Borrelia burgdorferi and autoimmune mechanisms: implications for mimicry, misdiagnosis, and mismanagement in Lyme disease and autoimmune disorders.

Autor: Doskaliuk B; Department of Patophysiology, Ivano-Frankivsk National Medical University, Halytska str. 2, Ivano-Frankivsk, 76000, Ukraine. Doskaliuk_Bo@ifnmu.edu.ua., Zimba O; Department of Clinical Rheumatology and Immunology, University Hospital in Krakow, Kraków, Poland.; National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland.; Department of Internal Medicine N2, Danylo Halytsky Lviv National Medical University, Lviv, Ukraine.
Jazyk: angličtina
Zdroj: Rheumatology international [Rheumatol Int] 2024 Nov; Vol. 44 (11), pp. 2265-2271. Date of Electronic Publication: 2024 Apr 05.
DOI: 10.1007/s00296-024-05580-x
Abstrakt: The genus Borrelia encompasses a diverse group of spirochetes transmitted primarily by ticks, with Borrelia burgdorferi causing Lyme disease, which is prevalent in North America and Europe. Borrelia's structural adaptations and ability to persist in diverse host tissues underscore its pathogenic potential. Beyond traditional infectious responses, Borrelia engages in complex interactions with the host immune system, contributing to autoimmune mechanisms such as molecular mimicry and persistent infections. This intricate interplay manifests in symptoms resembling various autoimmune diseases, including systemic lupus erythematosus, dermatomyositis, local scleroderma, and systemic sclerosis. However, these associations lack a precise explanation, emphasizing the need for further investigation. The cases of misdiagnosis between Lyme borreliosis and autoimmune diseases highlight the critical importance of accurate diagnostics and adherence to guidelines. Understanding Borrelia's impact on immune responses is pivotal for advancing diagnostics and targeted therapeutic interventions in Lyme borreliosis and its potential autoimmune implications.
(© 2024. The Author(s).)
Databáze: MEDLINE
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