Assessment of FOXP3 Gene Polymorphisms and Serum Interleukin 10 in Patients With ITP
NCT ID: NCT05410249
Last Updated: 2023-04-12
Study Results
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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UNKNOWN
130 participants
OBSERVATIONAL
2022-06-10
2023-09-30
Brief Summary
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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 \[7, 8\].
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Detailed Description
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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.
Conditions
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Study Design
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CASE_CONTROL
CROSS_SECTIONAL
Study Groups
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Patients with primary ITP
Patients with primary ITP and aged 18 and older will be included in the study. Patients under 18 and those with proven secondary ITP \[as cases initiated by or associated with infections due to human immunodeficiency virus (HIV-associated), hepatitis B virus, or hepatitis C virus-associated secondary ITP\] will be excluded. Moreover, patients with accompanying autoimmune disorders such as systemic lupus erythematosus (SLE) and patients of malignancies were excluded.
Serum IL10 By ELISA
measurement Of IL10 by ELISA
SNP -3279 A/C of FOXP3
Genotyping of -6054 del/ATT will be performed using the real-time polymerase chain reaction.
SNP-924 A/G Of FOXP3
Genotyping of -924 A/G polymorphisms was performed using the real-time polymerase chain reaction.
normal individuals
The control group will be age-matched and sex-matched normal healthy volunteers.
Serum IL10 By ELISA
measurement Of IL10 by ELISA
SNP -3279 A/C of FOXP3
Genotyping of -6054 del/ATT will be performed using the real-time polymerase chain reaction.
SNP-924 A/G Of FOXP3
Genotyping of -924 A/G polymorphisms was performed using the real-time polymerase chain reaction.
Interventions
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Serum IL10 By ELISA
measurement Of IL10 by ELISA
SNP -3279 A/C of FOXP3
Genotyping of -6054 del/ATT will be performed using the real-time polymerase chain reaction.
SNP-924 A/G Of FOXP3
Genotyping of -924 A/G polymorphisms was performed using the real-time polymerase chain reaction.
Eligibility Criteria
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Inclusion Criteria
Exclusion Criteria
2. Patients with accompanying autoimmune disorders such as systemic lupus erythematosus (SLE).
3. Patients with malignancies will be excluded
18 Years
ALL
Yes
Sponsors
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Sohag University
OTHER
Responsible Party
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Noha Saber Shafik
lecturer of medical microbiology and immunology, faculty of medicine
Principal Investigators
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Asmaa A Abdelbaset, lecturer
Role: PRINCIPAL_INVESTIGATOR
faculty of medicine, Sohag university
Locations
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Faculty Of Medicine
Sohag, , Egypt
Countries
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Central Contacts
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Facility Contacts
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References
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Ballantine LE, Ong J, Midgley A, Watson L, Flanagan BF, Beresford MW. The pro-inflammatory potential of T cells in juvenile-onset systemic lupus erythematosus. Pediatr Rheumatol Online J. 2014 Jan 16;12:4. doi: 10.1186/1546-0096-12-4.
Other Identifiers
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Soh-Med-22-4-34
Identifier Type: -
Identifier Source: org_study_id
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