Ankylosing spondylitis (AS) represents one kind of advanced arthritis formed via inflammatory stimuli long-term in the spin‘s joints. Interleukin (IL)-29 (interferon- lambda1(IFN- λ1)), interleukin (IL)-28A (interferon- lambda 2 (IFN- λ2)) and interleukin (IL)-28B (interferon- lambda 3(IFN-λ3)) are three interferon lambda (IFN- λs) molecules that have recently been identified as new members of the IFN family. IL-28B expression in ankylosing spondylitis (AS) is not well understood. 150 male healthy controls ((HC) and 160 males with AS as patients group participated in this study. Serum level and gene polymorphism were assessed using an enzyme-linked immunosorbent assay and Sanger sequencing for IL-28B, respectively. The results showed significantly lower serum IL-28B concentrations in the AS groups in comparison to the HC groups (both p values equal to 0.003). There was a large difference in IL-28B genotype and allele frequency between the two individuals. IL-28B heterozygote genotype CT of rs12979860 SNP exhibits a substantial correlation with AS (P = 0.008). While the genotypes of rs12980275 SNP were not shown any significant correlation with AS. The findings suggest that serum concentration of IL-28B is a potential diagnostic biomarker in patients with AS, and that the heterozygote CT of rs12979860 SNP serves as a potential risk factor for the onset of AS in the Iraqi population.

Autoimmune thyroid disease mainly includes Graves’ disease (GD) and autoimmune hypothyroidism (AIH), which is caused by individual genetics, autoimmune dysfunction, and a variety of external environmental factors. Interleukin IL-38 and IL- 40 are involved in a wide range of autoimmune diseases, but little is known about IL-38 and IL-40 expression in autoimmune thyroid disease. This research included 82 female patients with Graves' disease (GD), 78 females with autoimmune hypothyroidism (AIH), and 85 female healthy controls (HC). An enzyme linked immunosorbent assay and sequencing of IL-38 and IL-40 were used to evaluate serum levels and gene polymorphism, respectively. Results showed that significantly lower level of serum IL-38 levels in the GD and AIH groups in comparison with HC group (both p 0.0001). While there were highly significant differences in the GD and AIH groups than in the HC population (both p 0.0001). There was a significant variability in genotype and allele frequencies in the promoter region of IL-38 and IL-40 genes between patients with thyroid disease and healthy controls. The IL-38 homozygote genotype GG exhibits a substantial correlation with GD (P=0.000). While the CC genotype of IL-40 was shown to have a significant correlation with AIH. The findings suggest that serum concentrations of IL-38 and IL-40 are potential novel diagnostic biomarkers in patients with GD and AIH, and that the homozygotes GG and CC of IL-38 and IL-40, respectively, serve as a potential predisposing factor on GD and AIH development in the Iraqi population.

In spite of the high rate of morbidity and mortality heart failure (HF) is common, and none of the medications are now entirely available for HF treatment. In addition to many environmental influences and clinical diseases, genetic factors may also contribute to the progression and development of HF.  In the current study, samples of blood were collected from 150 heart failure patients and 130 healthy controls. We evaluated the association of four single nucleotide polymorphisms (snps) of Toll-like receptors (TLR6 and TLR5) with (HF) susceptibility in the Iraqi population. In this work, (SNP) called Toll-like receptor 5 (rs5744168, rs2072493) and Toll-like receptor 6 (rs1039559, rs5743810) were employed. (PCR-RFLP) for snps (rs5744168, rs2072493, and re5743810), and sequencing for snps were used to assess the allele and genotype frequencies in both the patient and control groups (rs1039559). In patients with heart failure and healthy controls, a significant difference was discovered in the genotypic and allelic frequencies of snps. From our results, we suggest that these snps act as a potential predisposing factor for HF development.