الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
Systemic lupus erythematous is a systemic autoimmune disorder that can affect any organ of the body as a result of immune system dysfunction, formation of autoantibodies and immune complexes, leading to chronic inflammation and potential damage to many organs. Cytokines e.g. IFNα, tumour necrosis factor and interleukins 6,17,2, aid in tissue injury and inflammation. Cytokines with their producing cells (macrophages, lymphocytes, leucocytes, and dendritic cells), are being investigated as potential therapeutic targets in SLE. For example, Interleukin-17 which is produced by CD4+ T helper 17 (TH17) cells. In SLE, the lung may be directly affected through aberrant systemic inflammatory response or indirectly affected as a complication of other organ dysfunction. In children affected with SLE, the incidence of pulmonary affection ranges from 5% to 67%. All parts of the pulmonary system can be involved including the pleura, lung parenchyma, airways, lung vasculature, and diaphragm. The most frequent manifestations are pleuritis, acute pneumonitis, chronic interstitial lung disease, alveolar hemorrhage, and diaphragmatic dysfunction. Many lupus patients that do not exhibit the clinical signs of respiratory involvement were reported to have abnormalities in pulmonary function tests. This can be considered a clear clue for subclinical affection which may be an early marker of progressive lung disease. In our study, we enrolled 42 pSLE patients (age 8–17.5 years, on treatment) and 45 age-matched healthy controls. Clinical and subclinical pulmonary affection was determined through careful history and examination in addition to pulmonary function tests and High-resolution CT chest. Serum IL-17 was determined by solid phase sandwich ELISA