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2015 ; 6
(ä): 610
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Disturbed T Cell Signaling and Altered Th17 and Regulatory T Cell Subsets in the
Pathogenesis of Systemic Lupus Erythematosus
#MMPMID26648939
Rother N
; van der Vlag J
Front Immunol
2015[]; 6
(ä): 610
PMID26648939
show ga
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the
presence of autoantibodies against nuclear components. Circulating immune
complexes of chromatin and autoantibodies deposit in various tissues leading to
inflammation and tissue damage. It has been well documented that autoimmunity in
SLE depends on autoreactive T cells. In this review, we summarize the literature
that addresses the roles of T cell signaling, and Th17 and regulatory T cells
(Tregs) in the development of SLE. T cell receptor (TCR) signaling appears to be
aberrant in T cells of patients with SLE. In particular, defects in the TCR?
chain, Syk kinase, and calcium signaling molecules have been associated with SLE,
which leads to hyperresponsive autoreactive T cells. Furthermore, in patients
with SLE increased numbers of autoreactive Th17 cells have been documented, and
Th17 cells appear to be responsible for tissue inflammation and damage. In
addition, reduced numbers of Tregs as well as Tregs with an impaired regulatory
function have been associated with SLE. The altered balance between the number of
Tregs and Th17 cells in SLE may result from changes in the cytokine milieu that
favors the development of Th17 cells over Tregs.