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RecruitingNCT06683690Updated Nov 12, 2024

TGF β 1 Expression Related Gene Polymorphism

An observational study in Leprosy, sponsored by Aswan University. Recruiting at 1 site in Egypt. Open to participants aged 18 Years to 50 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2024-11-12.

Sponsored by Aswan University · Observational

From the registry’s dates

  • Primary completion was expected by Jul 2025, 1 year 4 months ago, but the record still lists the study as recruiting.
  • Started Jul 2024; still recruiting 2 years 4 months later.
Study type
Observational
Model
Case-control
Time perspective
Prospective
Enrollment
60
Ages
18 Years to 50 Years
Sex
All
01

Study summary

Leprosy is one of the oldest human infectious diseases. It is a chronic infectious contagious, granulomatous disease caused by intracellular bacillus.

Mycobacterium leprae, this chronic granulomatous disease presents symptoms that mainly affected the skin, the nervous system and the reticuloendothelial system, also other systems can be affected, such as the upper respiratory tract, bones and joints, eyes and adrenal glands.

TGF- β is a pleiotropic cytokine that employs several functions on different types of cells. The effect of other cytokines may finally modulate the cellular response in the presence of TGF- β, causing a different effect depending on the activation state of the cell involved. In addition, TGF- β promotes the healing of inflamed tissue through the stimulation and regulation of extracellular matrix by fibroblasts, in addition to inducing the proliferation of endothelial cells required for angiogenesis. Thus, TGF- β is able to regulate the expression of other growth factors, increasing their level of activity.

Read the detailed description

The spectrum of clinical and histopathological manifestations reflects the immune response elicited by the microorganism in the host leprosy classified into polar groups:

Lepromatous (LL) and Tuberculoid (TT); and borderline spectrum: Borderline Tuberculoid (BT), Borderline Borderline (BB) and Borderline Lepromatous (BL). This classification, proposed by Ridley and Jopling This classification widely used in clinical, immunological, microbiological, and histopathological aspects. While The World Health Organization classifies leprosy clinically as multibacillary and paucibacillary, according to the number of skin lesions and nerve involvement.

In the tuberculoid form of leprosy (paucibacillary), the individual manifests an intense cell-mediated immune response that prevents proliferation of the bacillus, whereas the cell-mediated immune response is compromised in the lepromatous form (multibacillary) contributing to multiplication of the bacillus. In the intermediate forms,the patients exhibit characteristics that vary between the two types.

Leprosy is measured the first disease to be categorized based on the host's immune response. The clinical symptoms of leprosy vary from one patient to another based on the spectrum of disease but more importantly on the type of host's immune response to the bacteria. Both innate and acquired immune responses have been associated with leprosy, but the disease is typically described by the side of a Th1/Th2 response.

Patients with TT are decided by a relevant T-cell immune response, including interleukin-2 (IL-2), IL-4, IL-6, IL-10, interferon-γ (IFN-γ), tumor necrosis factor (TNF), and IL-17 and lymphotoxin, marked by some neural or cutaneous lesions with a few or no bacilli.

Infected macrophages are activated by IFN- γ and clonal expansion of T cells is induced by IL-2 which, in turn, leads to an increase in IFN- γ production. Tumor necrosis factor alpha (TNF- α) also plays a role in the Th1 response. This cytokine contributes to the maintenance of this pattern and acts in synchronism with IFN- γ in the activation of infected macrphages, developing a significant mechanism for the maintenance of the cell-mediated immune response.

In contrast, patients with LL show a superior humoral immune response, characterized by multiple lesions, elevated bacterial load, and reduced lymphocyte production develop a Th2 immune response characterized by intense production of transforming growth factor beta (TGF- β), IL-4, IL-5 and IL-10.

These cytokines induce an incompetent immune response characterized by the high production of antibodies that apply no protective effect against the bacterium.

IL-4 exerts an immunosuppressive effect that leads to an increase in bacterial proliferation and inhibits the proliferation of T cells and monocytes, the expression of CD14 on monocytes and the production of TNF- α, in addition to blocking the synthesis of nitric oxide which is essential for the destruction of intracellular microorganisms. In the 21st century, studies using modern genetic methods such as candidate gene association studies (CGASs) and genome wide association studies (GWASs) have gradually confirmed that the host genetic background play important role in the development of leprosy, and many leprosyassociated variants or genes have been reported. Most leprosy-associated genes are immune related, which is consistent with the finding that leprosy is caused by infection with pathogen.

TGF β1 plays roles in the suppression of T cell responses, inhibiting both IFN γ and IL-2 expression, and has the ability to inhibit the lytic activity of macrophages by suppressing the production of intermediate oxygen-reactive and nitrogen-reactive factors, leading to the progression of infection. So, the production of TGF β1 by macrophages in LL and BL skin lesions, probably as part of the M. leprae evasion mechanism.

Experimental studies on these pathogenic agents have demonstrated a role of TGF- β1 as a suppressor of macrophages. TGF-β1 production in lepromatous patients, which contributes to the anti-inflammatory situation and bacillary persistence observed

02

Conditions studied

  • Leprosy

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03

In context

Leprosy

52 studies on the registry are indexed under Leprosy; 13 are open to participants now.

Browse Leprosy studies →

Lead sponsor

Aswan University is the lead sponsor of 47 studies on the registry; 21 are open to participants now.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
18 Years to 50 Years
Sexes eligible
All
Accepts healthy volunteers
Yes
Sampling method
Probability sample

Study population

The study will include (30) leprosy patients and (30) normal control , selected from the outpatient clinic of the Dermatology, Venereology, and Andrology Department, at Aswan University Hospital.

Go through the criteria one by one — yes, no or not sure — and take the list to your doctor or the study team. Kept in this browser only.

Inclusion criteria

  • Patients of both sexes with leprosy.
  • Age above 18 years.
  • patients on multidrug therapy of leprosy.

Exclusion criteria

Exclusion Criteria:

  • Patients with other dermatological disease.
  • Patients with leprosy reaction.
  • Pregnancy and lactation.
  • Patients with disease.
Terms in these criteria, in plain language(1)

Underlined terms in the criteria open these too. Explained by clinicaltrials.gg, not part of the registry record. The study team decides who can take part.

Autoimmune disease

A condition in which the immune system attacks the body’s own tissues, such as rheumatoid arthritis, lupus, psoriasis, type 1 diabetes or inflammatory bowel disease.

Immunotherapy studies often leave out active autoimmune disease, and some name exceptions, such as thyroid disease on replacement hormone. Check the exceptions this study lists.

05

Study design

Observational model
Case-control
Time perspective
Prospective
Enrollment
60 participants (estimated)
Patient registry
No

Groups and cohorts

  • Group A: Leprosy Patients

    About 30 patients affected with Leorosy

    Procedure: Measurement of TGF- β1 in leprosy patients

  • Group B: Healthy People

    About 30 Healthy participants

    Procedure: Measurement of TGF- β1 in leprosy patients

Interventions

  • ProcedureMeasurement of TGF- β1 in leprosy patients

    Study TGF- β1gene polymorphism in leprosy patients, and Correlate their results with different types of leprosy before and after treatment.

06

What researchers measure

Primary outcomes

  1. Detection of serum TGF β1

    Detection of serum TGF β1 in leprosy patients and Correlate them with different clinical types of leprosy by taking Blood Samples will be collected from the patients to detect TGF β1gene by DNA extraction and SNP genotyping - Genomic DNA will be extracted from peripheral blood samples, then the polymorphism of the TGF β1 gene marker will be selected, The Blood Samples will be collected from the patients before and after treatment with multidrug therapy of leprosy to detect the level of TGF β1 concentrations by ELISA.

    Time frame: One Year

07

Study locations

1 of 1 sites recruiting
08

References and documents

Individual participant data

Plan to share: Undecided

No publications or documents are linked to this record.

09

Timeline

Tracking since Sep 25, 2026
ElapsedEstimatedEstimated, not yet reached

Started Jul 2024 (actual). Primary completion is estimated for Jul 2025, 11 months after the start.

How these figures are worked out, and which studies are left out of them.

Registered
Nov 8, 2024
First posted
Nov 12, 2024
StartActual
Jul 10, 2024
Primary completionEst.
Jul 5, 2025
CompletionEst.
Jul 10, 2025
Last update
Nov 12, 2024
What these dates mean
Start.
When the first participant enrolled; while estimated, when the study expects to open to recruitment.
Primary completion.
When the last participant was examined or treated to collect data for the study's main question, its primary outcome. A study that stopped early gives the date its data collection stopped.
Completion.
When the last participant's last visit took place, for every outcome, secondary ones and side effects included: the end of the study. Often later than primary completion, sometimes the same day.
Actual and Est.
Actual means the registry says the date has happened. Est. (estimated) is a date the sponsor plans or expects. It can still move, and the sponsor is expected to change it to actual once it has passed.
No changes since tracking began. The registry record was last updated on Nov 12, 2024, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
10

Registry details

Key details

Study ID
NCT06683690
Lead sponsor
Aswan University
Responsible party
Gehad Adel Abd El-Sabour Mohammed (Specialist of Dermatology, Aswan University) — Principal investigator
First posted
Nov 12, 2024
Start date
Jul 10, 2024
Primary completion
Jul 5, 2025 (estimated)
Completion
Jul 10, 2025 (estimated)
Last update
Nov 12, 2024

Study contacts

Gehad Adel Abd El-Sabour, M.D
Contact
gehada022@gmail.com
+201000415446
Moustafa Adam Ali El Taieb, Professor
study chair · Dermatology, Venereology and Andrology. Faculty of Medicine, Aswan University
Abdallah Mahmoud Abdallah, Professor
study director · Biochemistry and Molecular Biology. Faculty of Medicine, Aswan University

Oversight

Data monitoring committee
Yes
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

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