Thrombocytopenia
Conditions
Keywords
polymorphism, FOXp3, serum IL10
Brief summary
Immune thrombocytopenia (ITP) is an autoimmune condition characterized by increased platelet destruction and suppression of production resulting in isolated thrombocytopenia. The exact etiology of ITP is unknown; however, multiple disease mechanisms exist and are mostly related to immune dysregulation \[1\]. Many studies in recent years have indicated that regulatory T cells (Tregs) play a critical role in the maintenance of immunological tolerance, and they have been reported to be defective in ITP patients, either numerically or functionally. \[2-6\]. They inhibit the activation and proliferation of effector T cells by the secretion of cytokines such as interleukin-10 (IL-10) and tumor growth factor-β (TGF-β) and by cell-to-cell interaction \[7, 8\].
Detailed description
The suppressor function of Treg cells may be compromised if the FOXP3 gene is deficient. FOXP3 gene single nucleotide polymorphisms (SNPs), particularly regulatory polymorphisms in the promoter regions, have been linked to a variety of autoimmune diseases, including allergic rhinitis, type I diabetes (TID), systemic lupus erythematosus (SLE), multiple sclerosis (MS), and autoimmune thyroid diseases (AITD), according to numerous studies \[9-13\]. The FOXP3 gene's promoter region, which is crucial in gene expression and Treg activation, may contain important SNPs. The 6054 del/ATT and 924A \> G SNPs are functionally well-defined and are distinguished by the relevance of studies on them among these SNPs. \[14, 15\]. The Interleukin 10 (IL-10) cytokine is required for regulating immune functions by promoting the widespread suppression of immune responses through its pleiotropic effects. IL-10 secretion from CD4+CD25+FoxP3+ regulatory cells (Tregs), macrophages and other leukocytes followed by subsequent binding to IL-10 receptors on macrophages and dendritic cells (DCs) has been linked to reduced antigen presentation and increased T-cell anergy \[16\]. The relationship between the two FOXP3 polymorphisms and ITP has not been well elucidated, hence the objective of this study is to explore if these functional polymorphisms are linked to ITP, how they correlate to IL-10 levels, and how they relate to other features of clinical presentation in adult patients with ITP.
Interventions
DIAGNOSTIC_TESTSerum IL10 By ELISA
measurement Of IL10 by ELISA
DIAGNOSTIC_TESTSNP -3279 A/C of FOXP3
Genotyping of -6054 del/ATT will be performed using the real-time polymerase chain reaction.
DIAGNOSTIC_TESTSNP-924 A/G Of FOXP3
Genotyping of -924 A/G polymorphisms was performed using the real-time polymerase chain reaction.
Sponsors
Sohag University
Study design
Observational model
CASE_CONTROL
Time perspective
CROSS_SECTIONAL
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes
Inclusion criteria
* Patients with primary ITP and aged 18 and older will be included in the study.
Exclusion criteria
1. Patients under 18 and those with proven secondary ITP \[as cases initiated by or associated with infections due to human immunodeficiency virus (HIV-associated), hepatitis B virus, or hepatitis C virus-associated secondary ITP\] . 2. Patients with accompanying autoimmune disorders such as systemic lupus erythematosus (SLE). 3. Patients with malignancies will be excluded
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| SNP effect in FOXP3 gene in patients ITP | 26 May to August 2022 | different genotypes of FOXP3 in patients with ITP will be determined using real time PCR |
| Association of serum IL-10 levels in both groups( patients with ITP and normal control) | 26 May to August 2022 | measurement of serum IL10 in patients with ITP and normal controls using ELISA |
| Association of SNP in FOXP3 gene and the clinical presentation in adult patients with ITP | 26 May to August 2022 | evaluation and statistical analysis of effect of SNP in FOXP3 in the clinical picture in adult patients with ITP |
Countries
Egypt
Contacts
Primary ContactNoha S Shafik, lecturer
Backup ContactMahmoud G Mahmoud, lecturer
Outcome results
None listed