Immunome research最新文献

{"title":"Lipid Mediator Regulation of Group 2 Innate Lymphoid Cells","authors":"Maya R. Karta, T. Doherty, D. Broide","doi":"10.4172/1745-7580.10000116","DOIUrl":"https://doi.org/10.4172/1745-7580.10000116","url":null,"abstract":"ILC2s were originally found to be activated by epithelial cell derived cytokines to induce the secretion of Th2 cytokines, IL-5 and IL-13. Recent research has shown that lipid mediators play a large role in the activation and inhibition of ILC2 function. Unlike the traditional epithelial cell derived cytokines IL-33 and IL-25, lipid mediators have been shown to promote ILC2 secretion of not only IL-5 and IL-13, but the secretion of IL-4 as well. Prostaglandin D2 has been shown to be a potent chemoattractant of ILC2s as well as a potent activator of ILC2s to release Th2 cytokines. In addition to prostaglandin D2, cysteinyl leukotrienes also activate ILC2s to secrete Th2 cytokines during inflammation. Notably, lipid mediators have been shown to work in concert with epithelial cell derived cytokines to increase IL-5 and IL-13 secretion from ILC2s. On the other hand, lipid meditators prostaglandin I2 and lipoxin A4 are the first identified lipid mediator inhibitors of ILC2 function, and thus limit ILC2 contribution to Th2 inflammation. ILC2s play a potential significant role in Th2 mediated inflammation in a variety of allergic disease states, such as asthma, atopic dermatitis, and chronic rhinosinusitis. The identification of lipid mediators as activators and inhibitors of ILC2 function provides additional therapeutic targets for altering ILC2 function during disease states.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2016-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Levels of Endothelial Monocyte-Activating Polypeptide-II in Hepatitis CPatients","authors":"M. Saber, M. Clauss","doi":"10.4172/1745-7580.10000117","DOIUrl":"https://doi.org/10.4172/1745-7580.10000117","url":null,"abstract":"Objectives: Endothelial monocyte-activating polypeptide-II (EMAP-II) is a cytokine with pro-inflammatory and immune-suppressive properties. The goal of this study was to assess serum EMAP-II in treated and untreated Hepatitis C virus (HCV) patients. Furthermore, we determined the relationship between serum EMAP-II levels with the clinic pathological and laboratory parameters in patients with HCV. Methods: 25 control patients (Group I), 25 treated HCV patients (Group II) and 25 newly diagnosed, untreated patients with HCV (Group III) were included in this study. Serum EMAP-II levels were detected by Enzyme linked immunosorbent assay (ELISA), and HCV RNA was assessed by real time-PCR (RT-PCR). The results were evaluated against clinical and laboratory data. Results: Serum EMAP-II levels were significantly elevated in newly diagnosed, untreated HCV patients compared to treated HCV and control patients (p<0.001). We found that serum EMAP-II levels correlated positively with HCV RNA in untreated HCV patients (p<0.001). While serum albumin and platelet count correlated negatively with serum EMAP-II levels (p<0.001), a positive correlation was observed between EMAP-II and serum bilirubin (p<0.001). Conclusions: Increased serum EMAP-II levels are present in newly diagnosed HCV patients compared to treated HCV and control patients, suggesting EMAP-II as a novel biomarker for HCV diagnosis.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of LLLI on Expression of Micro RNA-21 and Ventricular Remodeling inRats after AMI","authors":"Firoj Mk, Fa Xe, Yusuf Hb","doi":"10.4172/1745-7580.10000118","DOIUrl":"https://doi.org/10.4172/1745-7580.10000118","url":null,"abstract":"Objective: To assess the effects of low-level laser irradiation (LLLI) on the expression of micro RNA-21 and ventricular remodelling in the model of rat myocardial infarction. Methods: 110 adult-female SD rats were randomly divided into sham operation (30), control (40), and treatment (40) groups. MI model was prepared by ligation of left anterior descending artery in the control and treatment groups while simply threading at the same site of MI model in sham group. LLLI treated using (635 nm, 6mW, 125s, 0.96 J/cm2) after three weeks of MI at infarct region in the treatment group. At 1 h, 24 h, 48 h, 72 h and 7 d after LLLI treatment, the expression of miR-21 at the infracted myocardial tissue were detected using qRT-PCR. At the end of 4 weeks after MI, hearts were harvested for histological analysis. Results: MiR-21 expression in the treatment group was lower than both sham group as well as the control group (P<0.05). LVEF (%) and LVFS (%) in the treatment group before and after LLLI; (39.37 ± 1.35 vs. 47.62 ± 2.75, P<0.05; (19.23 ± 3.12) vs (24.15± 2.53), P<0.05). Collagen fiber content in treatment group were significantly lower than control group (28.79 ± 2.06%) vs (69.22 ± 3.64%), (P<0.05). Conclusion: LLLI treatment of myocardial infarction can significantly down regulate the expression of tissue miR-21 in the infarct region, increase left ventricular function and decrease collagen fiber content suggesting the beneficial effect of LLLI on delaying myocardial fibrosis, reduce the pathological ventricular remodelling (VR) after MI.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"T Cell Immunoglobulin Mucin-3 (TIM-3) Expression on Peripheral BloodLymphocytes in Chronic Hepatitis Virus C Infection","authors":"Hydi Ahmed, Sahar Abo-Elfotoh Abdel Wahed, Zinab Mohammed Mahmoud Diab, A. Abdel-Gawad","doi":"10.4172/1745-7580.10000115","DOIUrl":"https://doi.org/10.4172/1745-7580.10000115","url":null,"abstract":"Introduction: T cell Immunoglobulin Mucin-3 (TIM-3) TIM-3 acts as a negative regulator of (T helper-1)Th1/ (T Cytotoxic-1)Tc1 cell function by triggering cell death upon interaction with its ligand Galectin-9, a feature observed in chronic viral diseases. Objective: To demonstrate the level of expression of TIM-3 on Peripheral Blood Mononuclear cells (PBCs) in cases of chronic HCV as a number of emerging molecules and pathways have been implicated in mediating the Tcell exhaustion characteristic of chronic viral infection. Patients and Methods: This study included 90 subjects, divided up as follows: Group 1 (35 patients) included HCV antibody positive with normal liver functions (Compensated), Group 2 (35 patients) comprised HCV antibody positive patients with abnormal liver functions (decompensated), and controls (Group 3) involved 20 apparently healthy persons (HCV antibody negative persons). The following laboratory investigations were performed for all participants in the 3 groups: Complete Blood Count (CBC), Blood Chemistry (liver functions), Special investigations (Flowcytometric study, and PCR for HCV RNA). Results: Comparing the control, compensated and decompensated groups regarding lymphocytic counts, ratios of TIM-3 positive cells within CD4, CD8, CD14 and CD56 cells in the three groups. Ratio of CD4 cells was higher in the compensated and control groups, than in the decompensated group, with non-significant difference. CD8 cells were maximum in the decompensated groups and minimum in the compensated group, with a significant p value. CD14 cells were maximum in the compensated group, followed by decompensated and minimum in the control group, again with a significant difference. CD56 showed non-significant differences between the three groups. A steady increase in the percentage of TIM +ve CD4, CD8, CD14 and CD 56 cells, with maximum percentages among the decompensated liver disease group, and least percentage among the control group was seen. The differences were significant regarding CD8 and CD56 and highly significant regarding CD4 and CD14 cells. Conclusions: Accumulation of TIM-3+ T cells is associated with functional impairment, and consequently with development of persistent HCV. The present study provides a basis for improving current therapies by simultaneous blockade of multiple inhibitory pathways that could result in additive efficacy without excessive toxicity. These findings have implications for the development of novel immunotherapeutic approaches to this common viral infection.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2016-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor microenvironment associated immune cells mediate platelet-activating factor induced tumor growth and treatment effectiveness","authors":"Ravi P Sahu","doi":"10.4172/1745-7580.C1.005","DOIUrl":"https://doi.org/10.4172/1745-7580.C1.005","url":null,"abstract":"","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70941507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3D1, a novel anti-nodal monoclonal antibody to target melanoma","authors":"Michael Foley","doi":"10.4172/1745-7580.C1.006","DOIUrl":"https://doi.org/10.4172/1745-7580.C1.006","url":null,"abstract":"N ligands are potent morphogens, belonging to the TGF-β superfamily. In humans, nodal is rarely expressed during late development and adulthood. Nodal physiological expression is typically observed only in embryonic tissues and embryonic stem (ES) cells. Aberrant re-activation of nodal expression in adults is associated with a number of tumours such as metastatic melanoma as well as breast, colon, prostate and ovarian carcinomas. Typically, nodal can trigger the Smad2/3 intracellular pathways by binding the type I (ALK 4/7) and type II (ActRIIB) activin-like serine-threonine kinase receptors, also in the presence of the co-receptor Cripto-1. In addition, like other ligands of the TGF-β superfamily, nodal can also activate MAPK cascade which, in a BRAF mutationdependent manner, converges on ERK and PI3K-AKT pathway. Nodal signaling plays a relevant role in the aggressive progression of metastatic melanoma; indeed its inhibition blocks the tumorigenic capacity and the plasticity of aggressive human melanoma cells. In this context, targeting and inhibition of nodal signaling represents an attractive and alternative strategy to block melanoma progression and other cancers. With the aim to produce antibodies able to recognize Nodal and to block it’s signaling by preventing also its association with Cripto-1, we have generated a set of monoclonal antibodies targeting one of the CBR (Cripto-BindingRegion) sites which encompass residues around Glu49 and Glu50 of Nodal. Using a subtractive ELISA screening we have selected a potential neutralizing monoclonal antibody, named 3D1, which recognizes the nodal E49 and E50 hot-spot residues. 3D1 mAb strongly associates with full-length rh Nodal (KD 1.4 nM) and recognizes the endogenous protein in a panel of human melanoma cell lines by western blot and FACS analyses. Melanoma cells treated in vitro with 3D1 show a significant reduction of nodal protein expression level and of its downstream signaling molecules P-Smad2 and P-ERK. 3D1 treatment blocks cell proliferation reducing P-H3 and Cyclin-B1 with a concomitant increase of p27 and prevents the anchorage-independent growth and vasculogenic network formation, too. Nude mice xenografts models, both subcutaneous orthotropic and lung colonization models, treated with 3D1 show anti-tumor effects in terms of reduced tumor volume and lung tumor burden, respectively. Collectively these data, suggest that 3D1 is a promising diagnostic reagent for detection of nodal and a novel bio-therapeutic agent for targeting nodal expressing cancers.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70941397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Trianni Mouse: The next generation transgenic platform for the isolation of fully human monoclonal antibodies","authors":"D. Meininger","doi":"10.4172/1745-7580.C1.004","DOIUrl":"https://doi.org/10.4172/1745-7580.C1.004","url":null,"abstract":"","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70941321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Jatropha Curcas Linn can Reduce the Expression of Hsp70 that will Result in Reduced Errors in Protein Folding and Promotion of Normal Protein Function in Proliferation and Apoptosis","authors":"A. Prayitno, M. S. Fitria, Elm, O. P. Astirin","doi":"10.4172/1745-7580.10000114","DOIUrl":"https://doi.org/10.4172/1745-7580.10000114","url":null,"abstract":"Background: Jatropha curcas (J. curcas) as a local plant have phytochemical contents like phenolic that effect as anti-inflammatory and cytotoxicity properties. Research in the last decade about cancers showed that over expression of heat shock protein 70 (Hsp70) does to mis-folding and continues to triggering proliferation and suppressing apoptosis. Increased expression of Hsp70 is responsible for mis-folding of proteins and implicated in functions that lead and play a role in the pathogenesis of pain including cancer incidence. In this study, we examined the expression of Hsp70, pRb and caspase3 in Raji cells after treatment with J. curcas. Methods: We first to determinethe plant. The plant is shrubby, woody and many are found in the tropics, names J.curcas sp. (Euphorbiaceae family). Second, to extraction of fresh leaves taken from J. curcas, washed clean, dried by the wind, sliced into small pieces and end dried by an oven at a temperature 65°C for 48 hours. And third, To developed a Raji cell culture (a cancer model) system and treated cells with fractionated extracts of J. curcas leaf. Fourth are evaluating the expression of Hsp70, pRb and caspase-3 that do by immuno histochemical analysis. A semi quantitative (devided into catagories: low, medium and strong) data was collected under light microscope view. Results: Our results showed that the expression of Hsp70 in Raji cells after treatment with fractionation J. curcas leaf was strong as much as 9(30.00%) lower than control (14:46.60%). The expression of pRb after treatment with fractionation J. curcas leaf was strong as much as 15(50.00%) higher than control (9:30.00%). And the expression of caspase-3 in Raji cells after treatment with fractionation J. curcas leaf was strong as much as 13(43.3%) higher than control (9:30.00%). Conclusion: Our results show that J. curcas leaf can reduce the expression of Hsp70, suggesting it can also reduce errors in protein folding and promotion of normal protein function in proliferation (by inhibit pRb protein expression) and apoptosis (by enhance caspase-3 protein expression).","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2016-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumoricidal Activation of Macrophages using Jatropha curcas Leaf Extract: Asa Proxy for the Treatment of Cancer","authors":"A. Prayitno, M. S. Fitria, Elm","doi":"10.4172/1745-7580.10000112","DOIUrl":"https://doi.org/10.4172/1745-7580.10000112","url":null,"abstract":"Abstract Background: Jatropha curcas (J. curcas) is a plant rich in methanolic. Macrophages can be activated to become tumoricidal through interactions with immunomodulators. The aim of this study was to investigate the effect of J. curcas leaf extracts on the phagocytic activity of macrophages. Methods: Peritoneal-derived macrophages from male BALB/c mice were obtained using the method of Colligan et al. with some modifications. Latex was added as an antigen to cultures of BALB/c mice macrophages treated with two different concentrations of J. curcas extract and the cultures were observed every 30 minutes for 2 hours. Results: Macrophage latex vacuoles were observed after treatment with 15 μg/mL J. curcas leaf extract, with a mean latex vacuole count of 7.2 vacuoles/cell and a phagocytic index (PI) of 369. Macrophage treatment with 250 μg/mL J. curcas leaf extract produced a mean latex vacuole count of 8.1 vacuoles/cell and a PI of 785. Conclusion: Treatment with J. curcas leaf extracts increased the phagocytic activity of mice macrophages.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2016-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/1745-7580.10000112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Maize Prolamins on Peripheral Blood Mononuclear Cells from CeliacDisease Patients","authors":"J. Sánchez, A. Barca","doi":"10.4172/1745-7580.10000110","DOIUrl":"https://doi.org/10.4172/1745-7580.10000110","url":null,"abstract":"Celiac disease (CD) is an enteropathy induced by wheat prolamins (gliadins) and in some rare cases by maize prolamins (zeins) possibly due to a similar immune response. The aim was to study the cellular immune response to zeins in comparison to gliadins of peripheral blood mononuclear cells (PBMC) from CD patients. Isolated PBMC from two treated CD patients and three non-CD controls were challenged in vitro with gliadins or zeins and released gamma-interferon (IFN-γ) in culture medium was measured. PBMC were stimulated with gliadin or zein immunogenic peptides or their digested fractions (3-5 kDa).The gliadin peptide G33-mer induced an expected IFN-γ releasing of PBMC from both patients 1 and 2, with a higher level between days 0 and 6 for patients 1 and no differences para patient 2. The zein peptide Z34-mer induced a higher increase of IFN-γ in both CD patients at 0 day, even higher that it of G33-mer for patient 2, and both of them were highly decreased at day 6. Finally, the zein digested fraction induce an IFN-γ release similar to that of gliadin digested fraction in both cases, although negligible for patient 1 and significant for patient 2. In conclusion, the cellular response to zeins was partially similar to it of gliadins after an in vitro challenge.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}