ArticleIndian dermatology online journal2025
Understanding Autoimmune Response Mechanisms in Leprosy.
Article in Indian dermatology online journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Utility of mimicking B cell epitopes between Mycobacterium leprae and host as prognostic biomarkers in type 1 reaction in leprosy.Scientific reports · 2026Article
- Lepromatous leprosy presenting with chronic painless ulcers and inflammatory arthropathy: a case report from a non-endemic setting.BMC infectious diseases · 2026Article
- Efficiency of the Sensory Mapping Score for Hansens's disease diagnosis and follow-up: a functional cure criterion?Frontiers in medicine · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractLeprosy is a persistent granulomatous disease that occurs due to Mycobacterium leprae infection. Leprosy primarily affects peripheral nerves, skin, and mucous membranes. Reactions in leprosy are immunological complications that may occur at any stage of disease progression, irrespective of treatment status. This review explores the potential link between M. leprae infection and autoimmune responses, emphasizing the role of immune dysregulation in leprosy reactions. We have delineated a comprehensive exploration of reactions in leprosy within the framework of autoimmunity, drawing insights from previously documented research. Biotic elements, including bacteria, might be associated with an imbalance in the host's homeostatic mechanism, leading to an autoimmune response. Mycobacteria have been reported for their potential to modulate host immune responses in both humans and experimental animal models. Pathogens can induce autoimmunity via molecular mimicry during the initiation of the disorder, and they may promote chronic pathologies with inflammation and/or superantigens, prompted by the loss of immunological tolerance to self-antigens, which can lead to systemic or organ-specific damage. Autoimmune manifestations in leprosy are triggered by the impairment of the regulatory mechanisms of the host due to M. leprae infection. Leprosy reactions are influenced by autoimmune processes triggered by M. leprae infection. Understanding the immunological interactions between the pathogen and the host may provide insights into disease management and therapeutic strategies.
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Registered trials
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