Publications by authors named "N Willcox"

Article Synopsis
  • APECED is a genetic immune disorder that affects various hormone-producing glands and increases vulnerability to candidiasis, with recent findings linking it to more severe COVID-19 and varicella infections.
  • In a study comparing APECED patients and healthy individuals, a higher percentage of APECED patients had anti-CMV IgG antibodies, although their antibody levels weren't significantly different from controls.
  • However, APECED patients showed lower levels of CMV-specific T cells, indicating a weakened immune response to CMV and solidifying the idea that APECED is associated with greater vulnerability to viral infections.
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Background And Objectives: Antibodies (Abs) specific for the low-density lipoprotein receptor-related protein 4 (LRP4) occur in up to 5% of patients with myasthenia gravis (MG). The objective of this study was to profile LRP4-Ab effector actions.

Methods: We evaluated the efficacy of LRP4-specific compared with AChR-specific IgG to induce Ab-dependent cellular phagocytosis (ADCP), Ab-dependent cellular cytotoxicity (ADCC), and Ab-dependent complement deposition (ADCD).

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Background And Purpose: Complement component 5 (C5) targeting therapies are clinically beneficial in patients with acetylcholine receptor antibody (AChR-Ab ) generalized myasthenia gravis (MG). That clearly implicates antibody-mediated complement activation in MG pathogenesis. Here, classical and alternative complement pathways were profiled in patients from different MG subgroups.

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Myasthenia gravis (MG) is an autoimmune disease in which pathogenic immunoglobulin G antibodies bind to acetylcholine receptors (or to functionally related molecules at the neuromuscular junction). B cell expression of the inhibitory immunoglobulin G receptor, Fc-gamma receptor (FcγR) IIB, maintains peripheral immune tolerance, and its absence renders B cells hyperresponsive to autoantigen. Here, we report that FcγRIIB expression levels are substantially reduced in B lineage cells derived from immunotherapy-naïve patients with acetylcholine receptor antibody-positive early-onset MG.

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Break . (Research Articles, 15 January 2021, eaay5731) conclude that T cell overproduction of interferon-γ causes chronic mucocutaneous candidiasis (CMC), a typical early feature of autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED). This contradicts studies implicating interleukin IL-17 and IL-22 deficiencies as a cause of CMC.

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