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[Pathophysiology of Behçet's disease]
1Service de médecine interne, hôpital la Rabta, 1007 Tunis, Tunisie; Unité de recherche 02/UR/08-15, faculté de médecine de Tunis, université El Manar 2, Tunis, Tunisie.
La Revue De Medecine Interne
|November 12, 2013
Summary
Behçet's disease involves immune system dysregulation in genetically susceptible individuals, potentially triggered by infections like Streptococcus sanguis, leading to inflammation and endothelial dysfunction. Understanding its pathogenesis aids in developing new therapies.
Area of Science:
- Immunology
- Genetics
- Pathophysiology
Context:
- Behçet's disease (BD) pathogenesis remains unclear, but involves genetic predisposition and immune system imbalance.
- Strongest genetic link is HLA-B51; genome-wide association studies identify IL-10, IL-23R, and IL-12RB2 as susceptibility genes.
- Infectious triggers, possibly Streptococcus sanguis, may initiate disease via molecular mimicry, perpetuating with auto-antigens.
Purpose:
- To review the current understanding of Behçet's disease etiopathogenesis based on recent scientific advances.
- To explore the roles of genetic factors, immune responses, and potential triggers in BD development.
Summary:
- BD pathogenesis involves disrupted immune homeostasis in genetically susceptible individuals, leading to altered innate and adaptive immunity.
- Key features include pathogenic T cell activation (Th1, Th17 expansion; suppressed Treg), significant roles for cytokines (IL-17, IL-23, IL-21), and endothelial dysfunction.
- Inflammatory lesions contain neutrophils, CD4(+) T cells, and cytotoxic cells.
Impact:
- Improved understanding of BD pathophysiology provides a foundation for developing novel and more effective therapeutic strategies.
- Highlights the complex interplay between genetic susceptibility, immune dysregulation, and potential environmental triggers in Behçet's disease.
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