الفهرس 
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Abstract
n
Systemic lupus erythematosus (SLE) is a chronic, immune-mediated
disease in which T and B cells cause systemic tissue injury. SLE is
characterized by the production of high levels of auto-antibodies against
nuclear antigens, resulting, at least in part, from a dysregulated T
lymphocyte response to autoantigens andthe immune system loses its ability
to tell the difference between foreign substances and its own cells and tissue.
The immune system then makes antibodies directed against “self”. This
debilitating disease affects each patient differently. The objective of this
study is to estimate the role of interferon gamma INFγin pediatric lupus
nephritis and to estimate the role ofT regulatory cells (Treg cells) .
For this purpose27 children with lupus nephritis were selected
fromMansoura University Children’s Hospital (MUCH) to be investigated.
The control group includes 11 healthy children.
The results shows
§ There were significant increase in the mean levels of ESR, ANA, CRP
and Anti-ds DNA in LN patients as compared to control group.
§ Hemoglobin and the frequency of peripheral blood INFγ %, CD8+
,
CD4+CD25+
, CD4+CD25+
FOXP3+
T cells (%),obtained from LN
patients were significantly decreased as compared to control group.
Summary & Conclusion
87
§ The frequencies of peripheral blood CD3+
, CD4+
, CD4+
/CD8+
T cells
(%) of LN patients were significantly elevated as compared with
control group.
§ The frequencies of urinary CD3+, CD4+ cells (%) were significantly
elevated as compared with control group. But the frequency of urinary
INFγ , CD8+
, were significantly reduced in control group as compared
with LN group.
In conclusion:The low expression of INFγ in T lymphocyte cells of LN
patients may be a good marker in prognosis and diagnosis of LN.The decreased
number of CD4+CD25+
and CD4+CD25+
FoxP3 T cells in the peripheral blood
of pediatrics patients with LN constitutes a defective Treg population and
contributes to the pathogenesis of LN. T cell subsets especially CD4+,
and CD8+
T cells could play a central and pivotal role in the pathophysilogy of LN.