Células T reguladoras em diferentes formas de hanseníase e reações hansênicas

Abstract

Leprosy is a chronic infectious contagious disease caused by Mycobacterium leprae. The disease is characterized by dermatoneurological manifestations and exhibits dynamic patterns of immune response to infection by the intracellular pathogen. Although regulatory T cells are fundamental in the immunoregulation of various pathological processes, their role in the immunology of leprosy has been addressed in few studies. In this context, this work was developed with the objective of determining the number of FoxP3, the main marker of Treg cells, in the different forms of leprosy and leprosy reaction. The following study groups were evaluated: patients diagnosed whit Paucibacillary Leprosy (PB); Multibacillary Leprosy (MB); Type 1 leprosy reaction (TR1); Type 2 leprosy reaction (TR2); Healthy endemic controls (HEC). The regulatory T cells expression was investigated using the ELISA method for the measurement of the FoxP3 marker in plasma and supernatant of PBMCs (Peripheral Blood Mononuclear Cell). Measurement of FoxP3 in plasma was performed in the absence of stimulation immediately after blood collection. Measurement of Tregs cells in the PBMCs supernatant was performed after incubation with 10 μg/ml M. leprae cells sonicated (MLCS) at 37 °C, 5 % CO2 for 72 hours. The results showed that there was no difference in FoxP3 expression measured directly in the plasma, in the absence of stimuli, between the studied groups. After stimulation with MLCS, PBMCs from all groups demonstrated a statistically significant increase in FoxP3 expression when compared to healthy subjects. A significant increase (p < 0,0001) in Treg cell expression in MB patients, with about 16 ng/ml FoxP3, was observed when compared to PB (6,83 ng/ml). TR1 individuals was the group that presented higher FoxP3 expression, with a median of 33,3 ng/ml. The amount of Treg FoxP3+ in TR1 patients was about six times that of healthy individuals and more than twice that of TR2 individuals. Thus, our data suggest a very important role of Tregs in the etiopathogenesis of leprosy. These cells would regulate the acute inflammatory process, avoiding a common exacerbated inflammation in TR1, which could lead to severe and incapacitating lesions on the tissues and nerves.