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- W4313350043 abstract "Abstract Biological strategies that selectively harness the therapeutic benefits of glucocorticoids (GC) are highly attractive in the management of inflammatory conditions such as multiple sclerosis (MS). Glucocorticoid induced leucine zipper (GILZ), is a GC induced protein that binds the p65 subunit of nuclear factor kappa B(NF-κB, prevents its nuclear translocation and suppress inflammatory cytokines. GILZ over-expressing mice exhibit reduced T-bet expression and IFN-γ secretion, a canonical Th1 transcription factor and prototype Th1 cytokine respectively. We hypothesized that the intracellular delivery of GILZ protein may suppress delayed type hypersensitivity reaction, a Th1 response that mimic inflammation in MS. IFN-γ and IL-12 secretion was significantly reduced and that of IL-10 was elevated in human peripheral blood mononuclear cells stimulated with protein peptide derivative in the presence of GC or exogenous GILZ. We next investigated the therapeutic potential of GILZ supplement in experimental autoimmune encephalomyelitis (EAE), an animal model for MS. Groups of SJL/J mice induced EAE and administered GILZ protein exhibited significantly reduced clinical disease than vehicle treated mice. Upon re-stimulation with CNS antigens lymphocytes from GILZ protein administered mice exhibited significantly lower proliferation and inflammatory cytokine secretion (TNF-α and IL-12). These observations suggest a therapeutic potential for exogenous GILZ in MS." @default.
- W4313350043 created "2023-01-06" @default.
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- W4313350043 date "2011-04-01" @default.
- W4313350043 modified "2023-10-14" @default.
- W4313350043 title "Novel strategies to suppress NF-κB in experimental autoimmune encephalomyelitis (164.17)" @default.
- W4313350043 doi "https://doi.org/10.4049/jimmunol.186.supp.164.17" @default.
- W4313350043 hasPublicationYear "2011" @default.
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