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Abstract

The neurological invasion of pathogens into the central nervous system (CNS) causes inflammatory host–cell interactions, which inexplicably control the pathogens’ ability to replicate or to be removed from the host. Undoubtedly, the pathogen’s mechanism of entering the CNS determines how the immune response develops. The portal of entry and the types of pathogens determine the exact mechanism of immune response in the CNS. Furthermore, immunological cellular interactions within this kind of ecosystem encourage the expression of inflammatory mediators, which has an acute impact on neuronal function at the cellular level. An increase in neutrophil chemoattractant molecules (like CXCL2), cellular adhesion molecules (ICAM), and complement C5a is observed if pathogen invasion happens. Antigen-presenting cells which are present in both meninges and choroid plexus support ongoing stimulation of T cells upon viral and fungal infections. However, high levels of TH1 cell cytokines, such as tumor necrosis factor, interferon, and IL-1, may potentially cause sustained cognitive function impairment even after the eradication of neurotropic pathogens. Autoimmune diseases in CNS could be better treated once the exact mechanism of molecular mimicry due to infections is clearly understood.

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Correspondence to Kyu Kyu Win .

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© 2023 The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd.

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Win, K.K., Parmasivam, P.A. (2023). Immune Responses in Infections of the Central Nervous System. In: Sami, H., Firoze, S., Khan, P.A. (eds) Viral and Fungal Infections of the Central Nervous System: A Microbiological Perspective . Springer, Singapore. https://doi.org/10.1007/978-981-99-6445-1_4

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