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Increased expression of histocompatibility leukocyte antigen-G in the tuberculoid form of leprosy
Fabiana Covolo de Souza Santana1, Débora Regina Fernandes2, Luciana Raquel Vicenzi Fachin2
1Immunology Technical Team, Lauro de Souza Lima Institute, Brazil.
Abstract:
Background The immunological context of leprosy is influenced by mechanisms closely associated with the human leukocyte antigen (HLA). HLA-G, a non-classical class I (Ib) molecule, plays a key role in regulating immune responses and has been linked to the progression and prognosis of various diseases. Objectives This study aimed to investigate HLA-G expression both in situ and in its soluble form in patients with different forms of leprosy, such as tuberculoid (TT), borderline tuberculoid (BT), borderline lepromatous (BL), and lepromatous leprosy (LL) and leprosy reactions, such as reversal reaction (RR) and erythema nodosum leprosum (ENL). Methods Biopsy samples from 71 patients and eight healthy controls were used for HLA-G immunohistochemistry. Serum samples from 43 patients and five controls were used to detect soluble HLA-G by ELISA. Results In situ HLA-G expression was observed in 78.6% of TT, 58.8% of BT, 60.0% of BB, 31.2% of BL, and 21.4% of LL patients. Among patients with leprosy reactions, 72.7% of RR and 33.3% of ENL showed HLA-G expression. TT patients exhibited higher expression than healthy controls (p=0.007) and LL patients (p=0.043). The levels of soluble HLA-G were similar in all clinical forms and leprosy reactions. Limitations This study was limited by a small sample size, particularly in the ENL group of patients. This may have influenced the results. Furthermore, the ability to investigate soluble HLA-G (sHLA-G) was limited by the number of patients available for this analysis. Additionally, the study's cross-sectional design did not allow for assessing changes in HLA-G expression and sHLA-G levels over time. Conclusions HLA-G expression was higher in TT leprosy patients and decreased across the clinical forms, suggesting that this molecule may modulate the course of leprosy.
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