Publications by authors named "H S Houssaini"

The inducible T-cell costimulator (ICOS) may play an important role in adaptive immunity by regulating the interaction between T cells and antigen-presenting cells. Disruption of this molecule can lead to autoimmune diseases, in particular systemic lupus erythematosus (SLE). In this study, we aimed to explore the possible association between ICOS gene polymorphisms and SLE as well as their influence on disease susceptibility and clinical outcomes.

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Lupus nephritis (LN) is a type of immunological complex glomerulonephritis characterized by chronic renal inflammation which is exacerbated by infiltrating leukocytes and fueled by a variety of pro-inflammatory cytokines. A profound understanding of the pathogenesis of LN is necessary to identify the optimal molecular targets. The role of RNA-binding proteins (RBPs) in post-transcriptional gene regulation in the immune system is being explored in greater depth to better understand how this regulation is implicated in inflammatory and autoimmune diseases.

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Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by T cells imbalance. Indeed, a correlation between levels of Th17 cells and disease activity has been reported. Our work aimed to study the functional association of subpopulations of Th cells and SLE with (lupus nephritis, LN) or without (lupus erythematosus, LE) renal involvement in Tunisian patients through the detection of intracellular cytokines and surface marker expression.

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Background: Extracellular hydrolases (phospholipase, aspartyl protease and haemolysin) and biofilm production are considered as major virulence factors of the opportunistic pathogenic fungus Candida albicans. However, the impact of antifungal therapy on such virulence attributes is not well investigated. The common antifungal agents may disturb the production of secreted hydrolases as well as biofilm formation.

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Candida albicans is considered as the leading species causing vulvovaginal candidiasis. Numerous virulence determinants and escalating resistance to antifungal therapy have contributed to its pathogenicity. However, correlation between resistance profiles and virulence patterns of C.

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