Assessment of FOXP3 Gene Polymorphisms and Serum Interleukin 10 in Patients With ITP

NCT ID: NCT05410249

Last Updated: 2023-04-12

Study Results

Results pending

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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Recruitment Status

UNKNOWN

Total Enrollment

130 participants

Study Classification

OBSERVATIONAL

Study Start Date

2022-06-10

Study Completion Date

2023-09-30

Brief Summary

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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

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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.

Conditions

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Thrombocytopenia

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

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

Intervention Type DIAGNOSTIC_TEST

measurement Of IL10 by ELISA

SNP -3279 A/C of FOXP3

Intervention Type DIAGNOSTIC_TEST

Genotyping of -6054 del/ATT will be performed using the real-time polymerase chain reaction.

SNP-924 A/G Of FOXP3

Intervention Type DIAGNOSTIC_TEST

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

Intervention Type DIAGNOSTIC_TEST

measurement Of IL10 by ELISA

SNP -3279 A/C of FOXP3

Intervention Type DIAGNOSTIC_TEST

Genotyping of -6054 del/ATT will be performed using the real-time polymerase chain reaction.

SNP-924 A/G Of FOXP3

Intervention Type DIAGNOSTIC_TEST

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

Intervention Type DIAGNOSTIC_TEST

SNP -3279 A/C of FOXP3

Genotyping of -6054 del/ATT will be performed using the real-time polymerase chain reaction.

Intervention Type DIAGNOSTIC_TEST

SNP-924 A/G Of FOXP3

Genotyping of -924 A/G polymorphisms was performed using the real-time polymerase chain reaction.

Intervention Type DIAGNOSTIC_TEST

Eligibility Criteria

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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
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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Sohag University

OTHER

Sponsor Role lead

Responsible Party

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Noha Saber Shafik

lecturer of medical microbiology and immunology, faculty of medicine

Responsibility Role PRINCIPAL_INVESTIGATOR

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

Site Status RECRUITING

Countries

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Egypt

Central Contacts

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Noha S Shafik, lecturer

Role: CONTACT

01067261504

Mahmoud G Mahmoud, lecturer

Role: CONTACT

Facility Contacts

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Noha S Shafik, lecturer

Role: primary

00201067261504

Mahmoud G Mahmoud, Lecturer

Role: backup

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.

Reference Type BACKGROUND
PMID: 24433387 (View on PubMed)

Other Identifiers

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Soh-Med-22-4-34

Identifier Type: -

Identifier Source: org_study_id

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