Publications by authors named "S El Azbaoui"

Setting: The utility of interferon-gamma release assays (IGRAs), such as the QuantiFERON-TB Gold In-Tube (QFT-GIT) test, in diagnosing active tuberculosis (TB) in children is unclear and depends on the epidemiological setting.

Objective: To evaluate the performance of QFT-GIT for TB diagnosis in children living in Morocco, an intermediate TB incidence country with high bacille Calmette-Gurin vaccination coverage.

Design: We prospectively recruited 109 Moroccan children hospitalised for clinically suspected TB, all of whom were tested using QFT-GIT.

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Setting: Tuberculosis spondylodiscitis (TS), or Pott's disease, an extra-pulmonary form of tuberculosis (TB), is rare and difficult to diagnose in children. Some cases of severe TB in children were recently explained by inborn errors of immunity affecting the interleukin-12/interferon-gamma (IL-12/IFN-γ) axis.

Objective: To analyse clinical data on Moroccan children with TS, and to perform immunological and genetic explorations of the IL-12/IFN-γ axis.

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Article Synopsis
  • Autosomal recessive TYK2 deficiency can lead to increased susceptibility to bacterial and viral infections, with varying symptoms among affected individuals.
  • Eight patients from different ethnicities were studied, revealing that while they all faced infections due to impaired immune responses, none exhibited the full hyper-IgE syndrome features seen in the first patient described.
  • The core issue in TYK2 deficiency is the inability to effectively respond to certain interleukins (IL-12 and IFN-α/β), which causes the infections, but the lack of HIES symptoms suggests that impaired IL-6 responses are not a fundamental aspect of this deficiency.
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Tuberculosis (TB), caused by Mycobacterium tuberculosis (M.tb) and a few related mycobacteria, is a devastating disease, killing more than a million individuals per year worldwide. However, its pathogenesis remains largely elusive, as only a small proportion of infected individuals develop clinical disease either during primary infection or during reactivation from latency or secondary infection.

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Background: Only a minority of individuals infected with Mycobacterium tuberculosis develop clinical tuberculosis. Genetic epidemiological evidence suggests that pulmonary tuberculosis has a strong human genetic component. Previous genetic findings in Mendelian predisposition to more severe mycobacterial infections, including by M.

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