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.

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.

Olga Radinsky is a PhD student under supervision of Professor Angel Porgador, doing research at the immunology field at Ben Gurion University of Negev in Israel. As a part of PhD studying, they 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 they 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.

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.

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.

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.

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.

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 poly-morphisms (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.rnrnMethods: 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.rnrnResults: 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.rnrnConclusion: The ERAP1 gene polymorphisms are associated with ankylosing spondylitis (AS) pathogenesis and could be considered as risk factors of this autoimmune disease.