In Semliki Forest virus encephalitis, suppressor of cytokine signalling 4 (SOCS4) is an essential modulator of immune responses that mediates the balance between immunopathology and virus clearance
Journal Title
Immunology & Cell Biology
Publication Type
epub ahead of print
Abstract
Central nervous system (CNS) virus infections are a major cause of morbidity and mortality worldwide and a significant global public health concern. As in many tissues, inflammation and immune responses in the brain, despite their protective roles, can also be harmful. Control of brain inflammation is important in many neurological diseases from encephalitis to multiple sclerosis and neurogenerative disease. The suppressors of cytokine signalling (SOCS) proteins are a key mechanism controlling inflammatory and immune responses across all tissues including the brain. Using a mouse model system, we demonstrate that lack of SOCS4 results in changes in the pathogenesis and clinical outcome of a neurotropic virus infection. Relative to wild type mice, SOCS4-deficient mice showed accelerated clearance of virus from the brain, lower levels of persisting viral RNA in the brain, increased neuroinflammation and more severe neuropathology. We conclude that in the mouse brain, SOCS4 is a vital regulator of anti-viral immunity that mediates the critical balance between immunopathology and virus persistence.
Publisher
Wiley
Keywords
Socs; Semliki Forest virus; brain immunology; encephalitis
Research Division(s)
Inflammation
PubMed ID
36702633
Open Access at Publisher's Site
https://doi.org/10.1111/imcb.12625
Terms of Use/Rights Notice
Refer to copyright notice on published article.


Creation Date: 2023-03-17 11:09:10
Last Modified: 2023-03-17 11:15:09
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