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Open AccessArticle

Inflammatory Immune Responses in the Pathogenesis of Tick-Borne Encephalitis

1
Department of Infectious Diseases, University Medical Center Ljubljana, Japljeva 2, 1525 Ljubljana, Slovenia
2
Institute for Biostatistics and Medical Informatics, Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1000 Ljubljana, Slovenia
3
Department of Mathematics, Faculty of Mathematics, Natural Sciences and Information Technologies, University of Primorska, Glagoljaška 8, 6000 Koper, Slovenia
4
Institute for Microbiology and Immunology, Faculty of Medicine, University of Ljubljana, Zaloška 4, 1000 Ljubljana, Slovenia
5
Division of Rheumatology, Allergy, and Immunology, Center for Immunology and Inflammatory Diseases, Masachusetts General Hospital/Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2019, 8(5), 731; https://doi.org/10.3390/jcm8050731
Received: 27 March 2019 / Revised: 26 April 2019 / Accepted: 16 May 2019 / Published: 22 May 2019
(This article belongs to the Section Clinical Neurology)
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. View Full-Text
Keywords: tick-borne encephalitis; inflammatory mediators; innate immunity; adaptive immunity; cytokines; chemokines; cerebrospinal fluid; severity of illness tick-borne encephalitis; inflammatory mediators; innate immunity; adaptive immunity; cytokines; chemokines; cerebrospinal fluid; severity of illness
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Bogovič, P.; Lusa, L.; Korva, M.; Pavletič, M.; Resman Rus, K.; Lotrič-Furlan, S.; Avšič-Županc, T.; Strle, K.; Strle, F. Inflammatory Immune Responses in the Pathogenesis of Tick-Borne Encephalitis. J. Clin. Med. 2019, 8, 731.

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