related mortalities in the United States. By the time of diagnosis, only 15–25% patient have a chance to undergo resection surgery. Looking for buy Metformin new serum biomarkers to diagnose pancreatic cancer early has become a top priority. ULBP-2 (UL16-binding protein 2) is a family of ULBPs. The ULBPs are ligands for NKG2D/DAP10, an activating receptor expressed by natural killer (NK) cell. MIC-1 (macrophage inhibitory cytokine-1) is a novel family of TGF-β. Both biomarkers are increased CH5424802 manufacturer expression in pancreatic cancer in several cohort studies. The aim of this case-control study is to compare the diagnostic ability

of ULBP-2, MIC-1 and CA19-9. In this study, we also estimate the correlation among different tumor markers with pancreatic cancer metastasis and TNM stage. Methods: The serum sample of pancreatic cancer patients, chronic pancreatitis patients, diabetes patients and age/sex-matched normal persons were collected in Ruijin Hospital during Dec 2008 and Jan 2012. We collected the clinical data of the research objects, including

sex, age, compliant, history of diabetes, history of hypertension, results of liver function tests and classical tumor markers, pathological diagnosis, surgery way and so on. The serum ULBP-2 and MIC-1 levels were determined by using the ELISA kit. Meanwhile, we adopted CA19-9 results of ruijin hospital. Differences in serum levels of target proteins among groups were compared. Area under the ROC medchemexpress curves (AUCs) were analyzed among serum target proteins. Results: The serum levels of ULBP-2, MIC-1 among all PC patients were significantly higher than those in benign Pancreatic tumor, chronic pancreatitis and healthy controls (p < 0.0001). And the ULBP-2, MIC-1 concentrations were associated with pancreatic cancer progression. The combination of ULBP-2, MIC-1 and CA 199 performed better than each marker alone in distinguishing PC patients from healthy individuals. An analysis of the area under ROC curves showed that ULBP-2 was superior to CA19-9 in discriminating patients with PC from healthy controls, and MIC-1 was superior to CA19-9 in diagnosing early-stage PC. Conclusion: 1.

The resin was polymerized in a 60°C oven for 2-3 days. Sections were cut with a Dupont diamond knife in Reichert-Jung UltraCut

E ultramicrotome, collected on copper grids, and doubly stained with saturated aqueous uranyl acetate and lead citrate. Ultrathin sections GPCR Compound Library were imaged for Paneth cells using a JEM-1200EX electron microscope manufactured by JEOL. Protein contents were determined with a bicinchoninic acid protein assay kit (Pierce Chemical, Rockford, IL), using bovine serum albumin as a standard. All data are reported as mean ± standard error. The overall significance of the results was examined using one-way analysis of variance and the significant differences between the groups were considered at P < 0.05 with the appropriate Tukey's post hoc test made for multiple comparisons. The ordinal values of the liver and kidney injury scores were analyzed by the Mann-Whitney nonparametric test. Histological examination of small intestines from sham-operated mice showed Paneth cells containing densely packed eosinophilic STAT inhibitor secretory granules (Fig. 1A). In contrast, after hepatic IR rapid and extensive degranulation of Paneth cells was observed (magnification 400×, representative of five experiments, arrows and magnified insert)

compared to sham-operated animals. Further evidence of Paneth cell degranulation was apparent by electron microscopy of small intestines following hepatic IR (Fig. 1B). The crypt lumen from sham-operated mice was devoid of Paneth cell granules, whereas the crypt lumen from mice subjected to hepatic IR showed granules being released into the lumen. With LCM we selectively isolated Paneth cells to determine whether Paneth cells produce increased IL-17A mRNA 5 hours after liver IR. mRNA recoveries were sufficient

for performance of semiquantitative RT-PCR for GAPDH and IL-17A, which demonstrated increased IL-17A mRNA after bilateral nephrectomy (11 ± 1-fold over sham, n = 4, P < 0.01, Fig. 2). We also isolated intact small intestinal crypts containing Paneth cells 24 hours after sham-operation or liver IR. Small intestinal crypts isolated with the distended sac method and stained with eosin-Y showed MCE公司 red staining characteristic of Paneth cells (Supporting Fig. 1). IL-17A ELISA performed in these isolated crypts showed that IL-17A protein levels were significantly increased (59 ± 4 pg/mg protein, n = 4) compared to sham-operated mice (9 ± 3 pg/mg protein, n = 4). Wildtype (C57BL/6) mice subjected to 60 minutes liver IR increased both systemic (Fig. 3A) and portal venous (Fig. 3B) IL-17A levels compared with the sham-operated mice (undetectable levels). The rise in systemic plasma was very rapid, occurring within 1 hour after reperfusion. Moreover, the rise in portal venous levels of IL-17A was significantly greater (P < 0.05) than the level detected in the systemic circulation.

Stop mutations are also reported in inhibitor cases, whereas missense mutations carry the lowest inhibitor risk [45, 49]. The clinical manifestations of haemophilia A and B are similar; however, differences in bleeding frequency, clinical scores, prophylaxis use and requirement for joint prosthesis have been highlighted and conflicting evidence continues to be debated [28, 42, 50, 51]. Already in 1959, the first report about a milder clinical expression of haemophilia B in comparison with haemophilia A was provided by Armand Quick [52]. More recently, an interesting observation was carried out during the validation of a scoring system aimed at assessing the clinical severity

of Selleckchem Birinapant haemophilia in patients without inhibitors [28]. This composite HSS included: incidence of joint bleeding; orthopaedic joint score and factor consumption. The HSS result

was higher in severe haemophilia A than in severe haemophilia B [28]. However, in contrast with these results, a subsequent study carried out in a single centre in Italy did not confirm any significant difference between patients with haemophilia A and B [53]. In a Canadian survey conducted in 2006 to collect information on the use of regular prophylaxis, it was Selleck IWR1 shown that this therapeutic regimen was less frequently adopted by patients with severe haemophilia B than by those with severe haemophilia A (32% vs. 69%) [50]. Even more unexpectedly, it appeared that among patients with haemophilia B a limited proportion of children younger than 2 years of age was on prophylaxis (20%), while more than half of the patients with haemophilia A belonging to the same-age medchemexpress group were already on regular prophylaxis

[50]. A different retrospective survey was carried out by Italian investigators to compare the orthopaedic outcome in severe haemophilia A and B. All joint arthroplasties performed at the 29 participating centres were analysed [42]. Overall, 347 surgeries were performed in 268 patients (328 operations in 253 patients with severe haemophilia A, 19 in 15 with severe haemophilia B). Patients with haemophilia A showed a three-fold greater risk of undergoing joint replacement and this result was confirmed after adjustment for confounders (age and viral infections) [42]. Since joint replacement is an indirect marker of advanced arthropathy and the most solid long-term outcome of the severe bleeding phenotype in haemophilia, this piece of evidence supports the view that haemophilia B has a milder bleeding tendency than haemophilia A [42]. Nevertheless, a single-centre study carried out in the Netherlands did not confirm any difference in the arthroplasty rate across haemophilia types [54]. Other conflicting results came from a small study conducted in Canadian patients with severe and moderate haemophilia [51].

1 Enthusiasm for further characterization of functional significance of new genes and cell signaling pathways remains high because of the potential for finding novel therapies to stimulate liver regeneration in acute and chronic liver diseases that negatively

impact liver regeneration. The report by Gazit et al. in this issue of Hepatology offers new insights into mechanisms of liver regeneration focusing on Selleckchem AZD2014 the contribution of peripheral lipid stores and systemic lipolysis in the liver’s ability to regenerate in response to 70% partial hepatectomy.7 The present study was prompted by previous observations that partial hepatectomy induces transient hypoglycemia followed by lipid accumulation within hepatocytes that precedes the time of peak hepatocyte proliferation in mice. The authors previously reported that pharmacologic and genetic interventions that suppress the early induction of transient hypoglycemia and hepatic steatosis are able to inhibit liver regeneration in mice.8-10 They reason that the early induction of hypoglycemia may be a potential trigger for the release of fatty acids from peripheral lipid stores and that fatty acids derived from peripheral adipose tissues, in turn, may be responsible for transient lipid accumulation within hepatocytes in

regenerating livers (Fig. 1). To test their hypothesis that catabolism of systemic

adipose stores are essential for liver regeneration, the authors performed 70% partial hepatectomy on fatty liver dystrophy (fld) mice, which exhibit partial lipodystrophy and have diminished find more peripheral adipose MCE stores. Supporting their hypothesis, fld mice exhibited attenuated development of hypoglycemia, hepatic lipid accumulation, and impaired hepatocyte proliferation in response to 70% partial hepatectomy.7 They conclude that hepatic insufficiency is the primary trigger for the induction of a systemic catabolic response based on their observation in two independent experimental models, partial hepatectomy, and carbon tetrachloride–mediated injury in mice. Data presented in this study supports the notion that catabolism of total body and fat mass after partial hepatectomy occurs in proportion to the degree of induced hepatic insufficiency. However, the decline in lean mass did not correlate with the extent of hepatic insufficiency induced after one-third versus two-thirds partial hepatectomy.7 These findings provide direction for future studies to address key questions pertaining to liver:body mass regulation and identification of relevant body mass compartments that impact growth responses in the liver. Maintenance of metabolic homeostasis by balancing extrahepatic energy consumption with dietary nutrient uptake is one of the essential functions of the liver.

Unfortunately, little is known about its role in the process of tumor angiogenesis. In this study, we investigated the effects

and potential mechanisms of parthenolide LY2606368 in vitro on angiogenesis in human colorectal cancer (CRC). Methods: HUVEC, human umbilical vein endothelial cells, was treated with PT at different concentrations. The MTT assay and flow cytometry analysis using PI were used to analyze cell death. We determined the effect of PT on tube formation and migration in HUVEC cells. Then, protein level of the angiogenesis related factors such as VEGF, VEGFR-1 and VEGFR-2 were observed in HUVEC cells and human colorectal cancer cells (HT-29, SW620, HCT-116). HT-29 cells xenograft model in nude mice was also used to investigate the in vivo inhibitory effects on angiogenesis by PT. Results: Suppression of proliferation, migration, check details and the tube formation capacity of HUVEC cells were observed after PT treatment. Angiogenesis related

proteins are also decreased by PT in HUVEC cells. Moreover, PT effectively inhibited proliferation of colorectal cancer cells and expression of angiogenesis related proteins in vitro. Intraperitoneal injection of PT showed significant inhibition of growth in the xenograft model via decreased production of VEGF. Conclusion: These results demonstrate that PT exhibits inhibitory effect on angiogenesis in human colorectal cancer in vitro and in vivo. Key Word(s): 1. MCE Angiogenesis; 2. Colorectal cancer; 3. Parthenolide; 4. Apoptosis; Presenting Author: DEQIANG HUANG Additional Authors: HUI LIN, SANSAN JIANG, NIANSHUAN NIANSHUAN, LINGYU LUO, NONGHUA NONGHUA Corresponding Author: NONGHUA NONGHUA Affiliations: The first affilated hospital of Nanchang University; The first affiliated hospital of Nachang University; The first affiliated hospital

of Nanchang University; The first affiliated hospital of Nanchang university Objective: Metformin, a derivative of biguanide, is a first-line therapy for type 2 diabetes mellitus, Previous studies have demonstrated the anti-cancer activity of metformin in various types of cancer cells, However, the manner in which metformin regulate migration or related epithelial-to-mesenchymal transitions (EMT) has yet to be elucidated. The aim of this study was to explore the effect of meformine on growth and migration using AGS gastric cancer cells. Methods: Cell viability was determined by the conventional MTT assay; Cell migration (wound healing) assay was conducted to determine the capacity of cell migration; The expression of EMT markers was analyzed by Western blotting. Results: We found that metformin reduced growth of AGS cells in a dose-dependent manner (Fig. 1). In addition, the drug significantly inhibited the migration of AGS cells (Fig. 2). Furthermore (Fig. 3), metformin strongly decreased vimentin (a mesenchymal marker) expression, while increasing E-cadherin (an epithelial marker) expression.

017 and P= 0.011, Selleck GSK3235025 respectively) and significantly lower triglycerides level (P=0.023), total cholesterol, HDL-C and LDL-C levels (all Ps<0.001) than 480 controls. In multivariate logistic regression analyses, a low total cholesterol,

a low triglycerides and a high HOMA-IR are independent factors significantly associated with chronic HCV Infection. In the 160 CHC patients [41 patients with high HOMA-IR (>2.5)], a high BMI, triglycerides and HCV RNA level are independent factors significantly associated with high HOMA-IR in multivariate logistic analyses. Chronic HCV infection was associated with metabolic characteristics including IR and lipid profile. IR was also associated with virological characteristics. “
“Cancer/testis (CT) antigens have been considered therapeutic targets

for treating cancers. However, a central question is whether their expression contributes to tumorigenesis or if they are functionally irrelevant by-products derived from the process of cellular transformation. In any case, these CT antigens are essential for cancer cell survival and may serve as potential therapeutic targets. Recently, the cell-based RNA interference (RNAi) screen has proven to be a powerful approach for identifying potential therapeutic targets. In this study we sought to identify new CT antigens as potential therapeutic targets for human hepatocellular carcinoma (HCC), and 179 potential CT genes on the X chromosome were screened through a bioinformatics analysis of gene expression DZNeP datasheet profiles. Then an RNAi screen against these potential CT genes identified nine that were required for sustaining the survival of Focus and PLC/PRF/5 cells. Among the nine genes, the physiologically testis-restricted dual specificity phosphatase 21 (DUSP21) encoding a dual specificity phosphatase was up-regulated in 39 (33%) of 118 human HCC specimens. Ectopic DUSP21 had no obvious impact on proliferation and colony formation in HCC cells. However, DUSP21 silencing significantly suppressed cell proliferation, colony formation, and in vivo tumorigenicity in HCC cells. The administration of adenovirus-mediated RNAi and an atelocollagen/siRNA mixture against

endogenous DUSP21 significantly suppressed xenograft HCC tumors in mice. Further investigations showed that DUSP21 knockdown led 上海皓元 to arrest of the cell cycle in G1 phase, cell senescence, and expression changes of some factors with functions in the cell cycle and/or senescence. Furthermore, the antiproliferative role of DUSP21 knockdown is through activation of p38 mitogen-activated protein kinase in HCC. Conclusion: DUSP21 plays an important role in sustaining HCC cell proliferation and may thus act as a potential therapeutic target in HCC treatment. (Hepatology 2014;59:518–530) “
“Background and Aim:  In human blood, two main subsets of antigen-presenting-cells (APCs) have been described: plasmocytoid dendritic cells (pDC) and myeloid dendritic cells (mDC) which are further subdivided in CD11c-mDC and CD16-mDC DC.