Understanding Autoimmune Response Mechanisms in Leprosy

Abstract

Leprosy 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.

Figure 1

The effect of the stimulus on the development of the macrophage lineage

Figure 2

Autoantibodies in leprosy

Figure 3

Frequency of positivity of autoantibodies across the leprosy spectrum

Figure 4

A comparative view of the level of autoantibodies against the host-specific proteins across T1R and Non-reactional TT/BT leprosy patients