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Altered homeostasis of CD4 + FoxP3 + regulatory T‐cell subpopulations in systemic lupus erythematosus
Author(s) -
Suen JauLing,
Li HsiaoTing,
Jong YuhJyh,
Chiang BorLuen,
Yen JengHsien
Publication year - 2009
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2008.02937.x
Subject(s) - foxp3 , il 2 receptor , immunology , flow cytometry , homeostasis , pathogenesis , biology , regulatory t cell , t cell , endocrinology , medicine , immune system
Summary The role of naturally occurring regulatory T cells (Treg), known to be phenotypically heterogeneous, in controlling the expression of systemic lupus erythematosus (SLE) is incompletely defined. Therefore, different subpopulations of CD4 + FoxP3 + Tregs in patients with active or inactive SLE were investigated and compared with those of healthy subjects and patients with ankylosing spondylitis (AS). Characterization of different subsets of circulating CD4 + FoxP3 + Tregs was examined using flow cytometry. CD4 + CD25 high T cells were sorted and examined for suppressive activity in vitro . The results showed first that a significant decrease in the frequency of CD4 + CD25 high FoxP3 + T cells was present in patients with active SLE ( n = 58), compared with healthy controls ( n = 36) and AS patients ( n = 23). In contrast, the frequencies of CD25 low FoxP3 + and CD25 − FoxP3 + CD4 + T cells were significantly increased in patients with active SLE by comparison with the control subjects. The elevation of these two putative Treg subpopulations was associated with lower plasma levels of complement C3 and C4 in patients with SLE. In addition, the ratios of the three subsets of CD4 + FoxP3 + Tregs versus effector T cells (CD4 + CD25 + FoxP3 − ) were inversely correlated with the titer of anti‐double‐stranded DNA IgG in patients with inactive, but not active, SLE. These results suggest that the pathogenesis of SLE may be associated with a defect in the homeostatic control of different Treg subsets.