Biography
Eman Albataineh has her expertise in Immunologic research projects about molecular immunology, allergic diseases epidemiology in Jordan as well as thernAllergy-triggering factors and associated diseases. She has been working in research for 6 years in two different universities, i.e.; Jordan University of science and technology and Mutah University.
Abstract
Alkaptonuria (AKU; MIM no. 203500) is a recessive inborn error disorder in the phenylalanine and tyrosine metabolism pathway, arising due to the deficient activity of the enzyme homogentisate 1,2-dioxygenase (HGD). Consequently, the homogentisic acid (HGA; 2,5-dihydroxyphenylacetic acid) will deposit in the connective tissue of various organs, causing a pigmentation known as ochronosis, leading to dramatic tissue degeneration, inflammation and arthritis. The disease prevalence worldwide is estimated as an ultra-rare, although higher incidence rates are recorded in Jordan.rnData regarding the levels of inflammatory mediators in patients suffering of the rare disease Alkaptonuria are limited. C-reactive protein (CRP), Interleukin-1 Beta (IL-1β) and Interleukin-6 (IL-6) are acute-phase markers associated with joint inflammation. The aim of the present study is to compare the serum levels of the pro-inflammatory mediators, CRP, IL-1β and IL-6 in alkaptonuria patients (n=17) with those measured for age-matched healthy controls (n=17). Moreover, we attempt to determine the association between cytokine levels with the disease severity score and age using the Spearman correlation and multiple linear regression. The results show that the serum concentrations of the IL-1 β, IL-6 and CRP are higher in AKU patients compared with healthy controls, with a significant difference in IL-6 (p=0.02). Moreover, a positive correlation is found between the patients\' serum IL-6 and patients\' age and the AKU Severity Score (ro=0.73 and 0.7, respectively; p<0.05). Thus, the patients\' IL-6 serum levels can predict the disease severity score in alkaptonuria patients (p<0.05). These findings suggest that the IL-6 might play a role in the pathogenesis of inflammation in AKU patients and thus targeting it may be one mode of treatment in future. However, these findings need to be supported by further studies, conducted on a larger sample of patients.rn
Biography
Sawsan Said is a PhD candidate in the Department of Molecular Biology and Genetics at the Istanbul Technical University, Istanbul, Turkey. She has been working on a subset of B cells, namely regulatory B cells in the Lab of Dr. Ayca Sayi Yazgan.
Abstract
The regulatory B and T cells have a pivotal role in balancing between immune pathogenicity and protection. Recently, it has been shown that the regulatory T cells could reduce H. pylori-induced gastritis in mice, at the same time allows the bacterium to colonize the mucosa at higher densities. Moreover, it was reported that IL-10+B cells were activated upon Helicobacter infection through TLR2-MyD88 activation, which leads to differentiation of T regulatory-1 (Tr-1) cells from naïve T cells. The interaction between Tr-1 and IL10+B cells may prevent the gastric precancerous lesions and serve as a good immune modulator against Helicobacter. Recently, RNA profile of B10 cells was investigated by RNA-seq, and differentially expressed genes in B10+ and B10-B cells were identified. CD9 was identified as a key surface marker for most mouse IL-10+ B cells, and PD-1was differentially expressed in IL10+/IL10-B cells. In our study, we focus on understanding the expression profile of Helicobacter activated regulatory B cells by microarray analysis, Agilent SurePrint G3 Gene Expression Microarrays of mouse (v2) 8x60K models. Furthermore, gene expression profiling of IL-10 producing regulatory B cells would provide detailed information of B cell genes, including immune function of specific genes. Next, we aim to investigate the expression levels of the recently described genes that are expressed in B 10 cells; CD9, and PDCD1(PD1) in our samples, unstimulated B cells, H. felis stimulated B cells, stimulated IL-10+ B cells and IL-10- B cells. Based on our microarray and real-time PCR data, we wanted to investigate the immune functions of PD1+ regulatory B cells on T cell differentiation to regulatory Tr-1 cells. The PD1 functional study directed the PD1/PD-L 1 interaction blockade as tool to understand the role of PD-1 upregulated B cells in induction (Tr1) upon PD1-PD-L 1 interaction.