MedDataX Logo

Serum IL 26 as a Marker of Disease Activity in SLE

NCT ID: NCT05161988

Last Updated: 2021-12-17

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

Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.

Recruitment Status

UNKNOWN

Total Enrollment

52 participants

Study Classification

OBSERVATIONAL

Study Start Date

2021-12-10

Study Completion Date

2025-05-01

Brief Summary

Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.

Assessment of serum Interleukin 26 level in SLE patients and compare it with healthy controls.

Association of serum interleukin 26 with SLE activity and severity.

Detailed Description

Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease characterized by diverse autoantibodies and varied clinical manifestations(mainly targeting the skin, kidneys, and brain). Autoantibodies directed against double-stranded (ds) DNA play a key role in the initiation and maintenance of inflammatory lesions in SLE(1).

Pathogenesis of SLE is mirrored by its complex aetiopathogenesis as genetic factors , environmental triggers (exposure to sunlight, drugs and infections, particularly with Epstein-Barr virus. . Causing secretion of inflammatory mediators , antibody and cytokines . But still pathological mechanisms of SLE are still not fully understood. (2) Immune system dysregulation such as incomplete clearance of apoptotic materials, hyperactivation of immune cells, overproduction of antibodies and abundant immune complex deposits are prominent in SLE (3) Clinical manifestations of SLE are Malar rash, Discoid rash ,Photosensitivity, Oral or nasopharyngeal ulcers, Pleurisy, Renal abnormalities, Immunologic abnormalities, Nonscarring alopecia, Synovitis, Hemolytic anemia, Leukopenia, Thrombocytopenia Proteinuria Seizures Psychosis Serositis and Arthritis (4) IL-26 is a 171-amino acid protein that belongs to the IL-10 family of cytokines, a family that includes IL-10, IL-19, IL-20, IL-22 and IL-24 . The IL-26 protein is encoded by the IL26 gene located on chromosome 12q15 between genes for interferon (IFN)-γ and IL-22 , and is conserved in several vertebrate species but not in mice and rats . The cytokine IL-26 was originally named AK155(5) IL-26 was initially identified as a pro-inflammatory cytokine , inducing the production of inflammatory cytokines by myeloid cells that are involved in the differentiation of naïve CD4+ T cells into Th17 cells (6) The involvement of IL 26 in numerous chronic auto inflammatory diseases and in two major pathogenic processes in SLE, namely the induction of IFN I and its production by Th 17 lymphocytes, makes the analysis of its role in SLE essential (7) Brilland et al., 2021 report that the levels of IL 26 are higher in SLE patients than healthy subjects and show a significant correlation with disease activity

Conditions

See the medical conditions and disease areas that this research is targeting or investigating.

SLE

Study Design

Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.

Observational Model Type

CASE_CONTROL

Study Time Perspective

PROSPECTIVE

Eligibility Criteria

Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.

Inclusion Criteria

* Adult SLE Patients who fulfilled the 2012 systemic lupus international collaborating clinics (SLICC) criteria

Exclusion Criteria

* Individuals with other autoimmune diseases (rheumatoid arthritis dermatomyositis, scleroderma, mixed connective tissue disease).
Minimum Eligible Age

15 Years

Maximum Eligible Age

80 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

Meet the organizations funding or collaborating on the study and learn about their roles.

Assiut University

OTHER

Sponsor Role lead

Responsible Party

Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.

Fatma alzahraa Mustafa Abdelbary Thabet

resident

Responsibility Role PRINCIPAL_INVESTIGATOR

Central Contacts

Reach out to these primary contacts for questions about participation or study logistics.

Fatma Al-zahraa M. Abdel-bary, resident

Role: CONTACT

Phone: 0201014363853

Email: [email protected]

Sherif H. Jalal, professor

Role: CONTACT

Phone: 0201222675000

Email: [email protected]

References

Explore related publications, articles, or registry entries linked to this study.

Knappe A, Hor S, Wittmann S, Fickenscher H. Induction of a novel cellular homolog of interleukin-10, AK155, by transformation of T lymphocytes with herpesvirus saimiri. J Virol. 2000 Apr;74(8):3881-7. doi: 10.1128/jvi.74.8.3881-3887.2000.

Reference Type BACKGROUND
PMID: 10729163 (View on PubMed)

Maidhof W, Hilas O. Lupus: an overview of the disease and management options. P T. 2012 Apr;37(4):240-9.

Reference Type BACKGROUND
PMID: 22593636 (View on PubMed)

Manson JJ, Rahman A. Systemic lupus erythematosus. Orphanet J Rare Dis. 2006 Mar 27;1:6. doi: 10.1186/1750-1172-1-6.

Reference Type BACKGROUND
PMID: 16722594 (View on PubMed)

Roberts AL, Rizzolo D. Systemic lupus erythematosus: an update on treat-to-target. JAAPA. 2015 Sep;28(9):22-8. doi: 10.1097/01.JAA.0000470432.76823.93.

Reference Type BACKGROUND
PMID: 26251978 (View on PubMed)

Other Identifiers

Review additional registry numbers or institutional identifiers associated with this trial.

SLE IL26

Identifier Type: -

Identifier Source: org_study_id