Background and Aim of Study:
Interleukin-10 (IL-10) is an important immunoregulatory cytokine. Many studies suggesting that a genetically controlled high innate IL-10 production
may predispose to systemic lupus erythematosis (SLE) development. The aim of our study was to investigate IL-10 gene -592 A/C polymorphism
in Egyptian patients with SLE and lupus nephritis (LN) and evaluate the role of lL-10 in the pathogenesis and clinical/pathological diversity of LN.
Patients and Methods:
The study was conducted on 64 patients with SLE. Patients were divided into LN group [group 1; 42 patients with mean age 29.63 ± 8.91 yrs]
and non nephritis group [group 2; 22 patients with mean age 31.81 ± 0.20yrs]. The IL-10 gene polymorphism of –592 A/C was determined by
polymerase chain reaction and restriction fragment length polymorphism in LN and non LN patients.IL-10 was determined by ELISA.
Frequencies of the genotypes were compared between LN and non LN patients and among LN patients with different pathological classes.
The clinical and pathological characteristics of the patients with different genotypes were also analyzed. Patients of group1 were followed
up for 6 months and 24 hrs urinary protein, Anti-ds DNA and IL-10 were measured after 6 months for group 1 to determine responders therapy.
Results:
There was significant increase in serum level of IL-10 (p=0.0161) in (group 1) compared to (group 2) and significant positive correlation between serum
IL-10 and SLEDAI (r=0.576,p=0.032) in group1.There was no significant differences in the distribution of the IL-10 -592 genotypes, or the alleles
frequencies between (group 1) and (group 2).There was no significant difference between AC/CC and AA genotypes with disease activity(SLEDAI),
proteinuria, hematuria, anti-ds DNA and IL-10 in (group 1).There was no significant difference in the distribution of AC and CC genotypes among
different LN classes. There was significant decrease in serum IL-10 (p=0.0039), anti- ds DNA(P=0004), 24 hrs urinary protein (p=0.042), and SLEDAI
(p=0047) after 6 months of therapy.
Conclusion:
The IL-10 gene -592 A/C polymorphism not associated with LN susceptibility or serum IL-10 levels. IL-10 gene polymorphism may or may not play
a role in the clinical and pathological diversity of LN and multiple factors are most likely responsible. IL-10 gene polymorphism may act indirectly
through linkages with some other genes that play a role in the pathological lesions in lupus nephritis.
Author(s): Emad Abdallah, Emam Waked, Malak Nabil, and Omnya El-Bendary