Author/Authors :
Rastin, Maryam Immunology Research Center - Bu-Ali Research Institute - Faculty of Medicine - Mashhad University of Medical Sciences, Mashhad, Iran , Soltani, Samaneh Immunology Research Center - Bu-Ali Research Institute - Faculty of Medicine - Mashhad University of Medical Sciences, Mashhad, Iran , Nazemian, Fatemeh Department of Internal Medicine - Imam Reza Hospital - Mashhad University of Medical Sciences, Mashhad, Iran , Sahebari, Maryam Rheumatic Diseases Research Center - Ghaem Hospital - Internal Medicine Section, Mashhad University of Medical Sciences, Mashhad, Iran , Mirfeizi, Seiede Zahra Rheumatic Diseases Research Center - Imam Reza Hospital - Internal Medicine Section - Mashhad University of Medical Sciences, Mashhad, Iran , Tabasi, Nafiseh Immunology Research Center - Bu-Ali Research Institute - Faculty of Medicine - Mashhad University of Medical Sciences, Mashhad, Iran , Mahmoudi, Mahmoud Immunology Research Center - Bu-Ali Research Institute - Faculty of Medicine - Mashhad University of Medical Sciences, Mashhad, Iran
Abstract :
Introduction. Lupus nephritis is a serious organ involvement
with unknown etiology, and glomerulonephritis class IV is one of
the most severe forms of the disease which correlates with poor
prognosis and death. Immunological abnormalities are implicated
in the expression of lupus nephritis. In this study, we examined
some T helper 17 and regulatory T-related cytokines and molecules
in systemic lupus erythematosus patients with glomerulonephritis
class IV.
Materials and Methods. The study group comprised of 20
glomerulonephritis class IV SLE patients and 20 sex- and age-matched
SLE patients without kidney involvement as control group. Blood
samples was collected from each participant, lymphocytes were
isolated, and RNA was extracted from lymphocytes. Then cDNA
was synthesized using reverse transcription enzyme‚ and finally
using specific primers and probes, the expression levels of forkhead
box P3 (Foxp3), transforming growth factor (TGF)-β, interferon
(IFN)-γ‚ interleukin (IL)-6, and IL-17 genes were analyzed by realtime
polymerase chain reaction based on the TaqMan method.
Results. The expression levels of IL-6‚ IL-17, IFN-γ, and Foxp3 genes
were significantly higher in SLE patients with glomerulonephritis
class IV than those with non-nephritis SLE. However, the expression
of TGF-β was not significantly different between the SLE patients
with and without glomerulonephritis class IV involvement.
Conclusions. According to our results, it seems that in class IV
glomerulonephritis patients, increased Foxp3-producing regulatory
T cells has an imperfect capacity to control the pathogenic IL-17-
and IFN-g-producing cells.
Keywords :
diffuse proliferative glomerulonephritis , regulatory T lymphocyte , T helper 17 lymphocyte , systemic lupus erythematous