Over the past decade, B-cell depletion has become an increasingly used treatment to maintain remission without oral immunosupressive drugs in complicated frequently relapsing, or steroid-dependent nephrotic syndrome (FR/SDNS) with a good safety profile. However, hypogammaglobulinemia occurs in 14-50 % of patients during B-cell depletion and some patients experience prolonged hypogammaglobulinemia long after their B-cell levels have returned to the normal range. We hypothesize that patients with persistent hypogammaglobulinemia may exhibit alterations in B-cell homeostasis. Additionally, since T-follicular Helpers (TfH) play a critical role in B-cell maturation and differentiation into memory B-cells and plasma cells, we also investigated T-cell homeostasis. We compared levels of IgG, IgA, IgM, IgE and IgG subclasses, analyzed B-cell subpopulations and T-cell subpopulations using flow cytometry on fresh blood, and evaluated B cell differentiation capacity into antibody-secreting cells (ASC) following non-specific polyclonal stimulation by B-cell ELISpot assay. Further analyses are ongoing to better understand this mechanism: B cell cultures to investigate a potential impact on T-independent B-cell maturation pathways in controls, and single-cell RNA sequencing analysis on B and T cells to determine transcriptomic alterations linked to the suspected class-switching process impairment
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