Biography:

Victor Alexander is MD, PhD in Medicine. He finished his high school with Gold Medal (1969).  He graduated in State Medical University of Azerbaijan in 1976. He pursued MD degree and obtained License in Prophylactics and Treatment of Internal Diseases and worked as MD in hospital for 3 years. He completed his Postgraduation in embryonic, pre- and postnatal Pharmacology area.  In 1984 he got his PhD in Embryonic, pre- & post-natal Pharmacology area of Medicine, which has been recognized in USA. He worked as an Academic PhD Research Scientist in Pharmacology Department of State Medical University and as an Assistant Professor for 12 years. He has been trained in Stem Cell and Molecular Biology area in UC Davis, CA, USA.  He was the Owner and PI of Capital Stem Cell Research Inc. in Sacramento, CA, USA (2008-2012). He is the author of 23 publications (3 in USA), 1 Patent Certificate (1989), 1 Invention (2008) in Stem Cell area registered by UC Davis, CA, participated and published in 3 World Congresses in Molecular Biology and Stem Cells areas (2008; 2011; 2013). He is retired, but actively promotes his new Concept about Ig synthesis in B-cells and novel SAb Technology projects.

Abstract:

Many unexplainable evidences in contemporary Molecular Immunology about Immune Globulin (Ig) synthesis (existence of high quantity of exons in V parts of Ig gene; formation of 2-4 palindromic (p-) sequences in L and H chains of Ig gene after 1st rearrangement; unexplainable “Hyper-mutation” phenomenon; localization of “Hyper-mutation” in the 3 CDRs (Complementarity-determining regions) of V chains; wasting of enormous quantity of new Lymphoid cells in B-Cell development is also evolutionary and scientifically unbelievable and allowed us to propose a New Conception about synthesis of Ig in B Lymphocytes as follows: 1. the 1st rearrangement of V segments of H and L chains in Pro-B and Pre-B lymphocytes in bone marrow is not a random, but a pattern rearrangement which is undergoing under toll-like receptor signaling through MSC to Pro- and Pre-B cells which are developing on the MSC.  Choosing of particular V exon also isn’t a random event, but pattern rearrangement under particular toll-like receptor signaling. 2. affinity maturation of naïve B-cells is not a random event, but undergo by undiscovered yet Reverse Pathway mechanism, which passes exact genetic information about the best matching amino-acids (aa) chain to given antigen on MHC-2, through synthesis of short RNA in a special vesicle of cytoplasm of B-cells. 3. this nascent RNA which is carrying exact genetic information about high affine short amino-acid chain to given antigen, after connection with 2 steroid nuclear receptors moves to nucleus of B cell and connect with 2 palindromic sequences of V-(D)-J section of Ig gene, which are already formed after 1st pattern rearrangement and substitutes all of N nucleotides. And that way Ig gene is getting exact genetic information about the best matching (aa) to given antigen and transcribes high affinity m-RNA and consequently high affinity Ig. It is obvious that our new conception will change the central dogma of molecular biology and will create a novel, very effective and fast Super-Antibody (SAb) Technology for treatment and cure of all infectious diseases and cancer.

Biography:

Zheng Shuo Jin, being a doctor is my dream which I have been keeping in my heart since I was a child. My grandpa was a doctor and he was very brilliant, but finally still killed by cancer. I was really upset and I hope I can help more people who are suffering from disease and pain, also using the science to find a new way to cure cancer .I believe that doctors are not only help patient to have a treatment, also need to research and implementation something new to help their patient feel better, that why I joined the MD program in Tsinghua University. Since 2015 I joined professor Dong Wang’s Lab at Tsinghua University, research in breast cancer and epigenetics.

Abstract:

RSC001 is a small molecule we had screened by HTS technology which can recruit chemokine in cells and these molecules belong to kinases inhibitor, serine kinases which are essential for cell proliferation. It can help in cell division and proliferation, the enzyme controlling chromatid segregation in cell cycle. Defects in this segregation can cause genetic instability, a condition which is highly associated with tumorigenesis, several cancer patients have detected higher expression of aurora kinases. The incidence of breast cancer has continued to rise over the last decade and has become the first major cause of cancer deaths in women in developing countries. The current treatment of breast cancer always uses chemotherapy or surgery treatment, experiments show that accurate treatment can be more effective in treating breast cancer and reduce the side effect during treatment. In the preliminary experiments held by Haiyan Wang shows that aurora kinases inhibitor can effectively inhibit tumor development. So, we decided to continue studying the role of the drug in breast cancer treatment, in the animal experiment the result shows that RSC001 can increase the recruit of immune cells around the tumor cells. From this phenomenon we hope we can explore the mechanism of these kinase inhibitor drug induced chemokine, Through the experiment, we noticed that breast cancer cell line 231 which added RSC001 molecule had high expression of chemokine CXCL11 and CXCL10 when STAT3 had low expression. Considering the chemokine activation pathway, we concentrated on JAK-STAT signal pathway and found the relationship between STAT1 and STAT3 and also the regulation of chemokine and autoimmune cell thus to make an immunotherapy of breast cancer. Immunotherapy combined with precision medicine can better solve breast cancer in the future.

Biography:

Jennifer Alagu obtained her BSc in Biomedical Sciences at Durham University UK in 2011. She then went to work at the Chiba Cancer Center, Japan until 2013 as a Research Assistant where she co-authored 3 publications in the field of Neuroblastoma. Since then, she has been working on her PhD thesis at Duke-NUS Medical School, Singapore in the Laboratory of Tumour Suppression under Prof. Koji Itahana, specifically researching the involvement of major tumour suppresser p14ARF in the regulation of inflammatory responses such as those activated by oncogenic viruses and tumour progression.

Abstract:

Background: Tumour suppressor p14ARF (alternative reading frame) is activated by oncogenic stress to oncogene-induced senescence via activation of p53. The function of ARF is lost in 40% of cancers. Interestingly, loss of ARF has been shown to compound the effect of p53 inactivation highlighting the need to understand the additional functions of ARF. ARF has emerged as a potent up-regulator of global intracellular SUMOylation, independent of p53 activity. However, few targets of ARF-enhanced SUMOylation have been identified and the functional consequences to cancer aetiology remain to be elucidated.

Methods: We employed a novel screening approach combining ARF with SUMO overexpression. Immunoprecipitation of SUMO was performed to identify the proteins SUMOylated in response to ARF by mass spectrometry.

Results: We identified and validated a novel protein target of ARF-enhanced SUMOylation which is a negative regulator of pro-inflammatory transcription factors STAT1 and NF-kB. ARF has been shown to be inducible by IFN-γ and TNF-α, upstream regulators of STAT1 and NF-kB respectively. Our results show that ARF promotes these pro-inflammatory responses by inhibiting this protein by enhancing its SUMOylation status.

Conclusions: Identification of our novel ARF-mediated SUMOylation target reveals ARF’s p53-independent role in the pro-inflammatory processes that are activated by tumour invasion or infection of oncogenic viruses to prevent tumourigenesis. Our findings present a novel role of ARF in tumour immunology and given the exceptionally high incidence of ARF loss reported in human cancers, may aid in the development of new therapeutic opportunities for dysregulations observed in the ARF-SUMOylation pathway.

Biography:

Seong Kug Eo in his lab, has focused on unveiling how hosts response to pathogen infection They have used various infectious models to prove host responses upon pathogenic infection. His lab has recently found the detailed pathway that IFN-I signal pathway orchestrated environments to provide effective protection against mucosal viral infection. Moreover, his lab is expert on viral acute encephalitis caused by flavivirus infection.

Abstract:

Possible risk mediators in primary dengue virus (DenV) infection that favor secondary DenV infection to life-threatening dengue hemorrhagic fever (DHF) and shock syndrome (DSS) via antibody-dependent enhancement (ADE) have not yet been described. Here, DenV infection enhanced the expression of inflammatory mediators and activation molecules in dendritic cells (DCs) through TLR2/MyD88 pathway. TLR2 appeared to facilitate DenV infection in DCs that were less permissive than macrophages for viral replication. In experiments using separate evaluations of DenV-infected and uninfected bystander DCs, infected DCs showed impaired maturation accompanied with TLR2-dependent production of inflammatory cytokines, by which uninfected bystander DCs showed increased expression of co-stimulatory molecules. Differential phosphorylation of MAPK and STAT3 was also detected between DenV-infected and uninfected DCs. Furthermore, DenV infection stimulated Th2-polarized humoral and cellular immunity against foreign and DenV Ag via TLR2/MyD88 pathway, and DenV-infected DCs were revealed to facilitate Th2-biased immune responses in TLR2-dependent manner. TLR2/MyD88-mediated Th2-biased Ab responses to primary DenV infection increased the infectivity of secondary homotypic or heterotypic DenV via ADE. Collectively, these results indicate that TLR2/MyD88 pathway in DC-priming receptors can drive Th2-biased immune responses during primary DenV infection, which could favor secondary DenV infection to DHF/DSS via ADE.

Biography:

Seong Kug Eo in his lab, has focused on unveiling how hosts response to pathogen infection They have used various infectious models to prove host responses upon pathogenic infection. His lab has recently found the detailed pathway that IFN-I signal pathway orchestrated environments to provide effective protection against mucosal viral infection. Moreover, his lab is expert on viral acute encephalitis caused by flavivirus infection.

Abstract:

Type I interferon (IFN-I)-dependent orchestrated mobilization of innate cells in inflamed tissues is believed to play a critical role in controlling replication and CNS-invasion of herpes simplex virus (HSV). However, the crucial regulators and cell populations that are affected by IFN-I to establish the early environment of innate cells in HSV-infected mucosal tissues are largely unknown. Here, we found that IFN-I signaling promoted the differentiation of CCL2-producing Ly-6Chi monocytes and IFN-g/granzyme B-producing NK cells, whereas deficiency of IFN-I signaling induced Ly-6Clo monocytes producing CXCL1 and CXCL2. More interestingly, recruitment of Ly-6Chi monocytes preceded that of NK cells with the levels peaked at 24 h post-infection in IFN-I–dependent manner, which was kinetically associated with the CCL2-CCL3 cascade response. Early Ly-6Chi monocyte recruitment was governed by CCL2 produced from hematopoietic stem cell (HSC)-derived leukocytes, whereas NK cell recruitment predominantly depended on CC chemokines produced by resident epithelial cells. Also, IFN-I signaling in HSC-derived leukocytes appeared to suppress Ly-6Ghi neutrophil recruitment to ameliorate immunopathology. Finally, tissue resident CD11bhiF4/80hi macrophages and CD11chiEpCAM⁺ dendritic cells appeared to produce initial CCL2 for migration-based self-amplification of early infiltrated Ly-6Chi monocytes upon stimulation by IFN-I produced from infected epithelial cells. Ultimately, these results decipher a detailed IFN-I–dependent pathway that establishes orchestrated mobilization of Ly-6Chi monocytes and NK cells through CCL2-CCL3 cascade response of HSC-derived leukocytes and epithelium-resident cells. Therefore, this cascade response of resident to-hematopoietic–to-resident cells that drives cytokine–to-chemokine–to-cytokine production to recruit orchestrated innate cells is critical for attenuation of HSV replication in inflamed tissues.

Biography:

Eunjin Hyeon is student who is studying Medical Science in Chonbuk National University. She is particularly researching about allergic diseases such as asthma and rhinitis.

Abstract:

Allergic rhinitis is a common heterogeneous chronic upper airway disorder and is an IgE-mediated inflammation characterized by one or more nasal symptoms such as sneezing, itching, nasal discharge, rhinorrhea, post nasal drainage and nasal blockage. In the present study, the effects of Skullcapflavone II (SCFII) on upper airway inflammation, Th2 cytokines, and NF-kb signaling in an ovalbumin (OVA)-induced allergic rhinitis (AR) murine model in vivo were investigated. OVA-induced AR mice increased nasal symptoms, eosinophils and mast cells infiltration into nasal cavity, OVA-specific IgE/IgG1and histamine in serum, Th2 cytokines including IL-13 and GATA3, and NF-κB signaling in NALF and lung homogenate. Interestingly, treatment of SCFII reduced the levels of OVA-specific IgE/IgG1 and histamine in serum, of Th2 cytokines and of NF-κB signaling in the NALF and the lung homogenate, and histopathological changes in the nasal tissue and the lung. Also, dexamethasone suppressed such increases. The results of this study suggested that SCFII may ameliorate allergic inflammation of upper airway in AR mice model by blocking the Th2 cytokine production, the NF-κB signal pathway and the mast cell histamine release. Taken together, we suggest that SCFII may be used as a therapeutic agent for patients with Th2-mediated or mast cell-mediated allergic diseases.

Biography:

Thi Tho Bui  has his expertise in evaluation the herbal medicine as well as bioactive compounds for immunology-related deseases treatment.

Abstract:

Bupleurum Chinense has been used as traditional herbal medicine for more than a thousand years. It has been found to have anti-inflammatory, anti-oxidant, hepato-protective, antipyretic, analgesic, anti-fibrotic and immunomodulatory effect. However, the effect of B. Chinense on allergic rhinitis remains unclear. We clarified whether or not Bupleurum Chinense extracts (BCE) could ameliorate inflammatory response in OVA-induced AR mice model. The oral administrations of BCE inhibited the accumulation of eosinophils in NALF (nasal lavage fluid) and nasal epithelium and their active production such as CCL24. BCE may also prevented allergic response via suppressing mast cells accumulation in nasal epithelium and serum histamine release simultaneously with inhibiting the serum anti-OVA IgE, IgG1 and elevating the anti-OVA IgG2a at BCE dose-dependent treatment. Accordingly, nasal epithelial swelling and goblet cells hyperplasia were clearly attenuated. In addition, BCE regulated the balance of Th1, Th2 and Treg-related cytokines that could prevent inflammatory cells activation such as eosinophils ans mast cells; briefly; down-regulated the expression of IL-4, IL-5, IL-13 in NALF and nasal tissue and up-regulated the secretion of IL-10, IL-12 and IFN-γ. These results suggest that BCE may have therapeutic potential for treating allergic rhinitis by preventing the accumulation and activation of the inflammatory cells such as eosinophils and mast cells.

Biography:

Yan Jing Fan is a Master’s student of Medical Science in Chonbuk National University, Department of Anatomy.

Abstract:

Fructus Amomi Cardamomi (FA) is the mature fruit of Amomum villosum Lour of the family Zingiberaceae. It has been used in Chinese medicine for the treatment of a variety of gastrointestinal disorders. However, the anti-allergic rhinitis effects of FA are less known. We investigated the immunomodulatory effect of FA on allergic inflammation in an allergic rhinitis (AR) mouse model. Administrated by nasal installation of FA (10, 20, 40 mg/kg) ameliorated the nasal symptom and alleviated the swelling of nasal epithelium. FA reduced the goblet cell number and eosinophil number in nasal epithelium. FA also inhibited the lung hyperplasia in lung tissue. Meanwhile, FA treatment groups evidently decreased the expression of Th2 cytokines (IL-4, IL-5), increased the secretion of Th1 cytokines (IL-12, IFN-γ) in lung homogenate. FA also reduces the OVA-specific IgE and OVA-specific IgG1 level in serum. In this study, our data suggests that FA has a significant anti-allergic inflammation effect and it may prove to be an efficacious therapeutic regent on allergic rhinitis.

Biography:

Chunhua Piao is a PhD candidate in the Department of Medicine at Chonbuk National University.

Abstract:

Dryopteris crassirhizoma (DC) is used as a traditional herbal remedy to treat various diseases, the tapeworm infection, common cold, and cancer in Korea, Japan, and China. DC also has the antioxidant anti-inflammatory and antibacterial activities. However, anti-allergic inflammatory effect of DC and some of its mechanisms in allergic rhinitis model is unknown well. The purpose of this study is to investigate the anti-allergic inflammatory effect of DC on the allergic rhinitis model, mast cell activation and histamine release. Allergic rhinitis was induced in BALB/c mice by sensitization and challenge with OVA. Each various concentration of DC and Dexamethasone was administrated by oral administration on 1 hour before OVA challenge. Mice of control group were treated with saline only. Then mice were evaluated for the presence of nasal mucosa inflammation, the production of allergen-specific cytokine response and the histology of nasal mucosa. DC significantly ameliorated the nasal symptoms and the inflammation of nasal mucosa. DC also reduced the infiltration of eosinophils and mast cells in these tissues and the release of histamine in blood. Meanwhile, DC evidently inhibited the overproduction of Th2 cytokine, and increased reduction of Th1 and Treg cytokines in nasal lavage fluid by OVA. DC also reduced the levels of OVA specific IgE, IgG1 and IgG2a in blood. This study suggests that DC has a significant anti-allergic inflammatory effect in nasal cavity. DC may have the therapeutic effect for allergic rhinitis.

Biography:

Maha Bakhuraysah has her expertise in evaluation and passion in improving the health and wellbeing. Her research focuses on the role of the Nogo receptor in multiple sclerosis, she and her team are working on Experimental Autoimmune Encephalomyelitis (EAE). Previous data has mentioned that there was no new role associated with Nogo receptor, thus she focused on the immunological arm in this model and discovered the existence of B-cells expressing NgR in EAE. It has been published recently that in MS patients’ B cells are localized in the brain, which she and her team found it in mice. The studies haven't mentioned anything about the Nogo receptor, but she and her team found them too.  

Abstract:

Despite clear evidence demonstrating that the deletion of Nogo-receptor 1 (NgR1) can protect against axonal degeneration and thus progression of experimental autoimmune encephalomyelitis (EAE), an immunological role for this receptor is yet to yield mechanistic evidence. However, recently NgR has been suggested as an alternate receptor for the B-cell activating factor (BAFF) in the central nervous system (CNS).  Therefore, our strategic aim was to define whether NgR contributes in the modulation of the adaptive immune response during EAE by promoting maturation and differentiation of BAFF-reactive B-cells within follicles during the induction of disease. The results showed that CNS-infiltrating blood cells revealed an augmented response in the B-cells, which expressed NgR1 and NgR3, observed in ngr1^+/+ mice with the onset and progression of the disease that could not be demonstrated within the spinal cords of EAE-induced ngr1^-/- mice. Remarkably, a cluster of B-cells-expressing NgR was present at the meninges of lumbosacral spinal cords of the of ngr1^+/+ EAE-induced mice at clinical score 1. Furthermore, there were significant increases of secreted immunoglobulins from these NgR1-expressing B-cells. Importantly, these cells could be directed into the synthesis phase of the cell cycle, after stimulating sorted cells by extracellular BAFF in vitro; however, when BAFF signaling was blocked using either rBAFF-R, or NgR1-Fc, or NgR3 peptides, the cells were observed to be into G0/G1 phase. As a consequence, when we blocked NgR1-ligand signaling using a novel hematopoietic stem cell-based delivery of a therapeutic protein, immune lineage-differentiated cells, including ZsGreen and fusion protein, were trafficking into the CNS during acute EAE. Collectively, these data indicate that the existence of an inducible expression of NgR1 and NgR3 in specific immune lineage cells upon the induction of EAE, and that the follicular-like NgR1 and NgR3-positive B-cells in the meninges may play an active role during the induction of EAE. Thus, our data reinforce the idea that blocking the interaction of BAFF and NgR1 and NgR3 may be vital for neuroprotection during inflammatory insults.

Biography:

Chang Duk Jun discovered several crucial molecules involved in the immunological synapse (IS). Among them, TAGLN2 localizes at the distal area of supramolecular activation clusters (d-SMAC) in IS and stabilizes actin structure that prolongs the duration of IS. In macrophages, TAGLN2 plays an important role by enhancing the phagocytic function of macrophages. He is also interested in mutual communication between T cells and antigen-presenting cells in the process of immune synapses and kinapses. 

Abstract:

Activated macrophages have a greater ability of phagocytosis against pathogens that is mediated by large-scale actin rearrangement. However, molecular machineries that conduct this task have not been fully identified. Here, we demonstrate an unanticipated role of TAGLN2, a 22-kDa actin-binding protein, in Toll-like receptor (TLR)-stimulated phagocytosis. TAGLN2 was greatly induced in macrophages in response to lipopolysaccharide (LPS), a ligand for TLR4, partly via the NF-κB pathway. TAGLN2-deficient macrophages (TAGLN2-/-) showed defective phagocytic functions of IgM- and IgG-coated sheep red blood cells as well as bacteria. Cell signaling pathways involved in actin rearrangement-PI3 kinase/AKT and Ras-ERK were also down-regulated in LPS-stimulated TAGLN2-deficient macrophages. Moreover, TAGLN2-/- mice showed higher mortality after bacterial infection than wild-type littermates. Thus, our results revealed a novel function of TAGLN2 as a molecular armament required for host defense.

Biography:

Daniela Rojas is a Medical Technologist working at the Department of Veterinary Pathology, University of Concepción. She has worked with different research groups in the Faculty of Veterinary Science for over 15 years.

Abstract:

Obesity and overweight are increasingly common conditions associated with poor-quality diet. These conditions trigger hyperplasia and hypertrophy of adipocytes and inflammation, therefore targeting this tissue and its local inflammation became the most effective therapeutic approach to overcome obesity. Previous studies have revealed that oils derived from the Pinaceae family, commonly used as a dressing in the Asian cuisine, suppress appetite, however it remains unknown whether seed oil from Pinus radiata exhibit any beneficial effect on adipose tissue morphology or inflammatory state. In this study, we analysed the effect of a P. radiata seed oil-based supplement (SuplD) on a murine model of high fat diet (HFD)-induced obesity. Female C57BL/6J mice were fed with HFD for 3 months until obesity was established. Then, obese mice were randomized and divided into 3 groups: under HFD supplemented with 15% w/w SuplD, under HFD supplemented with 15% w/w Glycine max oil as a negative control, and under HFD without supplementation as untreated control. After 3 months post supplementation, mice treated with SuplD showed increased frequency of small adipocytes within the visceral adipose tissue in comparison with controls. Moreover, increased presence of small adipocytes niches containing pre-adipocytes, identified as CD34⁺, CD29⁺ and CD45^-, and increased Von Willenbrand Factor expression, indicating increased adipose vascularity, were also observed in tissues from mice treated with SuplD. Finally, when immunological parameters were evaluated, we observed increased IL-10 and Arginase-1, and reduced TNF-α and IL-6 expression in visceral adipose tissue samples from mice treated with SuplD compared to control groups. Altogether, our results suggest that oral administration of a P. radiate-based supplement in obese mice promotes hyperplasic growth of small adipocytes, increases vascularity in the visceral adipose tissue and an anti-inflammatory local environment. These observations suggest that P. radiate seed oil could be clinically relevant in human obesity. 

Biography:

Yuan Liu has her expertise in research of pathogenesis mechanism of autoimmune diseases and using proteomic approaches to identify biomarkers in autoimmune diseases.

Abstract:

Hydroxychloroquine (HCQ) is an antimalarial drug that has been used for treating a large variety of diseases for many years. However, its specific mechanism is still not well demonstrated. In this study, we investigated the effects of HCQ on regulating dendritic cells (DC) function. The surface molecule expression, secretion of inflammatory cytokines and ability in promoting naïve CD4+ T cells proliferation and differentiation of bone marrow-derived DCs (BMDCs) were investigated after HCQ treatment. We found that HCQ treatment could significantly reduce the expression level of MHC II, CD86 and CD40. HCQ could also inhibit the production of cytokines including IL-1β, IL-6, IL-23 and TNF-α by LPS (Lipopolysaccharide) stimulated DC. Additionally, the ability of DC in promoting naïve CD4+ T cells proliferation and Th17 cells differentiation was decreased by HCQ. The effect of HCQ on DC may be partly associated to inhibition of phosphorylation of ERK1/2 and p38 MAP kinase proteins. These findings provided new understanding about the mechanism of HCQ in immune regulation.

Biography:

Shiju Chen has her experience in diagnosis and treatment of rheumatoid diseases and clinical research. She has been engaged in busy clinical work for a long time and keeps a great passion and interest in dealing with patents and their diseases. She has some experience in osteoporosis and osteoarthritis disease in basic and clinical research including Wnt/beta - catenin signaling pathway and mi-RNA regulation function in the osteoblast. Now the main research focus on microRNAs and exosome in inflammatory arthritis.

Abstract:

The acute gouty arthritis (GA) is one most painful acute inflammation induced by monosodium urate (MSU) deposition. The pathogenesis of inflammation remains unclear. Activation of MyD88/ NF-kB signal pathway is involved in acute GA, giving rise to the increase of cytokines including TNF-, IL-1, and IL-6. MicroRNAs(miRNAs), severing as post-transcriptional regulation, is reported to participate in many inflammatory diseases including acute GA. Previous study demonstrated miR-920 down-regulated in the peripheral white blood cells of GA which negative regulated target IL-1ß. This may be the role of miR-920 in regulating the production of proinflammatory cytokines in the pathogenesis of GA. To further explore the function of miR-920 in acute GA, we detected miR-920 by qRT-PCR in the peripheral blood mononuclear cells (PBMCs) of 9 acute gouty arthritis patients and 9 healthy controls. However, overexpression of miR-920 was found in PBMCs and MyD88 was predicated as another target gene by bioinformatics. After transfecting the miR-920 mimics or negative control mimics into human monocytic THP-1 cell line, expression of MyD88 decreased. This may hint an opposite role of miR-920 in acute gouty arthritis.

Biography:

Farida Karim has completed her MBBS from Jinnah Medical and Dental College Karachi and internship from Aga Khan University Hospital. She is working currently as Medical Officer in  the Aga Khan University Hospital, Pakistan’s best and most advanced healthcare service organization. She has published three articles and is working on several other projects that are under reviewing process.  

Abstract:

Objective: To determine the clinical and immunological characteristics and short term outcome of children with systemic lupus erythematosus (cSLE) presented at a tertiary care center in Karachi, Pakistan.

Design: A descriptive observational study conducted at the Pediatric Rheumatology Clinic of Aga Khan University Hospital (AKUH), Karachi, from January 2011 to April 2015.

Methodology: Data of children <16 years of age, admitted at the Pediatric ward, diagnosed with cSLE, was studied.

Results: 32 children satisfying the criteria of American College of Rheumatology (ACR) for cSLE were enrolled. A female predominance was observed, with 87.5% of the patients being female. Mean age at symptom onset was 10.5+2.7 years and 8.8+2.1 years in females and males respectively. Mean age at diagnosis was 11.3+2.8 years in females and 9.4+1.9 years in males. Fever was the most common non-specific symptom found in 84% patients. Sixty nine percent children were found to be anemic and 56% had signs of arthritis at presentation. Renal involvement was observed in 47% patients. The most common immunological markers were found to be serum Anti-neutrophil antibodies (ANA), positive in  88% patients, followed by Anti double-stranded DNA antibodies (anti ds-DNA), raised in 81% cases. Overall response rate to therapy was 50% in 20 children who were followed for  4 years.

Conclusion: We found that cSLE encompasses a wide variety of manifestations with  female preponderance. Fever and Arthralgia  are the most frequent clinical findings. Hemolytic anemia is the most common laboratory abnormality, with ANA and Anti ds-DNA positivity in majority of patients.

Biography:

Olga Radinsky is a PhD student under supervision of Professor Angel Porgador, doing her research in the Immunology field at Ben Gurion University of Negev in Israel. As a part of PhD studying, she developed cell-based reporter system based on the expression of CD3zeta-fused FcγRs in BW cells to quantitate total and pathogen-specific antibody binding to Fcγ-Receptors. Using this system, she completed analysis of sera from patients with different health conditions: Alzheimer patients, cancer patients, recurrent abortions in women, and long-recovered survivors of SUDV infection.

Abstract:

Ebolavirus is a highly lethal pathogen, causing a severe hemorrhagic disease with a high fatality rate. To better understand immune correlates of protection by virus specific IgG, we investigated the evolution of the Fcγ receptors (FcγRs)-activating capabilities of antiviral IgG in serum samples of long recovered survivors. To this end, longitudinal serum samples from survivors of Sudan ebolavirus (SUDV) infection, studied over years, were examined for the presence of Ebola-GP specific IgG subclasses, and for their binding to FcγRs. We developed a cell-based reporter system to quantitate pathogen-specific antibody binding to FcγRIIIA, FcγRIIA, FcγRIIB and FcγRI. With this system, we demonstrate that anti-GP-specific stimulation of the FcγRI reporter by survivors’ sera was substantially high one year after acute infection, with a slight reduction in activity over a decade post infection. We further demonstrate that GP-specific IgG1 is by far the seroprevalent subclass that retained and even enhanced its presence in the sera, over ten years post infection; the prevalence of other GP-specific IgG subclasses was considerably reduced over time. In accordance, GP-specific FcγRI reporter response and GP-specific total IgG1 subclass correlated in the studied group of Ebola survivors. These observations are important for further informing Ebola vaccine and therapeutic development.

Biography:

Radwa H Ghoraba is a Pharmacist, graduated from Faculty of Pharmacy and Drug Manufacturing, Pharos University 2012, Alexandria, Egypt. She has a Master’s Degree in Diagnostic and Molecular Microbiology, Medical Research Institute (MRI), Alexandria University 2017, Egypt. Her involvement in research has given her first-hand exposure to the process of active scientific research, resulted in incredible research experiences, and instilled in her a passion for science and exploration. She is interested in improving public health through research.

Abstract:

Viral infections in hematological patients may result from reactivation of latent infection or, rarely, from acquisition of a new infection. It is extremely important to identify which patients or which treatment strategies are particularly at risk of viral infections to choose the suitable therapeutic procedure. Both acute lymphoblastic leukemia and acute myeloid leukemia patients receiving induction or consolidation chemotherapy are at the highest risk of viral infection. Thus, screening of patients with hematological malignancies for HHV-6 might be considered mandatory. The aim of this study is to evaluate a possible association between Human Herpesvirus-6 (HHV-6) infection and acute leukemia in adults after receiving chemotherapy treatment for acute leukemia. The patients were divided into two main groups according to the type of leukemia: Group I; 36 patients with newly diagnosed acute myeloid leukemia (AML) and Group II; 27 patients with newly diagnosed acute lymphoblastic leukemia (ALL); 21 patients with B-ALL and 6 patients with T-ALL. All 63 studied adult patients with newly diagnosed acute leukemia were subjected to history taking, complete clinical examination for the presence of organomegaly and routine laboratory investigations. Peripheral blood samples were collected from all patients for quantitative determination of HHV6 viral load by Taqman probe technique (real time PCR) at day 0 and day 100 of induction chemotherapy. The results argued against an etiological relationship between HHV-6 infection and the genesis of acute leukemia in adults, however, it supports the hypothesis of viral latency and the possibility of virus reactivation in immunocompromised hosts. The possible presence of HHV-6 as an associated or a putative causative agent in leukemia should however be considered. The following recommendations include: screening of patients with hematological malignancies for HHV-6 might be considered among the routine initial laboratory work-up.

Biography:

Dr. Shobha Sehgal is an emeritus professor of immunopathology at the Post Graduate Institute of Medical Education and Research, Chandigarh, India. She is the past president of the Indian Immunology Society and founder president of the Indian Society of Primary Immune Deficiencies. Has worked in HIV and AIDS in North India including early spread, the type of virus prevalent, spectrum and immunological characteristics of Clade C virus. She has interest in other infectious diseases like leishmaniasis tuberculosis, autoimmune diseases including SLE. She has more than 250 publications to her credit. Currently she is working in the field of ocular immunology.

Abstract:

Toll like receptor (TLR) engagement is primarily a function of innate immune cells yet recent reports indicate that TLR9 may be expressed on certain subsets of T lymphocytes but their precise role in T effector (Teff) cells has not been elucidated. We made a chance observation that purified Teff cells from healthy individuals consistently bind to the TLR9 ligand ODN 2216. We confirmed intracellular localization of ODN 2216 FITC as well as intracellular expression of TLR9 in Teff cells. Furthermore, ODN 2216 FITC was also co localized with the lysosomal membrane associated protein 1 (LAMP1). In the whole blood, on the other hand, 98% of monocytes showed binding to ODN 2216 FITC indicating that the monocytes compete with the lymphocytes for ligand binding. The uptake of TLR ligand culminated in cellular proliferation, up-regulation of cytokines and increased mRNA expression of TLR9 and IRF7 in T effector cells. ODN uptake by Teff cells was inhibited by an endocytosis inhibitor, promethazine, as well as by TLR9 antagonist.  Our results show a direct engagement of TLR9 ligand in Teff cells giving new insight into the role of TLR9 signalling and novel mechanisms of action of TLR inhibitors. 

Biography:

Zohreh Babaloo is an Associate Professor of Immunology and has completed her PhD and Lab MD Fellowship from the Immunology London School of Hygiene and Tropical Medicine. Her main researches interests are immune responses and immunogenetics of autoimmune diseases; multiple sclerosis, behcet, ankylosing spondylitis, and infectious diseases; visceral leishmaniasis. She is the Head of Immunology Department and Director of Immunology Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Abstract:

Background: Ankylosing spondylitis (AS) is a chronic inflammatory arthritis; a type of seronegative spondyloarthropathies. AS typically affects the joints of the spinal and axial skeleton. Among the non-HLA predisposing loci, the strongest association has been observed for single nucleotide poly­morphisms (SNPs) of endoplasmic reticulum amino peptidase ERAP1 gene. ERAP1 reduces the ability of signal transmission by cleaving cytokine receptors which affects the inflammation process. It also causes cleavage of some cell proteins into small peptides which exported to the cell surface, where they attach to MHC class I molecules and trigger an autoimmune response.

Methods: In this study the frequencies of ERAP1 allelic variants and genotypes for three non-synonymous SNPs have been determined in 160 AS patients and 160 healthy individuals, as control group, from an Iranian population in north-west Iran. Both AS patients and healthy control groups consist HLA-B27 positive and HLA-B27 negative individuals. The implemented method was SSP-PCR for genotyping three SNPs of ERAP1 gene including rs30187, rs2287987, and rs10050860 in AS patients and healthy controls.

Results: Our investigation showed considerable differences in alleles frequencies within AS patients vs. healthy controls. The association of three SNPs; rs30187, rs2287987, and rs10050860 with the risk of AS [odds ratio (OR) 0.775, 95% CI 0.566–1.06, P=0.12 for rs30187, OR 0.561, 95% CI 0.359–0.877, P=0.01 for 10050860 and OR 1.91, 95% CI 1.16-3.15, P=0.014 for rs2287987] was the most important result of this study.

Conclusion: The ERAP1 gene polymorphisms are associated with ankylosing spondylitis (AS) pathogenesis and could be considered as risk factors of this autoimmune disease.