الفهرس 
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Abstract
The immune system in our body’s is designed to protect us from infections . that caused by any invaders such as bacteria, parasites and viruses by causing inflammation that act as defense against the pathogen infection and damage of tissues, However, when immune system cannot distinguish between self (body cells) and non-self (any invader cells) antigens begin to attack the cells, tissues and organs of the body this result is called the autoimmune diseases, such as rheumatoid arthritis RA, systemic lupus erythematous SLE and other autoimmune diseases.
Human autoimmune diseases ADs affecting more than 5% of the population worldwide, there are over 81 types of autoimmune diseases . The development of ADs depends on combination between environmental and genetic factors.
Treg cells and Th17 cells have the same signaling pathway that is mediated by TGF-β, in which in the presence of interleukin IL-6 and IL-21 together with TGF-β the naïve CD4+ T cells differentiate into Th17 cells; while in the absence of IL-6 and IL-21 TGF-β drives differentiation into Treg cells.
Th17 cells secret proinflammatory cytokines which provide the recruitment of neutrophils, and provide inflammation at the infection site.
On the other hand Treg cells produce anti-inflammatory cytokines include those suppressing activity of different types of immune cells and inhibit the immune responses.
Thus, both Treg cells and Th17 play opposite roles during inflammatory and immune responses, in which Th17 cells cause, whereas Treg cells inhibit, autoimmunity. Thus, the reciprocal generation of Th17 and Treg cells is critically important.
The aim of our study was study of the balance between th17 and Treg cells in systemic lupus erythematosus (SLE) patients and Rheumatoid arthritis (RA) patients by estimating Th17 and Treg by flow cytometery and evaluate how balance between Th17 and Treg related to diseases (SLE, RA) activity.
The patients were divided into four groups .
group (1) 80 SLE patients who were divided into: 40 adult SLE patients (18 had active SLE and 22 inactive SLE patients) and 40 juvenile SLE patients (15 had active SLE and 25 had inactive SLE patients).
group (2) 80 healthy normal 40 adults and 40 children matched in age, gender, and geographical location, were used as the control group for SLE patients both adult and juvenile.
group 1 and group 2 were subjected to history taking, clinical examination and laboratory investigations including CBC, serum creatinine, C3, C4, ANA, Anti ds-DNA and protein / creatinine ratio in urine and count ,assessment of Th17 cells and Treg cells by flow cytometry.
group (3) 80 Rheumatoid Arthritis (RA) patients, divided into 40 adults and 40 juvenile ( 22 of them had inactive disease and 18 had active disease).
group (4) 80 healthy normal 40 adults and 40 children matched in age, gender, and geographical location, were used as the control group for RA patients both adult and juvenile.
group 3 and group 4 were subjected to history taking, clinical examination and laboratory investigations including -complete blood count, ESR , CRP , RF , ANTI-CCP , ANA and count, assessment of TH17and T/reg by flow cytometry
Our study showed a significant difference in Anti-ds-DNA, and protein/creatinine ratio between adults, juvenile groups and controls. Our study showed a significant increase in absolute number and percentage of Th17 cells and a significant decrease in absolute number and percentage of Treg cells with increased Th17/Treg ratio in active adult and juvenile SLE when compared with inactive SLE and healthy control. The results showed that between inactive SLE and healthy control, there was no significant difference
The study also indicated a significant correlation between Th17/Treg ratio and parameters of the SLE disease activity. There was also a positive correlation with ANA, ANTI-DNA, protein/creatinine ratio and SLEDAI with negative correlation with C3 and C4.
In patients with adult and juvenile RA. The results revealed that the absolute count of the CD4+ T lymphocyte subpopulation was significantly higher in both the adult and juvenile RA groups compared to the controls. Additionally, there were significant increases in the absolute number and the percentage of Th17 cells and significant decreases in the absolute number and the percentage of Treg cells, with the consequent increase in the Th17/Treg ratio, in the patients with active adult and juvenile RA compared with those with inactive adult and juvenile RA and the healthy controls. Finally, there were no significant differences in these parameters between the patients with inactive RA and the healthy controls (p value 0.228,0.643,0.755)
In the present study, we also observed increased frequencies of peripheral Th17 cells in the patients with active RA compared to those with inactive RA among the patients with adult RA;Th17 cell frequencies were positively correlated with DAS28 ,ESR ,ANA , CRP ,anti-CCP and RF.
We also found a significant decrease in the percentage of Treg cells and a significant increase in the Th17/Treg ratio in the adult patients with active RA compared to those with inactive disease (P <0.001). Furthermore, there was a significant negative correlation between the Treg cells percentage and DAS28, ESR, CRP, and anti CCP, which might be associated with an increase in RA severity.
In the juvenile group included in the current study, we observed that percentages of peripheral Th17 cells were higher in those with active RA than those with inactive RA and that the frequencies were positively correlated with all disease parameters except disease duration. There was a significant decrease in Treg cells and a significant increase in the Th17/Treg ratio in those with active juvenile RA compared with the inactive juvenile RA group (P < 0.001), as well as significant negative correlations between Treg cells and DAS28, ESR, CRP, anti-CCP, and ANA.