ArticleScientific reports2021
Mimicking B and T cell epitopes between Mycobacterium leprae and host as predictive biomarkers in type 1 reaction in leprosy.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Integrated skin-lesion transcriptomics prioritises biomarker-candidate host-response genes with pharmacological annotation in leprosy type 1 reaction.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Utility of mimicking B cell epitopes between Mycobacterium leprae and host as prognostic biomarkers in type 1 reaction in leprosy.Scientific reports · 2026Article
- Understanding Autoimmune Response Mechanisms in Leprosy.Indian dermatology online journal · 2025Article
- Characteristics of Serum Autoantibody Repertoire and Immune Subgroup Variation of Tuberculosis-Associated Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Article
- Corroboration of cross-reactivity betweenFrontiers in microbiology · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several Mycobacterial infections including leprosy and tuberculosis are known to evoke autoimmune responses by modulating homeostatic mechanism of the host. Presence of autoantibodies like, rheumatoid factor, anti-nuclear factor and antibodies to host, collagen, keratin, myelin basic protein (MBP) and myosin, have been earlier reported in leprosy patients. In the present study, we detected the role of mimicking epitopes between Mycobacterium leprae and host components in the induction of autoimmune response in leprosy. Based on our previous findings, we predicted and synthesized a total of 15 mimicking linear B cell epitopes (BCE) and 9 mimicking linear T cell epitopes (TCE) of keratin and MBP. Humoral and cell-mediated immune responses against these epitopes were investigated in Non-reaction (NR), Type 1 reaction (T1R) leprosy patients, and healthy controls. We observed significantly higher levels of antibodies against 8 BCE in T1R in comparison to NR leprosy patients. Further, we also found 5 TCE significantly associated with lymphocyte proliferation in the T1R group. Our results indicated that these epitopes play a key role in the induction of autoimmune response in leprosy and are also strongly associated with the inflammatory episodes of T1R. Conclusively, these molecules may be employed as a biomarker to predict the inflammatory episodes of T1R.
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