Abstract:
:In systemic lupus erythematosus (SLE), T helper cells exhibit increased and prolonged expression of cell-surface CD40 ligand (CD154), spontaneously overproduce interleukin-10 (IL-10), but underproduce interferon-gamma (IFN-gamma). We tested the hypothesis that the imbalance of these gene products reflects skewed expression of CD154, IL-10, and IFN-gamma genes. Here, we demonstrate that the histone deacetylase inhibitor, trichostatin A, significantly down-regulated CD154 and IL-10 and up-regulated IFN-gamma gene expression in SLE T cells. This reversal corrected the aberrant expression of these gene products, thereby enhancing IFN-gamma production and inhibiting IL-10 and CD154 expression. That trichostatin A can simultaneously reverse the skewed expression of multiple genes implicated in the immunopathogenesis of SLE suggests that this pharmacologic agent may be a candidate for the treatment of this autoimmune disease.
journal_name
Proc Natl Acad Sci U S Aauthors
Mishra N,Brown DR,Olorenshaw IM,Kammer GMdoi
10.1073/pnas.051507098keywords:
subject
Has Abstractpub_date
2001-02-27 00:00:00pages
2628-33issue
5eissn
0027-8424issn
1091-6490pii
051507098journal_volume
98pub_type
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