TY - JOUR KW - General Medicine AU - Yuniati R AU - Riawan W AU - Widayati A AU - Khrisna MB AU - Kristina TN AB -

Background Neural lesions are one of the main pathologies occurring in leprosy, which can result in devastating consequences due to disability and deformity. Transforming Growth Factor β (TGF-β) is important in the development of tissue fibrosis. The signaling process for TGF-β starts when it binds to TβRI and TβRII, activating and inducing the phosphorylation of Smad2 and Smad3. SUMOylation is a posttranslational modification, mediating the phosphorylation of Smad3 and regulating the TGF-β response. S100b is a marker of nerve damage. Objectives This study evaluates the in-vivo expression levels of SUMO-1 and SUMO2/3/4, the distribution of Schwann cells and mononuclear cells, and the distribution of S100b and collagen-1 in nerve biopsies of patients with leprosy reversal reactions. Methods Biopsies from twenty-six leprosy patients with reversal reactions (RR) and twenty-four leprosy patients without reversal reactions were stained for SUMO-1, SUMO-2/3/4, S100b, and collagen. We analyzed the cells using a Nikon microscope under 400× magnification. Results We found an increased distribution of SUMO-1, SUMO-2/3/4, macrophages, S100b, and collagen staining in neural lesions of reversal reaction patients, compared to leprosy patients without reversal reactions. Conclusion TGF-β plays an important role in the development of fibrosis in the neural lesions of patients with leprosy. Regulation of the transcription process is mediated by TGF-β1 signaling by SUMO-1 and/or SUMO-2/3/4. The increase in macrophages and collagen, with the decrease in S100b, in patients with neural lesions reflects the  damage to nerves in leprosy reversal reactions.

BT - Leprosy Review DO - 10.47276/lr.93.2.138 IS - 2 LA - eng N2 -

Background Neural lesions are one of the main pathologies occurring in leprosy, which can result in devastating consequences due to disability and deformity. Transforming Growth Factor β (TGF-β) is important in the development of tissue fibrosis. The signaling process for TGF-β starts when it binds to TβRI and TβRII, activating and inducing the phosphorylation of Smad2 and Smad3. SUMOylation is a posttranslational modification, mediating the phosphorylation of Smad3 and regulating the TGF-β response. S100b is a marker of nerve damage. Objectives This study evaluates the in-vivo expression levels of SUMO-1 and SUMO2/3/4, the distribution of Schwann cells and mononuclear cells, and the distribution of S100b and collagen-1 in nerve biopsies of patients with leprosy reversal reactions. Methods Biopsies from twenty-six leprosy patients with reversal reactions (RR) and twenty-four leprosy patients without reversal reactions were stained for SUMO-1, SUMO-2/3/4, S100b, and collagen. We analyzed the cells using a Nikon microscope under 400× magnification. Results We found an increased distribution of SUMO-1, SUMO-2/3/4, macrophages, S100b, and collagen staining in neural lesions of reversal reaction patients, compared to leprosy patients without reversal reactions. Conclusion TGF-β plays an important role in the development of fibrosis in the neural lesions of patients with leprosy. Regulation of the transcription process is mediated by TGF-β1 signaling by SUMO-1 and/or SUMO-2/3/4. The increase in macrophages and collagen, with the decrease in S100b, in patients with neural lesions reflects the  damage to nerves in leprosy reversal reactions.

PB - Lepra PY - 2022 SP - 138 EP - 148 T2 - Leprosy Review TI - Histopathology of SUMO in TGF-β1 signaling in neural lesions of leprosy reversal reactions UR - https://leprosyreview.org/admin/public/api/lepra/website/getDownload/6298a32fafaac119da731702 VL - 93 SN - 2162-8807 ER -