Receptores Toll-like 2: ativação e regulação da imunidade inata e adaptativa em pacientes com hanseníase

Abstract

Leprosy is a chronic infectious disease caused by the Mycobacterium leprae. It remains a significant public health challenge worldwide, particularly in Brazil, which ranks second in global disease prevalence. Although curable, the disease possesses a high potential for causing physical disabilities and sequelae, making early diagnosis and appropriate treatment essential. Due to its complex pathogenesis and the varied immune responses that determine its clinical forms, this study focused on understanding innate immunity mechanisms, specifically the Toll-like receptor (TLR) pathway—with an emphasis on TLR2 and its interaction with adaptive immune cells, namely CD4+ and CD8+ T lymphocytes. In this study, the expression and functionality of these markers were investigated following in vitro stimulation with soluble M. leprae antigen in leprosy patients, categorized into paucibacillary (PB) and multibacillary (MB) forms. Significant differences in immune responses were observed between these groups, reflecting the complexity of the host response to the pathogen. There was a predominance of TLR2-mediated responses, with notable macrophage activation and a trend toward a TH1 polarization in PB patients. In contrast, MB patients exhibited a more regulatory response, characterized by higher levels of IL-10. This study underscores the fundamental role of TLRs in modulating the immune response in leprosy, providing insights into the immunological mechanisms that differentiate the clinical forms of the disease. Furthermore, the findings reinforce the need for innovative therapeutic approaches that account for the complexity of the involved immunological interactions. Furthering these investigations may contribute to the development of more precise diagnostics and effective treatments, with the potential to prevent disease progression and reduce transmission.