IL-1 beta gene expression in B cells derived from the murine MRL/lpr model of lupus.

Abstract:

:The MRL/lpr model of SLE resembles human lupus in its various immunopathologic characteristics including the presence of high-level IgG and anti-DNA antibody production and multisystem organ involvement (nephritis, arthritis, and vasculitis). Our previous studies have shown that IL-1 overactivity in B cells plays a potentially important role in driving IgG and autoantibody production. However, the underlying mechanisms determining IL-1 overactivity are poorly understood. We studied IL-1 beta gene expression and transcriptional rates in B cells derived from old and young MRL/lpr, MRL/+ +, and non-autoimmune control mice using semi-quantitative RT-PCR and the nuclear run-on assay. RT-PCR demonstrated increased steady-state IL-1 beta gene expression in B cells derived from old MRL/lpr mice as compared to either young MRL/lpr or control mice. Furthermore, IL-1 beta gene expression in B cells was associated with the presence of the lpr mutation because heightened IL-1 beta message was observed in RNA obtained from MRL/lpr but not MRL/+ + B cells. IL-1 beta transcriptional rates measured by the nuclear run-on assay were very similar in B cells from old and young MRL/lpr and control mice. These observations suggest that IL-1 overactivity in B cells obtained from old diseased MRL/lpr results from heightened IL-1 beta message, is associated with the presence of the lpr mutation, and is likely to reflect post-transcriptional stabilization of IL-1 beta mRNA.

journal_name

Autoimmunity

journal_title

Autoimmunity

authors

Mao C,Singh AK

doi

10.3109/08916939609001949

subject

Has Abstract

pub_date

1996-01-01 00:00:00

pages

71-9

issue

2

eissn

0891-6934

issn

1607-842X

journal_volume

24

pub_type

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