INTRODUCTIONGiardia is one of the most prevalent intestinal flagellated protozoans that causes diarrhea in both children and adults [1] . Giardiasis has a worldwide distribution with a higher incidence rate in developing countries than developed ones and a higher infection rate in children than adults [2] . In certain localities in Egypt, the prevalence of giardiasis is up to 30.2%, a fact that makes Egypt a hyper-endemic region according to the World Health Organization (WHO) criteria [3] . Giardiasis is transmitted via the fecal-oral route through direct or indirect ingestion of cysts. Symptoms of infection vary from asymptomatic to acute steatorrhea, nausea, epigastric pain, and weight loss [1] . Post-infection complications may arise after Giardia elimination in the form of stunting, failure to thrive, chronic fatigue syndrome, irritable bowel syndrome, allergies and arthritis [4] .The host defense against giardiasis includes both innate and adaptive immune responses that act in synchrony to control the infection. Innate immune mechanisms are the first line of defense against

Background This study aimed to describe the prevalence of the various clinical features and severity of juvenile systemic lupus erythematosus (jSLE) and to assess predictors of AQP4-Ab positivity in jSLE. In addition, we assessed the relationship of AQP4-Abs with neuropsychiatric disorders and white matter lesions in jSLE. Method For 90 patients with jSLE, demographic data, clinical manifestations, and treatments received were recorded, and all of the patients were underwent clinical examinations, including assessments for the neurological manifestations of jSLE and neuropsychiatric disorders; Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score evaluations; laboratory investigations, including serum AQP4-Ab assays; and 1.5 Tesla brain MRI. Echocardiography and renal biopsy were performed for the indicated patients. Result Fifty-six patients (62.2%) tested positive for AQP4-Abs. These patients were more likely to have higher disease activity scores (p < 0.001); discoid lesions (p = 0.039); neurological disorders (p = 0.001), mainly psychosis and seizures (p = 0.009 and p = 0.032, respectively); renal and cardiac involvement (p = 0.004 and p = 0.013, respectively); lower C3 levels (p = 0.006); white matter hyperintensities (p = 0.008); and white matter atrophy (p = 0.03) than patients who were negative for AQP4-Abs. Furthermore, AQP4-Ab-positive patients were more likely to have received cyclophosphamide (p = 0.028), antiepileptic drugs (p = 0.032) and plasma exchange therapy (p = 0.049). Conclusion jSLE patients with higher severity scores, neurological disorders, or white matter lesions could develop antibodies against AQP4. We recommend more studies for systematic screening of AQP4-Ab positivity in jSLE patients to confirm its relationship with neurological disorders.