Background: Tumor necrosis factor-alpha (TNF-α) and interleukins play important roles in the pathogenesis of rheumatoid arthritis (RA). Genetic research has been employed to find many of the missing connections between genetic risk variations and causal genetic components. Objective: The goal of this study is to look at the genetic variations of TNF-α and interleukins in Iraqi RA patients and see how they relate to disease severity or response to biological therapy. Method: Using specific keywords, the authors conducted a systematic and comprehensive search to identify relevant Iraqi studies examining the genetic variations of TNF-α and interleukins in Iraqi RA patients and how they relate to disease severity or response to biolo

Background: Rheumatoid arthritis (RA) is a chronic and systemic autoimmune disease that is characterized by severe synovial inflammation, cartilage erosion, bone loss, and generalized vasculopathy. Although the immunologic mechanism of RA is still unclear, it is now thought to be a primarily Th17-driven disease. Along with other factors, IL-23 stimulates the expansion of Th17 cells from naive CD4+ T cells.

Objective: The objective of this study is to assess the circulating levels of interleukin (IL)-23 in rheumatoid arthritis (RA) and determine the correlation between plasma/serum IL-23 levels and disease activity. So, we performed a systematic review with meta-analysis comparing

Abstract Introduction: MMP3 plays a crucial role in the process of bone erosion in the pathomechanism of rheumatoid arthritis (RA). It acts by removing the outer osteoid layer, which allows the osteoclasts to tightly connect and carry out the subsequent damage to the underlying bone. MMP3 can trigger the production of other MMPs like MMP-1, MMP-7, and MMP-9, it plays a pivotal role in the remodeling of connective tissues. Aim of the study: to assess the influence of MMP-3 serum levels and single-nucleotide polymorphisms of rs679620 in the rheumatoid arthritis patients' group in comparison to the control group. Subjects: eighty eight samples, 45 rheumatoid arthritis patients after being referred by their treating physician for regular RA

It was aimed to understand the interleukin-4 (IL-4) role in etio-pathogenesis of rheumatoid arthritis (RA). Two approaches were adopted. In the first one, a quantitative expression of IL4 gene was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and such findings were correlated with some demographic, clinical and laboratory parameters, which included gender, duration of disease, disease activity score (DAS-28), rheumatoid factors (RFs), C-reactive protein (CRP) and anti-cyclic citrullinated peptide (ACCP) antibodies. In the second approach, a single nucleotide polymorphism (SNP) of IL4 gene (rs2243250) was inspected by DNA sequencing using specific primers. Fifty-one Iraqi RA patients (22 males and 29 fem

Background In rheumatoid arthritis, your immune system attacks the tissue lining the joints on both sides of your body. Other parts of the body may also be affected. Unsure of the exact cause. Two separate genes termed IL12A (p35) and IL12 encode the heterodimeric cytokine known as IL12 (p40). Several different hematopoietic cell types can have several different hematopoietic cell types that can generate antigen-presenting cells (APCs), including DCs and macrophages. Objectives This study aimed to investigate if the interleukin IL-12B gene's common polymorphisms in an Iraqi population were associated with RA. Material and methods Blood samples were taken from 70 Iraqi patients with RA illnesses and 30 Iraqi controls during the periods from

Diabetic foot ulcer (DFU) or Lower limb ulcers are one of the major complications caused by diabetes mellitus especially when patients fail to maintain tight glycemic control. DFU is linked to multiple risk factors along with the genetic factors and ethnicity which play a significant role in the development of DFUs through their effects on multiple aspects of the pathophysiological process. This narrative review aimed to summarize all the previous studies within the last ten years associating gene polymorphism and DFU. Polymorphism associated with vascular endothelial growth factor (rs699947), the G894T polymorphism of the endothelial nitric oxide synthase gene, interleukin-6–174 G>C gene polymorphism, heat shock protein 70 gene polymorph

Rheumatoid arthritis is a worldwide inflammatory chronic autoimmune disease with varying severity. Due to no definitive cure for this disease, current therapies aim to decrease the pain and slow further damage. The interleukin (IL)‐36 cytokine was little known for its role in rheumatoid arthritis; this research aimed to evaluate the serum IL36 levels in RA patients compared to healthy controls. This study included 80 patients with rheumatoid arthritis registered at the Rheumatology Clinic in Baghdad teaching hospital. The patients were divided into three groups based on the treatments received. Group 1 included patients treated with biological therapy (etanercept, adalimumab), Group2 patients with non-biological treatment (methotr

Background: Alopecia areata(AA) is a common autoimmune disease that causes hair loss without scarring. It occurs as a result of T-helper 1 (Th1) and Th17 cells attacking the anagen hair follicles. Genetic factors play a role in the occurrence of infection, which stimulates the production of pro and anti-inflammatory interleukins. Polymorphisms of IL-37 play a role in autoimmune diseases. However, IL37 single nucleotide polymorphisms(SNP) have not been identified in patients with AA. Therefore, this study aimed to reveal the IL37 gene SNP and its relationship to AA. Methods: Genotyping of IL-37 gene single nucleotide polymorphisms SNPs were detected using sequence-specific primer-polymerase chain reaction (SSP-PCR) method was done following