[Research progress on the impact and formation mechanism of vascular endothelial cells in cutaneous tuberculosis].

Cutaneous Tuberculosis (CTB) is a dermatological manifestation caused by Mycobacterium tuberculosis (Mtb). Studies have shown that various immune cells are involved in its pathogenesis. Early perspectives suggested that Mtb primarily invades innate immune cells, but recent research has found that adaptive immune cells also play a crucial role during the infection process and significantly influence changes at the inflammation site. As the main component of the vascular endothelium, endothelial cells (ECs) can secrete various inflammatory mediators and chemokines during Mtb infection, recruiting and activating immune cells to promote host anti-tuberculosis immune responses and contribute to the formation of tuberculous granulomas. Oxidative stress enhances the pro-inflammatory state of ECs, while pattern recognition receptors (TLRs) recognize Mtb antigens and mediate antigen presentation. Additionally, ECs drive angiogenesis to maintain microcirculation at infection sites, balancing vascular barrier function and immune defense to collectively combat Mtb infection, which demonstrates significant immunomodulatory functions. This article reviews the mechanisms by which Mtb induces cutaneous tuberculosis, with a focus on the role of vascular ECs. It analyzes the interactions between Mtb and ECs and their contributions to the onset and progression of the disease, aiming to provide a theoretical basis for the development of new therapeutic targets and strategies.