ArticleJournal of clinical medicine2019
Inflammatory Immune Responses in the Pathogenesis of Tick-Borne Encephalitis.
Article in Journal of clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Tissue tropism and mRNA expression profiles of selected innate immunity-related genes following experimental tick-borne encephalitis virus and louping ill virus infection of sheep.Journal of virology · 2026Article
- Circulating miRNAs as Biomarkers of Tick-Borne Encephalitis Severity: Association with Cytokine Profile in Febrile, Meningeal, and Encephalitic Forms.International journal of molecular sciences · 2026Article
- Tick-Borne Encephalitis in the 21Le infezioni in medicina · 2026Review
- Article
- The Factors Associated with the Blood-Brain Barrier Dysfunction in Tick-Borne Encephalitis.International journal of molecular sciences · 2025Article
- Viruses and the Brain-A Relationship Prone to Trouble.Viruses · 2025Review
- An autochthonous case of severeIDCases · 2025Article
- Robust CXCL10/IP-10 and CCL5/RANTES Production Induced by Tick-Borne Encephalitis Virus in Human Brain Pericytes Despite Weak Infection.International journal of molecular sciences · 2024Article
- Proinflammatory Chemokine Levels in Cerebrospinal Fluid of Patients with Neuroinvasive Flavivirus Infections.Microorganisms · 2024Article
- Defining the "Correlate(s) of Protection" to tick-borne encephalitis vaccination and infection - key points and outstanding questions.Frontiers in immunology · 2024Review
- Tick-Borne Encephalitis (TBE): From Tick to Pathology.Journal of clinical medicine · 2023Review
- Tick-Borne Encephalitis Virus: A Comprehensive Review of Transmission, Pathogenesis, Epidemiology, Clinical Manifestations, Diagnosis, and Prevention.Microorganisms · 2023Review
- Activation of Early Proinflammatory Responses by TBEV NS1 Varies between the Strains of Various Subtypes.International journal of molecular sciences · 2023Article
- Comparison of laboratory and immune characteristics of the initial and second phase of tick-borne encephalitis.Emerging microbes & infections · 2022Article
- Quantification of Antiviral Cytokines in Serum, Cerebrospinal Fluid and Urine of Patients with Tick-Borne Encephalitis in Croatia.Vaccines · 2022Article
- Metabolic Response to Tick-Borne Encephalitis Virus Infection and Bacterial Co-Infections.Pathogens (Basel, Switzerland) · 2022Article
- Comparison of Clinical, Laboratory and Immune Characteristics of the Monophasic and Biphasic Course of Tick-Borne Encephalitis.Microorganisms · 2021Article
- Antiviral Cytokine Response in Neuroinvasive and Non-Neuroinvasive West Nile Virus Infection.Viruses · 2021Article
- Upregulated Intrathecal Expression of VEGF-A and Long Lasting Global Upregulation of Proinflammatory Immune Mediators in Vaccine Breakthrough Tick-Borne Encephalitis.Frontiers in cellular and infection microbiology · 2021Article
- Tick-borne encephalitis vaccination in multiple sclerosis: A prospective, multicenter study.Neurology(R) neuroimmunology & neuroinflammation · 2020Observational
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Clinical manifestations of tick-borne encephalitis (TBE) are thought to result from the host immune responses to infection, but knowledge of such responses is incomplete. We performed a detailed clinical evaluation and characterization of innate and adaptive inflammatory immune responses in matched serum and cerebrospinal fluid (CSF) samples from 81 adult patients with TBE. Immune responses were then correlated with laboratory and clinical findings. The inflammatory immune responses were generally site-specific. Cytokines and chemokines associated with innate and Th1 adaptive immune responses were significantly higher in CSF, while mediators associated with Th17 and B-cell responses were generally higher in serum. Furthermore, mediators associated with innate and Th1 adaptive immune responses were positively associated with disease severity, whereas Th17 and B cell immune responses were not. During the meningoencephalitic phase of TBE, innate and Th1 adaptive inflammatory mediators were highly concentrated in CSF, the site of the disease. The consequence of this robust immune response was more severe acute illness. In contrast, inflammatory mediators associated with B cell and particularly Th17 responses were concentrated in serum. These findings provide new insights into the immunopathogenesis of TBE and implicate innate and Th1 adaptive responses in severity and clinical presentation of acute illness.
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