Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease characterized by elevated levels of circulating anti-nuclear autoantibodies and interferon-alpha (INFs-α). Interferon regulatory factor-5 (IRF5) plays an important role in the induction of type I interferon and pro-inflammatory cytokines, and participates in the SLE pathogenesis. This study aimed to investigate the role of IRF5 gene expression levels in a sample of SLE Iraqi patients and its correlation with disease activity, and to identify its diagnostic ability as a biomarker reflecting disease activity. Blood samples were taken from 45 participants diagnosed with SLE cases classified according to the American College of Rheumatology (ACR) criteria. T

Interleukin-38 (IL-38), an inflammatory cytokine discovered in recent years, has been implicated in the pathogenesis of systemic lupus erythematosus (SLE). IL-38 is encoded by the IL1F10 (interleukin 1 family member 10) gene. Genetic variants of this gene have been associated with susceptibility to a number of autoimmune and inflammatory diseases, while their association with SLE risk has not been explored. In this case–control study, two novel variants of the 5 prime untranslated region (5′UTR) of the IL1F10 gene, rs3811050 C/T and rs3811051 T/G, were investigated

Background: Human leukocyte antigen-G (HLA-G)and Toll-like receptor-9 (TLR-9)play a role in the regulation of autoimmune diseases and inflammatory processes. Aim of the study: To detect the HLA-G + 3142G > C gene polymorphism that associated with the susceptibility to SLE patients and associated with Hepatitis B infection and TLR-9 serum level. Patients and methods: This study was done on 75 SLE patients and 75 healthy control groups. Genotyping of HLA-G + 3142G > C were detected by PCR and PCR-RFLP methods. In addition to the estimation of Hepatitis B surface (HBs)antigen status by immunochromatography technique and TLR-9 serum level by ELISA technique. Results: The HLA-G + 3142G > C gene polymorphism between the SLE patients and controls

Background: The etiology of Systemic lupus erythematosus seems to be multifactorial including environmental as well as genetic factors. The genetic predisposition was supported by the occurrence of Systemic lupus erythematosus in more than one member of a family as well as in identical twins.
Aim of the study: To determine the human leukocyte antigen typing class I (A and B) in patients with Systemic Lupus Erythematousus disease.
Methods: Patients group consisted of 44 Iraqi Arab Muslims patients with Systemic lupus erythematosus disease who presented to Baghdad Medical City from January 2010 to January 2012 from Baghdad Province. The second control group consisted from 80 Iraqi Arab Muslims volunteers from hospital employees and t

Background:

Recent accumulated evidences suggest that prolactin is an important immunomodulator and may have a role in the pathogenesis of systemic lupus erythematosus (SLE). The aim of this study was to assess the frequency of hyperprolactinemia in women with SLE and to evaluate its correlation with disease flares. Serum prolactin levels were measured in 62 women with SLE and 50 age- and sex-matched healthy controls. In patients and control groups prolactin levels were determined by immunoradiometric assay (IRMA). The prolactin level was found to be higher than normal rang in (40.3%) of SLE patients in active stage versus only (8.06%) of the same SLE patients but in the inactive stage and in (4%) of control group, the elevation was ranging between mi

  The study aimed to estimate  the role of glucagon-like peptide-1 (GLP-1)  and visfatin as a novel  pro inflammatory marker in Rheumatoid Arthritis (RA ) according to the activity scores of disease to assess the possibility of introducing glucagon-like peptide-1 and visfatin in the diagnosis and monitoring of RA patients and to found the correlation  of visfatin level with GLP-1 and AIP in patients prone to atherosclerosis ,fifty  healthy individuals as control group (G1) and fifty rheumatoid arthritis (RA) patients (G2) were enrolled in this study with middle age  ranged (30 – 40) years and BMI ≥24 kg/m2. ESR ,RF, lipid profile, CRP,insulin, visfatin and GLP-1were determined. Results in t

Certain bacterial and viral infectious agents may play a role in the activation of inflammation in atherosclerosis lesions. Epidemiological studies indicate that infectious agents may predispose patients to atherosclerosis as Infections have been associated with an increased risk of this disease. Moreover, a positive antibody status has been detected against some infectious organisms associated with atherosclerotic rupture. Infectious agents found in human atheroma, which may directly cause or accelerate atherosclerosis , include many pathogens but the present study focused on Helicobacter pylori, hepatitis B virus surface antigen and C. In order to evaluate the possible association between H. pylori, HBV, and HCV infections and the risk of