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347418

Regulatory T cells and Disease damage in systemic lupus erythematosus

Article

Last updated: 25 Dec 2024

Subjects

-

Tags

Diagnostic

Abstract

Background: Systemic lupus erythematosus (SLE) is an inflammatory, multisystem autoimmune disorder characterized by a multitude of autoantibody production and immune complex deposition, causing damage to multiple organs. Dysfunction of T and B cells are believed to be essential factors involved in the disease pathogenesis. A lack or defect in Treg function is generally considered to support SLE pathology. Aim: Our study aimed to assess CD4+ CD25+ Foxp3+ T regulatory cellspercentage in SLE patients and its relation to activity index and damage index. Methods: 50 SLE patients and 50 controls were enrolled in the study. Flowcytometric determination of peripheral Treg cells was done for all participants. Disease activity was measured using the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI -2k) while disease damage was measured using the Systemic Lupus international collaborating clinics American College of Rheumatology Damage Index (SLICC/ACR DI) which were correlated with T regulatory cells percentage in cases only. Results: Treg cells percentage was significantly decreased in SLE patients when compared with healthy controls (0.1% to 0.9% vs 0.9% to 2.1%) (p< 0.001).As regard SLEDAI -2k, there was a negative correlation between Treg cells percentile and SLEDAI-2k (p< 0.001). Also there was a negative correlation between Treg cells percentile and damage index (SLICC/ACR DI) (p< 0.001). Regarding the correlation between SLEDAI -2K with damage index (SLICC/ACR DI), we found highly significant positive correlation (p< 0.001). Conclusion: Our study showed that Tregs percentile were significantly lower in SLE patients when compared with healthy controls.Treg cells % have significant association with SLEDAI and damage index suggesting the value of Tregs as activity biomarker and marker of damage. 

DOI

10.21608/ejmr.2023.188321.1326

Keywords

Systemic lupus erythematosus, T Regulatory cells, Forkhead box p3, damage index

Authors

First Name

Lamiaa

Last Name

Abd elsalam

MiddleName

Salah Eldin

Affiliation

Clinical Pathology department, Faculty of Medicine, Helwan University, Cairo, Egypt.

Email

lamia.salah@med.helwan.edu.eg

City

Cairo

Orcid

0000-0001-8456-3350

First Name

Mostafa

Last Name

kamal

MiddleName

-

Affiliation

Clinical Pathology department, Faculty of Medicine, Helwan University, Cairo, Egypt.

Email

mostafa.kamal@med.helwan.edu.eg

City

-

Orcid

-

First Name

Hala

Last Name

Gabr

MiddleName

-

Affiliation

Clinical Pathology department, Faculty of Medicine, Cairo University, Cairo, Egypt.

Email

halagabr@kasralainy.edu.eg

City

-

Orcid

-

First Name

Somaya

Last Name

Anwar

MiddleName

-

Affiliation

Rheumatology and Rehabilitation department, Faculty of Medicine, Cairo University, Cairo, Egypt.

Email

somaya.anwar@kasralainy.edu.eg

City

-

Orcid

-

First Name

Samah

Last Name

Bastawy

MiddleName

-

Affiliation

Clinical Pathology department, Faculty of Medicine, Helwan University, Cairo, Egypt.

Email

bastawy.samah@med.helwan.edu.eg

City

-

Orcid

-

First Name

Manar

Last Name

Youssef

MiddleName

Ibrahim

Affiliation

Clinical Pathology department, Faculty of Medicine, Helwan University, Cairo, Egypt.

Email

manar.ibrahim@med.helwan.edu.eg

City

-

Orcid

0000-0002-3957-8454

Volume

5

Article Issue

2

Related Issue

46702

Issue Date

2024-04-01

Receive Date

2023-01-21

Publish Date

2024-04-01

Page Start

46

Page End

60

Print ISSN

2682-4396

Online ISSN

2682-440X

Link

https://ejmr.journals.ekb.eg/article_347418.html

Detail API

https://ejmr.journals.ekb.eg/service?article_code=347418

Order

347,418

Type

Original Article

Type Code

1,224

Publication Type

Journal

Publication Title

Egyptian Journal of Medical Research

Publication Link

https://ejmr.journals.ekb.eg/

MainTitle

Regulatory T cells and Disease damage in systemic lupus erythematosus

Details

Type

Article

Created At

25 Dec 2024