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• W1982536665 abstract "Multiple sclerosis (MS), one of the most frequent central nervous system (CNS) diseases in young adults, is a chronic demyelinating disease of unknown etiology and possibly multifactorial causes. Due to clinical and pathological similarities, Theiler’s murine encephalomyelitis (TME) represents a commonly used infectious animal model for the chronic-progressive form of human MS. Inadequate viral clearance in susceptible SJL mice leads to persistent infection of the CNS and immune mediated spinal cord demyelination. In contrast resistant C57BL/6 mice eliminate the virus from the CNS by specific cellular immunity, including effective CD8-mediated cytotoxicity. Previous studies have demonstrated that regulatory T cells (Treg) reduce antiviral immune responses in TME in susceptible mice strains. However, the function of Treg in resistant C57BL/6 mice remains undetermined. Thus the aim of the present study was to investigate the impact of in vivo-expansion of Treg by interleukin-2 immune complexes (Treg-expansion) and antibody-mediated CD8+ T cell depletion (CD8-depletion) upon TME virus-induced disease progression in C57BL/6 mice to get further insights into role of Treg and their interaction with other leukocyte subsets in persistent viral infections. Results of the present study confirmed the central role of antiviral cytotoxicity for TME virus elimination in resistant C57BL/6 mice. In agreement with previous reports simple manipulation of the Treg-compartment showed only minor effect upon the disease course in resistant mice, though Treg-expansion exerted profound inhibitory responses in an CD8-reduced environment. Flow cytometric analyses revealed an increased percentage of Foxp3+ Treg in the blood and spleen of C57BL/6 mice following Treg-expansion and CD8-depletion (combined treated animals) associated with an increased CD4/CD8 ratio. Furthermore, a prolonged effect of Treg-expansion was observed in combined treated mice, indicative of an inhibitory effect of CD8+ T cells upon Treg. Peripheral phenotypical changes were associated with an enhanced recruitment of lymphocytes to the brain and spinal cord of TME virus-infected C57BL/6 mice as determined by histology. Real time polymerase chain reaction confirmed chronic brain infection at 42 days post infection (dpi) in combined treated C57BL/6 mice. Immunohistochemistry revealed a predominent infection of hippocampal neurons and significant infiltrations of CD3+ T cells, CD45R+ B cells and CD107b+ microglia/macrophages till 14 dpi in the cerebrum. Foxp3+ Treg were found in the hippocampus also during the late phase (42 dpi), potentially attributed to termination of inflammatory responses. In the spinal cord CD8-depletion and combined treatment led to prolonged infection and leukomyelitis in mice. Immunohistochemistry revealed a significant loss of myelin basic protein expression at 42 dpi in combined treated mice. Moreover, spinal cord demyelination was associated with an increase of β-amyloid precursor protein-postitive axons predominetely in combined treated mice, indicative of axonal damage. Inflammatory responses in the spinal cord white matter were dominated by CD3+ T cells and CD107b+ macrophages/microglia, suggestive of T cell-mediated immunopathology. In addition, significant numbers of Foxp3+ Treg and CD45R+ B cells were found in the spinal cord white matter during the late phase in combined treated C57BL/6 mice. In conclusion, the present project demonstrates synergistic effects of combined Treg-expansion and CD8-depletion to efficiently reduce antiviral immune responses in TME virus-infected C57BL/6 mice, which renders them susceptible to develop chronic infection, leukomyelitis and myelin loss. In addtion to the well described inhibitory effect of Treg upon CD8+ T cells, also regulatory effects of cytotoxic cells upon Treg or bidirectional interaction of these two T cell subsets, respectively, may occur in infectious CNS disoders. C57BL/6 mice are widely used for genetic modification and several transgenic mice with this genetic background have been established for the use as animal models. Thus, findings will potentially support the development of novel therapeutic strategies for chronic inflammatory disorders and provide a base for future studies upon virus-induced immunopathology using transgenic mice." @default.
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• W1982536665 date "2015-01-01" @default.
• W1982536665 modified "2023-09-22" @default.
• W1982536665 title "Expansion of regulatory T cells in theiler’s murine encephalomyelitis virus-infected C57BL/6 mice" @default.
• W1982536665 doi "https://doi.org/10.1016/j.jcpa.2014.10.038" @default.
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