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IRF-4-Binding Protein Inhibits Interleukin-17 and Interleukin-21 Production by Controlling the Activity of IRF-4 Transcription Factor

December 29, 2009

Recent studies have uncovered the existence of a T helper cell
effector subset, the Th17 cell lineage, whose deregulation has
been implicated in the pathogenesis of autoimmunity (Bettelli
et al., 2007b; Weaver et al., 2006). In particular, Th17 cells are believed
to play a key role in rheumatoid arthritis (RA) (McInnes and
Schett, 2007; Toh and Miossec, 2007), a disease characterized
by destructive inflammatory lesions affecting the synovial membranes
of joints and by aberrant humoral responses that result
in the production of autoantibodies such as rheumatoid factor
and cyclic citrullinated peptide (CCP) antibodies. The ability of
the Th17 cell subset to produce IL-17 is critical to their role in
RA pathogenesis because IL-17 can induce the production of
proinflammatory cytokines such as TNF-a and IL-1 as well as
stimulate matrix metalloproteinase activity, matrix catabolism,
and bone resorption (Koenders et al., 2006; Stamp et al., 2004).
Th17 cells have also recently been shown to produce IL-21
(Korn et al., 2007; Nurieva et al., 2007; Zhou et al., 2007), a cytokine
that can amplify the differentiation of Th17 cells in an
autocrine manner as well as control T-dependent humoral
responses (Leonard and Spolski, 2005; Mehta et al., 2004).
Th17 cells develop via a pathway distinct from Th1 and Th2 cells.
Induction of IL-17 production depends on the presence of the
transcription factors STAT3 and RORgt (Ivanov et al., 2006; Laurence
et al., 2007; Yang et al., 2007), whereas IL-21 expression
requires the presence of STAT3 but not of RORgt (Nurieva
et al., 2007). Given the potentially deleterious effects of the
cytokines produced by Th17 cells, their production needs to be
strictly controlled so that acquisition of these effector functions
occurs only in response to the appropriate antigenic stimuli.
The regulatory pathways that prevent the inappropriate production
of IL-17 and IL-21 have, however, not been fully elucidated.

...

Read the full article here

Source lupusresearch.org


IRF-4-Binding Protein Inhibits Interleukin-17 and Interleukin-21 Production by Controlling the Activity of IRF-4 Transcription Factor

December 29, 2009

Recent studies have uncovered the existence of a T helper cell
effector subset, the Th17 cell lineage, whose deregulation has
been implicated in the pathogenesis of autoimmunity (Bettelli
et al., 2007b; Weaver et al., 2006). In particular, Th17 cells are believed
to play a key role in rheumatoid arthritis (RA) (McInnes and
Schett, 2007; Toh and Miossec, 2007), a disease characterized
by destructive inflammatory lesions affecting the synovial membranes
of joints and by aberrant humoral responses that result
in the production of autoantibodies such as rheumatoid factor
and cyclic citrullinated peptide (CCP) antibodies. The ability of
the Th17 cell subset to produce IL-17 is critical to their role in
RA pathogenesis because IL-17 can induce the production of
proinflammatory cytokines such as TNF-a and IL-1 as well as
stimulate matrix metalloproteinase activity, matrix catabolism,
and bone resorption (Koenders et al., 2006; Stamp et al., 2004).
Th17 cells have also recently been shown to produce IL-21
(Korn et al., 2007; Nurieva et al., 2007; Zhou et al., 2007), a cytokine
that can amplify the differentiation of Th17 cells in an
autocrine manner as well as control T-dependent humoral
responses (Leonard and Spolski, 2005; Mehta et al., 2004).
Th17 cells develop via a pathway distinct from Th1 and Th2 cells.
Induction of IL-17 production depends on the presence of the
transcription factors STAT3 and RORgt (Ivanov et al., 2006; Laurence
et al., 2007; Yang et al., 2007), whereas IL-21 expression
requires the presence of STAT3 but not of RORgt (Nurieva
et al., 2007). Given the potentially deleterious effects of the
cytokines produced by Th17 cells, their production needs to be
strictly controlled so that acquisition of these effector functions
occurs only in response to the appropriate antigenic stimuli.
The regulatory pathways that prevent the inappropriate production
of IL-17 and IL-21 have, however, not been fully elucidated.

...

Read the full article here

Source lupusresearch.org



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