Pub Date : 2016-05-02DOI: 10.4172/1745-7580.10000113
Mohamoud Lh, Yang Lt, L. Zeng, Xu Lz, Zhang Hp, Li Lj, Liu Jq, Xiao Xj, Liu Zg, Yang Pc
Dust mites are an important source of allergens. The mechanism by which dust mite allergens induce allergic diseases is to be further investigated. This study aims to elucidate the role of one of the components of dust mite allergens, the Dermatophagoides farinae-8 (Der f 8), in the induction of airway allergy. In this study, the expression of T cell immunoglobulin and mucin domain 4 (TIM4) in dendritic cells (DC) s was analyzed after stimulating with Der f 8 in the culture. The role of Der f 8 in the induction of T helper (Th) 2 inflammation was assessed with an airway allergy mouse model. We observed that, in 34 subtypes of dust mite allergens, Der f 8 uniquely and markedly induced high levels of the TIM4 expression in DCs by modulating the chromatin at the TIM4 promoter locus. Der f 8 played a critical role in the expansion of the Th2 response in the mouse airway via inducing DCs to produce TIM4. Administration with Der f 8-null dust mite extracts (DME) efficiently inhibited the allergic inflammation and induced regulatory T cells in the airway of mice. We conclude that Der f 8 plays an important role in the pathogenesis of dust mite allergy. Vaccination with the Der f 8-null DME is more efficient to inhibit the dust mite allergic inflammation in the airway than the wild DME.
{"title":"Dust Mite Allergen Der F 8 Promotes Th2 Polarization via Modulating Chromatin Structure at the TIM4 Gene Locus in Dendritic Cells","authors":"Mohamoud Lh, Yang Lt, L. Zeng, Xu Lz, Zhang Hp, Li Lj, Liu Jq, Xiao Xj, Liu Zg, Yang Pc","doi":"10.4172/1745-7580.10000113","DOIUrl":"https://doi.org/10.4172/1745-7580.10000113","url":null,"abstract":"Dust mites are an important source of allergens. The mechanism by which dust mite allergens induce allergic diseases is to be further investigated. This study aims to elucidate the role of one of the components of dust mite allergens, the Dermatophagoides farinae-8 (Der f 8), in the induction of airway allergy. In this study, the expression of T cell immunoglobulin and mucin domain 4 (TIM4) in dendritic cells (DC) s was analyzed after stimulating with Der f 8 in the culture. The role of Der f 8 in the induction of T helper (Th) 2 inflammation was assessed with an airway allergy mouse model. We observed that, in 34 subtypes of dust mite allergens, Der f 8 uniquely and markedly induced high levels of the TIM4 expression in DCs by modulating the chromatin at the TIM4 promoter locus. Der f 8 played a critical role in the expansion of the Th2 response in the mouse airway via inducing DCs to produce TIM4. Administration with Der f 8-null dust mite extracts (DME) efficiently inhibited the allergic inflammation and induced regulatory T cells in the airway of mice. We conclude that Der f 8 plays an important role in the pathogenesis of dust mite allergy. Vaccination with the Der f 8-null DME is more efficient to inhibit the dust mite allergic inflammation in the airway than the wild DME.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936638","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}
Pub Date : 2016-05-02DOI: 10.4172/1745-7580.10000111
E. Elharrar, Moamen Masalha, G. Lerman, R. Leibowitz-Amit, R. Kassem, M. Harats, Y. Sidi, D. Avni
Psoriasis is a chronic inflammatory skin disorder which results from pathological interactions between activated immunocytes and keratinocytes. Recent studies implicated the role of IL-17 and IL-22, secreted from Th17 and Th22 in the generation and propagation of the psoriatic plaque. Previously, we and others have shown that the expression of miR-197 is significantly decreased in psoriatic lesions. We further showed that miR-197 targets IL-22RA1 and that ectopic expression of miR-197 prevent IL-22 induced proliferation and migration of keratinocytes. Since the 3'UTR of the IL17RA subunit mRNA contains a putative binding site for miR-197, our aim was to expand our understanding of the miRNA-mediated crosstalk between immunocytes and keratinocytes by studying the effect of miR-197 expression on IL-17A signaling pathway. Luciferase reporter assays along with Western blot analysis revealed that miR-197 directly targets the 3'UTR of IL17RA. Furthermore, ectopic expression of miR-197 led to a significant decrease in IL-17A-induced expression of CCL20, a known downstream effector of IL-17A. Interestingly, the addition of IL-17A to keratinocytes led to a rapid and transient increase in the expression of miR-197. Chromatin immuno-precipitation assays showed that keratinocytes' treatment with IL-17 leads to C/EBP binding to the promoter region of miR-197, and that the expression level of miR-197 is directly proportional to the extent of C/EBP binding to the promoter. Moreover, following treatment with IL-17A, the histone acetylation pattern at the miR-197 promoter turns to become characteristic of transcribed chromatin. Taken together, our results suggest that a positive-negative feedback loop exists between IL-17A and miR-197 in keratinocytes; the cytokine induces the binding of C/EBPα to miR-197 promoter sequences, enhances miR-197 expression that negatively attenuates IL-17 receptor and decreases the input along the IL-17A pathway. Our work suggests that in psoriasis, decreased expression of miR-197 may prevent the miR-197-induced attenuation of the IL-17 cascade, leading to its over-activity.
{"title":"Positive-Negative Feedback Loop between miR-197 and IL-17A Signaling in Human Keratinocytes","authors":"E. Elharrar, Moamen Masalha, G. Lerman, R. Leibowitz-Amit, R. Kassem, M. Harats, Y. Sidi, D. Avni","doi":"10.4172/1745-7580.10000111","DOIUrl":"https://doi.org/10.4172/1745-7580.10000111","url":null,"abstract":"Psoriasis is a chronic inflammatory skin disorder which results from pathological interactions between activated immunocytes and keratinocytes. Recent studies implicated the role of IL-17 and IL-22, secreted from Th17 and Th22 in the generation and propagation of the psoriatic plaque. Previously, we and others have shown that the expression of miR-197 is significantly decreased in psoriatic lesions. We further showed that miR-197 targets IL-22RA1 and that ectopic expression of miR-197 prevent IL-22 induced proliferation and migration of keratinocytes. Since the 3'UTR of the IL17RA subunit mRNA contains a putative binding site for miR-197, our aim was to expand our understanding of the miRNA-mediated crosstalk between immunocytes and keratinocytes by studying the effect of miR-197 expression on IL-17A signaling pathway. Luciferase reporter assays along with Western blot analysis revealed that miR-197 directly targets the 3'UTR of IL17RA. Furthermore, ectopic expression of miR-197 led to a significant decrease in IL-17A-induced expression of CCL20, a known downstream effector of IL-17A. Interestingly, the addition of IL-17A to keratinocytes led to a rapid and transient increase in the expression of miR-197. Chromatin immuno-precipitation assays showed that keratinocytes' treatment with IL-17 leads to C/EBP binding to the promoter region of miR-197, and that the expression level of miR-197 is directly proportional to the extent of C/EBP binding to the promoter. Moreover, following treatment with IL-17A, the histone acetylation pattern at the miR-197 promoter turns to become characteristic of transcribed chromatin. Taken together, our results suggest that a positive-negative feedback loop exists between IL-17A and miR-197 in keratinocytes; the cytokine induces the binding of C/EBPα to miR-197 promoter sequences, enhances miR-197 expression that negatively attenuates IL-17 receptor and decreases the input along the IL-17A pathway. Our work suggests that in psoriasis, decreased expression of miR-197 may prevent the miR-197-induced attenuation of the IL-17 cascade, leading to its over-activity.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"43 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2016-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936450","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}
Pub Date : 2016-04-25DOI: 10.4172/1745-7580.10000E105
G. Razavi
Cross talk between antigen presenting cells, effector T cells and immune regulatory cells through co-stimulatory and inhibitory signals orchestrates the anti-tumor immune response that eventuates in either the effective tumor directed immune activity leading to the tumor removal or an immune suppressed tumor microenvironment leading to the tumor progression and metastasis. The co-stimulatory signals have been shown to be mediated by CD28 and members of the tumor necrosis factor receptor (TNFR) family, such as CD40, OX-40, 4-1BB, CD30, and CD27, while the regulatory signals are generally mediated through cytotoxic T lymphocyte activator-4 (CTLA-4) and programmed death -1 (PD-1) receptors that share structural homology with the CD28 co-stimulatory class and also bind to the B7 family members. Despite the observed similarities in their structure and receptors, CTLA-4 and PD-1 show the main regulatory role and considered as checkpoints. Targeting these co-stimulatory or inhibitory receptors with either stimulating or blocking antibodies may lead to the enhanced immune response within tumor microenvironment and clinical benefits.
{"title":"Cancer Treatment in the Checkpoint Inhibitor Era","authors":"G. Razavi","doi":"10.4172/1745-7580.10000E105","DOIUrl":"https://doi.org/10.4172/1745-7580.10000E105","url":null,"abstract":"Cross talk between antigen presenting cells, effector T cells and immune regulatory cells through co-stimulatory and inhibitory signals orchestrates the anti-tumor immune response that eventuates in either the effective tumor directed immune activity leading to the tumor removal or an immune suppressed tumor microenvironment leading to the tumor progression and metastasis. The co-stimulatory signals have been shown to be mediated by CD28 and members of the tumor necrosis factor receptor (TNFR) family, such as CD40, OX-40, 4-1BB, CD30, and CD27, while the regulatory signals are generally mediated through cytotoxic T lymphocyte activator-4 (CTLA-4) and programmed death -1 (PD-1) receptors that share structural homology with the CD28 co-stimulatory class and also bind to the B7 family members. Despite the observed similarities in their structure and receptors, CTLA-4 and PD-1 show the main regulatory role and considered as checkpoints. Targeting these co-stimulatory or inhibitory receptors with either stimulating or blocking antibodies may lead to the enhanced immune response within tumor microenvironment and clinical benefits.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2016-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70939490","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}
Pub Date : 2016-03-28DOI: 10.4172/1745-7580.10000108
E. Kozela, A. Juknat, F. Gao, G. Coppola, N. Kaushansky, Z. Vogel
Multiple Sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune diseases driven by pathogenic memory T cells. Using myelin oligodendrocyte glycoprotein (MOG) 35-55-specific encephalitogenic T cells (TMOG) isolated from MOG35-55-immunized EAE mice we describe here their gene expression profile following antigen specific activation. A vast number of pro-inflammatory genes including cytokines, chemokines and growth factors (e.g., Csf2, Il3, Ccl1, Ccl3) as well as signaling pathways (e.g., iNOS, MAPK, JAK/STAT, NFκβ) were dramatically upregulated following MOG35-55 stimulation of TMOG cells. A number of Th17-related pathways were induced confirming potent Th17-like activation of TMOG. Interestingly, genes known for their anti-inflammatory role (Sit1, Hsd11b1, Pias3, Pparg, Lgmn, Klk3, Tnfaip8l2) were down-regulated in response to MOG35-55 suggesting that silencing of intrinsic suppressory mechanisms may underlie the hyperactivation of memory T cells. MOG35-55 activation led to lower transcription of pro-apoptotic/autophagic genes (Ddit4, Bbc3, Dapk2, Wbp1) and to enhanced level of anti-apoptotic transcripts (Bcl2l1). Transcripts related to toll-like receptors and MyD88-signaling were induced, revealing the involvement of innate immunity pathways in T cell driven autoimmunity. This study reveals the transcriptional events that lead to enhanced cytotoxicity, proliferation and resistance to apoptosis of activated autoimmune T cells. We suggest that encephalitogenic T cells may serve as a reliable in vitro model for screening for possible therapeutics against T cell driven autoimmune diseases.
{"title":"Insights into Gene Expression of Activated Pathogenic Autoimmune T Cells - Studies in Experimental Multiple Sclerosis-like Model","authors":"E. Kozela, A. Juknat, F. Gao, G. Coppola, N. Kaushansky, Z. Vogel","doi":"10.4172/1745-7580.10000108","DOIUrl":"https://doi.org/10.4172/1745-7580.10000108","url":null,"abstract":"Multiple Sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune diseases driven by pathogenic memory T cells. Using myelin oligodendrocyte glycoprotein (MOG) 35-55-specific encephalitogenic T cells (TMOG) isolated from MOG35-55-immunized EAE mice we describe here their gene expression profile following antigen specific activation. A vast number of pro-inflammatory genes including cytokines, chemokines and growth factors (e.g., Csf2, Il3, Ccl1, Ccl3) as well as signaling pathways (e.g., iNOS, MAPK, JAK/STAT, NFκβ) were dramatically upregulated following MOG35-55 stimulation of TMOG cells. A number of Th17-related pathways were induced confirming potent Th17-like activation of TMOG. Interestingly, genes known for their anti-inflammatory role (Sit1, Hsd11b1, Pias3, Pparg, Lgmn, Klk3, Tnfaip8l2) were down-regulated in response to MOG35-55 suggesting that silencing of intrinsic suppressory mechanisms may underlie the hyperactivation of memory T cells. MOG35-55 activation led to lower transcription of pro-apoptotic/autophagic genes (Ddit4, Bbc3, Dapk2, Wbp1) and to enhanced level of anti-apoptotic transcripts (Bcl2l1). Transcripts related to toll-like receptors and MyD88-signaling were induced, revealing the involvement of innate immunity pathways in T cell driven autoimmunity. This study reveals the transcriptional events that lead to enhanced cytotoxicity, proliferation and resistance to apoptosis of activated autoimmune T cells. We suggest that encephalitogenic T cells may serve as a reliable in vitro model for screening for possible therapeutics against T cell driven autoimmune diseases.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-16"},"PeriodicalIF":0.0,"publicationDate":"2016-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936234","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}
Pub Date : 2016-03-22DOI: 10.4172/1745-7580.10000107
Doaa M Mahrous Alshareef, H. Kamel, W. M. A. E. Hameed, A. H. E. Amin
Background: Gene mutations are known to play a role in the development of cerebral palsy (CP). The aim of this study was to determine the frequency of factor V Leiden (fVL) mutation as an etiological novel marker in Egyptian children with cerebral palsy. Methods: The study included 70 children; 50 patients with cerebral palsy (Group I) and 20 healthy subjects (Group II) matched age and sex as a control group. Venous blood samples were used for DNA extraction using PCR testing. Polymerase chain reaction (PCR) primers were designed based on exon 10 sequence of human factor V gene. Key findings: There was insignificant difference between both groups regarding comparison of demographic characteristics and risk factors except for pre-term birth (26% in study group versus 5% in control group with P = 0.04). The frequency of fVL mutation was 42% in the study group, 15% in control group with significant difference between study and control groups. There was a significant association and for the first time between homozygous fVL mutation and severe type of cerebral palsy; 60% of homozygous mutations associated with severe CP versus 9% of heterozygous mutations. Conclusions: The fVL mutation is one of the major risk factors that may increase the likelihood of cerebral thrombo-embolism and subsequent cerebral palsy in Egyptian children.
{"title":"Factor V Leiden Mutation as a Novel Marker in Children with Cerebral Palsy","authors":"Doaa M Mahrous Alshareef, H. Kamel, W. M. A. E. Hameed, A. H. E. Amin","doi":"10.4172/1745-7580.10000107","DOIUrl":"https://doi.org/10.4172/1745-7580.10000107","url":null,"abstract":"Background: Gene mutations are known to play a role in the development of cerebral palsy (CP). The aim of this study was to determine the frequency of factor V Leiden (fVL) mutation as an etiological novel marker in Egyptian children with cerebral palsy. Methods: The study included 70 children; 50 patients with cerebral palsy (Group I) and 20 healthy subjects (Group II) matched age and sex as a control group. Venous blood samples were used for DNA extraction using PCR testing. Polymerase chain reaction (PCR) primers were designed based on exon 10 sequence of human factor V gene. Key findings: There was insignificant difference between both groups regarding comparison of demographic characteristics and risk factors except for pre-term birth (26% in study group versus 5% in control group with P = 0.04). The frequency of fVL mutation was 42% in the study group, 15% in control group with significant difference between study and control groups. There was a significant association and for the first time between homozygous fVL mutation and severe type of cerebral palsy; 60% of homozygous mutations associated with severe CP versus 9% of heterozygous mutations. Conclusions: The fVL mutation is one of the major risk factors that may increase the likelihood of cerebral thrombo-embolism and subsequent cerebral palsy in Egyptian children.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2016-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936114","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}
Pub Date : 2016-03-22DOI: 10.4172/1745-7580.10000109
P. Jena, Bhumika Prajapati, P. Mishra, S. Seshadri
Type 2 diabetes is characterized by peripheral insulin resistance. Besides immune and inflammatory mechanisms, other pathways involve interaction between gut microbiota and metabolic syndrome. The present study was designed to understand gut microbiota alteration following High Sugar Diet (HSD) and its effect on physiology and gastrointestinal immunology. Male wistar rats were fed with high fructose and HSD for 60 days. Composition of fecal microbiota by DGGE and proinflammatory cytokines in serum was investigated. Expressions of genes such as TLR2, TLR4 and NF-kB in various tissues were also studied. The bacteria coliforms and clostridium level were higher and Lactobacillus was lower in both sugar rich diet fed rats. Highly diverse and densely populated bands were observed in HSD group by DGGE fingerprint. The band profiles of sugar fed group have clustered together. Elevated mRNA expression of TLR2, TLR4, and NF-kB were observed in HSD groups. Increased inflammation was confirmed by blood and tissue biochemical assay and enhanced serum pro-inflammatory cytokines in HSD diet groups. Gut microbiota strongly influenced the metabolic profiling of individuals fed with high calorie intake. The diverse microbial population and increased coliforms and clostridium may affect host gene expression. Targeting TLRs and microbiota could be promising therapeutic approach
{"title":"Influence of Gut Microbiota on Inflammation and Pathogenesis of Sugar Rich Diet Induced Diabetes","authors":"P. Jena, Bhumika Prajapati, P. Mishra, S. Seshadri","doi":"10.4172/1745-7580.10000109","DOIUrl":"https://doi.org/10.4172/1745-7580.10000109","url":null,"abstract":"Type 2 diabetes is characterized by peripheral insulin resistance. Besides immune and inflammatory mechanisms, other pathways involve interaction between gut microbiota and metabolic syndrome. The present study was designed to understand gut microbiota alteration following High Sugar Diet (HSD) and its effect on physiology and gastrointestinal immunology. Male wistar rats were fed with high fructose and HSD for 60 days. Composition of fecal microbiota by DGGE and proinflammatory cytokines in serum was investigated. Expressions of genes such as TLR2, TLR4 and NF-kB in various tissues were also studied. The bacteria coliforms and clostridium level were higher and Lactobacillus was lower in both sugar rich diet fed rats. Highly diverse and densely populated bands were observed in HSD group by DGGE fingerprint. The band profiles of sugar fed group have clustered together. Elevated mRNA expression of TLR2, TLR4, and NF-kB were observed in HSD groups. Increased inflammation was confirmed by blood and tissue biochemical assay and enhanced serum pro-inflammatory cytokines in HSD diet groups. Gut microbiota strongly influenced the metabolic profiling of individuals fed with high calorie intake. The diverse microbial population and increased coliforms and clostridium may affect host gene expression. Targeting TLRs and microbiota could be promising therapeutic approach","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"46 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2016-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/1745-7580.10000109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936696","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}
Pub Date : 2016-02-15DOI: 10.4172/1745-7580.10000106
S. Shimodaira, K. Hirabayashi, Terutsugu Koya, Y. Higuchi, R. Yanagisawa, M. Okamoto, S. Koido
Although treating advanced cancers that affect organs with distant metastasis remains challenging, the pace of recent advances has accelerated; these advances have particularly focused on the inhibitors of key immune potentiates. Research on therapeutic vaccination involving active dendritic cell (DC)-based immunotherapy is also being performed for the induction of an effi cient immune response against cancer-associated antigens by the acquired immune system. Cancer vaccines prepared with autologous monocyte-derived mature DCs have been generated using granulocyte–macrophage colony-stimulating factor and interleukin-4, which are principally attributed to the presence of tumor-associated antigens. Wilms’ tumor 1 (WT1) is an attractive target antigen that is widely detected in many cancers. DC-based immunotherapy targeting WT1 may elicit a strong therapeutic response to cancers. DC vaccines primed with HLA class I/II-restricted WT1 peptides (WT1-DC) are a feasible option for patients with advanced cancers. Immune response monitoring using tetramer analysis and/or enzyme-linked immunosorbent spot assay has been applied to determine the effi cacy of WT1-DC. The inhibition of immune suppressors and acceleration of anti-cancer immunity with WT1-DC may comprise a promising future therapeutic strategy for treating advanced cancers.
{"title":"An update on Dendritic Cell-Based Cancer Immunotherapy","authors":"S. Shimodaira, K. Hirabayashi, Terutsugu Koya, Y. Higuchi, R. Yanagisawa, M. Okamoto, S. Koido","doi":"10.4172/1745-7580.10000106","DOIUrl":"https://doi.org/10.4172/1745-7580.10000106","url":null,"abstract":"Although treating advanced cancers that affect organs with distant metastasis remains challenging, the pace of recent advances has accelerated; these advances have particularly focused on the inhibitors of key immune potentiates. Research on therapeutic vaccination involving active dendritic cell (DC)-based immunotherapy is also being performed for the induction of an effi cient immune response against cancer-associated antigens by the acquired immune system. Cancer vaccines prepared with autologous monocyte-derived mature DCs have been generated using granulocyte–macrophage colony-stimulating factor and interleukin-4, which are principally attributed to the presence of tumor-associated antigens. Wilms’ tumor 1 (WT1) is an attractive target antigen that is widely detected in many cancers. DC-based immunotherapy targeting WT1 may elicit a strong therapeutic response to cancers. DC vaccines primed with HLA class I/II-restricted WT1 peptides (WT1-DC) are a feasible option for patients with advanced cancers. Immune response monitoring using tetramer analysis and/or enzyme-linked immunosorbent spot assay has been applied to determine the effi cacy of WT1-DC. The inhibition of immune suppressors and acceleration of anti-cancer immunity with WT1-DC may comprise a promising future therapeutic strategy for treating advanced cancers.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"2016 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2016-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/1745-7580.10000106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936021","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}
Pub Date : 2016-01-31DOI: 10.4172/1745-7580.10000105
Melese Yilma
Across sectional study was conducted with objective to determine sero-prevalence bovine brucellosis occurrence from Dec 2009 to Feb 2010 at Chencha district of Gamo Gofa zone. Total of 384 serum samples were collected from cattle and tested for the presence of brucell antibodies using Rose Bengal Plate Test (RBPT). Overall seroprevalence of 4 (1.04%) was recorded in the area. Among the risk factors Abortion and RFM (Retain Fetal membrane) were found significantly associated with sero-positivity (p<0.05). In conclusion the present work generally showed low sero prevalence of bovine brucellosis in the study area and brucellosis was clinically associated with abortion and retained fetal membrane.
{"title":"Rose Bengal Plate Test (RBPT) Based Sero-prevalence of Bovine Brucellosis in and around Chench, Gama Goffa, Southern Ethiopia","authors":"Melese Yilma","doi":"10.4172/1745-7580.10000105","DOIUrl":"https://doi.org/10.4172/1745-7580.10000105","url":null,"abstract":"Across sectional study was conducted with objective to determine sero-prevalence bovine brucellosis occurrence from Dec 2009 to Feb 2010 at Chencha district of Gamo Gofa zone. Total of 384 serum samples were collected from cattle and tested for the presence of brucell antibodies using Rose Bengal Plate Test (RBPT). Overall seroprevalence of 4 (1.04%) was recorded in the area. Among the risk factors Abortion and RFM (Retain Fetal membrane) were found significantly associated with sero-positivity (p<0.05). In conclusion the present work generally showed low sero prevalence of bovine brucellosis in the study area and brucellosis was clinically associated with abortion and retained fetal membrane.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"12 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2016-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/1745-7580.10000105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70935948","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}
Pub Date : 2015-12-28DOI: 10.4172/1745-7580.10000104
M. Carvajal-Moreno
Although aflatoxins are unavoidable toxins of food, many methods are available to control them, ranging from natural detoxifying methods to more sophisticated ones. The present review englobes the main characteristics of Aflatoxins as mutagens and carcinogens for humans, their physicochemical properties, the producing fungi, susceptible crops, effects and metabolism. In the metabolism of Aflatoxins the role of cytochromes and isoenzymes, epigenetics, glutathione-S-transferase enzymes, oncogenes and the role of aflatoxins as mutagens of the tumor suppressor gene p53, and the Wnt signaling pathway are briefly explained, as well as these toxins as biomarkers. The last section includes the Aflatoxin control methods, from the protection of the crop from the Aspergillus fungi, the biocontrol solution, the AFB1-DNA adduct control with the natural repair rates of adduct removal, induction to resistance to AFB1, the detoxification enzymes, recombinant yeasts, pre-exposure to Aflatoxin M1, the inhibition of AFB1 lesions by different compounds, chemoprevention and protective chemical compounds, cruciferous vegetables, dietary dithiolethiones, glucoraphanin, indol-3-carbinol, oltipraz, phenols (butylated hydroxytoluene and ellagic acid), indomethacin, selenium, natural nutrients, coumarin chemoprevention, cafestol and kahweol, terpenes and monoterpenes, grapefruit juice, vitamins, traditional Chinese medical plants (Oldenlandia diffusa and Scutellaria barbata), chlorophyllin, probiotic bacteria and additives as aluminosilicates and glucomannans are described here. Finally, the aflatoxin international legislation was briefly described.
虽然黄曲霉毒素是食物中不可避免的毒素，但有许多方法可以控制它们，从自然排毒方法到更复杂的排毒方法。本文综述了黄曲霉毒素作为人类诱变物和致癌物的主要特征、理化性质、产生真菌、易感作物、作用和代谢。在黄曲霉毒素的代谢中，细胞色素和同工酶的作用、表观遗传学、谷胱甘肽- s -转移酶、致癌基因和黄曲霉毒素作为肿瘤抑制基因p53的诱变剂的作用，以及Wnt信号通路，以及这些毒素作为生物标志物的作用。最后一节包括黄曲霉毒素的防治方法，从保护作物免受曲霉真菌的侵害，生物防治溶液，AFB1- dna加合物控制与加合物去除的自然修复率，诱导对AFB1的抗性，解毒酶，重组酵母，预暴露于黄曲霉毒素M1，不同化合物抑制AFB1损伤，化学预防和保护性化合物，十字花科蔬菜，饮食二硫代乙硫酮，葡萄糖苷，吲哚-3-甲醇、oltipraz、酚类(丁基羟基甲苯和鞣花酸)、吲哚美辛、硒、天然营养物质、香豆素化学预防、咖啡醇和咖啡豆醇、萜烯和单萜烯、葡萄柚汁、维生素、中药植物(白花玉兰和五花芩)、叶绿素、益生菌以及铝硅酸盐和葡甘露聚糖添加剂。最后简要介绍了黄曲霉毒素的国际立法。
{"title":"Metabolic Changes of Aflatoxin B1 to become an Active Carcinogen andthe Control of this Toxin","authors":"M. Carvajal-Moreno","doi":"10.4172/1745-7580.10000104","DOIUrl":"https://doi.org/10.4172/1745-7580.10000104","url":null,"abstract":"Although aflatoxins are unavoidable toxins of food, many methods are available to control them, ranging from natural detoxifying methods to more sophisticated ones. The present review englobes the main characteristics of Aflatoxins as mutagens and carcinogens for humans, their physicochemical properties, the producing fungi, susceptible crops, effects and metabolism. In the metabolism of Aflatoxins the role of cytochromes and isoenzymes, epigenetics, glutathione-S-transferase enzymes, oncogenes and the role of aflatoxins as mutagens of the tumor suppressor gene p53, and the Wnt signaling pathway are briefly explained, as well as these toxins as biomarkers. \u0000The last section includes the Aflatoxin control methods, from the protection of the crop from the Aspergillus fungi, the biocontrol solution, the AFB1-DNA adduct control with the natural repair rates of adduct removal, induction to resistance to AFB1, the detoxification enzymes, recombinant yeasts, pre-exposure to Aflatoxin M1, the inhibition of AFB1 lesions by different compounds, chemoprevention and protective chemical compounds, cruciferous vegetables, dietary dithiolethiones, glucoraphanin, indol-3-carbinol, oltipraz, phenols (butylated hydroxytoluene and ellagic acid), indomethacin, selenium, natural nutrients, coumarin chemoprevention, cafestol and kahweol, terpenes and monoterpenes, grapefruit juice, vitamins, traditional Chinese medical plants (Oldenlandia diffusa and Scutellaria barbata), chlorophyllin, probiotic bacteria and additives as aluminosilicates and glucomannans are described here. Finally, the aflatoxin international legislation was briefly described.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"11 1","pages":"1-15"},"PeriodicalIF":0.0,"publicationDate":"2015-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70935829","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}
Pub Date : 2015-12-07DOI: 10.4172/1745-7580.10000103
Neziri-Ahmetaj Luljeta, Bakir MehiÄ, R. Gojak, N. Arber
Viral infections augment immediate and late allergic responses in the lungs of patients with allergic asthma. Certain viruses that typically exacerbate asthma have been noted to induce release of the cytokine interleukin-11 (IL-11) which is associated with airway hyperreactivity (AHR). The aim of study: To determine the frequency of influenza-like illness in patients with allergic asthma on immunotherapy compared to the patients with allergic asthma receiving only antiasthmatic pharmacotherapy during the period of 1-year follow up. Methods: In our study, we included 60 patients with allergic asthma, both genders who were subsequently divided into two treatment groups. Study group included 30 patients who received immunotherapy (immunotherapy group) and control group included 30 patients treated with standard pharmacotherapy, but not with immunotherapy (GINA proposal). Results: There was a significant difference in influenza-like illness (ILI) between immunotherapy and control group of patients. A significantly higher percentages of patients in control group experienced cold and/or flu syndrome compared to immunotherapy group, which was observed at the 2nd, 3rd and 4th trimester (X2= 20.480 p=0.0001). During the first trimester there was no difference in the number of patients with the cold/flu symptoms between the immunotherapy and control group. During the 2nd trimester, there was a significant decrease in the number of patients with cold/flu symptoms 3/30 (10%) in the immunotherapy group, while in the control group there was significantly higher number of patients with the cold/flu symptoms (11/30 (36 %)). In the 3rd and 4th trimester the frequency of patients with cold/flu symptoms was unchanged compared to the 2nd trimester in the immunotherapy group, while in the control group the frequency of patients with cold/flu symptoms increased from 20/30 (66%) at the 3rd to 27/30 (90%) in the 4th trimester. The number of patients reported to the physician due to bronchial hyperreactivity was dependent on the immunotherapy treatment (p=0.0001) Conclusions: The frequency of influenza-like illness occurrence was significantly lower in patients treated with immunotherapy during one year of follow-up compared to the patients treated with antiasthmatic pharmacotherapy. The percentage of patients with influenza-like illness was 10% in the patients treated with immunotherapy at third and fourth trimester of the follow-up, whilst in patients on antiasthmatic pharmacotherapy, the percentage of patients with influenza-like illness increased from 66% in the third to 90% in the fourth trimester.
{"title":"The Frequency of Influenza-Like Illness in Patients with Allergic Asthmaon Immunotherapy","authors":"Neziri-Ahmetaj Luljeta, Bakir MehiÄ, R. Gojak, N. Arber","doi":"10.4172/1745-7580.10000103","DOIUrl":"https://doi.org/10.4172/1745-7580.10000103","url":null,"abstract":"Viral infections augment immediate and late allergic responses in the lungs of patients with allergic asthma. Certain viruses that typically exacerbate asthma have been noted to induce release of the cytokine interleukin-11 (IL-11) which is associated with airway hyperreactivity (AHR). The aim of study: To determine the frequency of influenza-like illness in patients with allergic asthma on immunotherapy compared to the patients with allergic asthma receiving only antiasthmatic pharmacotherapy during the period of 1-year follow up. Methods: In our study, we included 60 patients with allergic asthma, both genders who were subsequently divided into two treatment groups. Study group included 30 patients who received immunotherapy (immunotherapy group) and control group included 30 patients treated with standard pharmacotherapy, but not with immunotherapy (GINA proposal). Results: There was a significant difference in influenza-like illness (ILI) between immunotherapy and control group of patients. A significantly higher percentages of patients in control group experienced cold and/or flu syndrome compared to immunotherapy group, which was observed at the 2nd, 3rd and 4th trimester (X2= 20.480 p=0.0001). During the first trimester there was no difference in the number of patients with the cold/flu symptoms between the immunotherapy and control group. During the 2nd trimester, there was a significant decrease in the number of patients with cold/flu symptoms 3/30 (10%) in the immunotherapy group, while in the control group there was significantly higher number of patients with the cold/flu symptoms (11/30 (36 %)). In the 3rd and 4th trimester the frequency of patients with cold/flu symptoms was unchanged compared to the 2nd trimester in the immunotherapy group, while in the control group the frequency of patients with cold/flu symptoms increased from 20/30 (66%) at the 3rd to 27/30 (90%) in the 4th trimester. The number of patients reported to the physician due to bronchial hyperreactivity was dependent on the immunotherapy treatment (p=0.0001) Conclusions: The frequency of influenza-like illness occurrence was significantly lower in patients treated with immunotherapy during one year of follow-up compared to the patients treated with antiasthmatic pharmacotherapy. The percentage of patients with influenza-like illness was 10% in the patients treated with immunotherapy at third and fourth trimester of the follow-up, whilst in patients on antiasthmatic pharmacotherapy, the percentage of patients with influenza-like illness increased from 66% in the third to 90% in the fourth trimester.","PeriodicalId":73347,"journal":{"name":"Immunome research","volume":"11 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2015-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70936244","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}
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