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Clinical immunology (Orlando, Fla.) (1)
Rider, Virginia (2)
Abdou, Nabih I (1)
Abdou, Nabih I. (1)
Greenwell, Cindy (1)
Kimler, Bruce (1)
Kimler, Bruce F. (1)
Smith, Peter (1)
Svojanovsky, Stan (1)
Walters, Emily (1)
Ward, Julie M. (1)
Year of Publication
Estradiol Differentially Regulates Calreticulin: A Potential Link with Abnormal T Cell Function in Systemic Lupus Erythematosus?
Ward, Julie M.
Abdou, Nabih I.
Systemic lupus erythematosus (SLE) is an autoimmune disease that affects women nine times more often than men. The present study investigates estradiol-dependent control of the calcium buffering protein, calreticulin, to gain further insight into the molecular basis of abnormal T cell signaling in SLE T cells.
T cells were purified from blood samples obtained from healthy females and SLE patients. Calreticulin expression was quantified by real time polymerase chain amplification. Calreticulin and estrogen receptor-α were co-precipitated and analyzed by Western blotting to determine if the proteins associate in T cells.
Calreticulin expression increased (p= 0.034)in activated control T cells, while estradiol decreased (p = 0.044) calreticulin in resting T cells. Calreticulin expression decreased in activated SLE T cell samples and increased in approximately 50% of resting T cell samples. Plasma estradiol was similar (p > 0.05) among SLE patients and control volunteers. Estrogen receptor-αand calreticulin co-precipitated from nuclear and cytoplasmic T cell compartments.
The results indicate that estradiol tightly regulates calreticulin expression in normal human T cells and the dynamics are different between activated and resting T cells. The absence of this tight regulation in SLE T cells could contribute to abnormal T cell function.
SLE; human T cells; estradiol; calreticulin; estrogen receptor-α
1 Estradiol Targets T Cell Signaling Pathways in Human Systemic Lupus
Abdou, Nabih I
Kimler, Bruce F.
Clinical immunology (Orlando, Fla.)
The major risk factor for developing systemic lupus erythematosus (SLE) is being female. The present study utilized gene profiles of activated T cells from females with SLE and healthy controls to identify signaling pathways uniquely regulated by estradiol that could contribute to SLE pathogenesis. Selected downstream pathway genes (+/− estradiol) were measured by real time polymerase chain amplification. Estradiol uniquely upregulated six pathways in SLE T cells that control T cell function including interferon-α signaling. Measurement of interferon-α pathway target gene expression revealed significant differences (p = 0.043) in DRIP150 (+/− estradiol) in SLE T cell samples while IFIT1 expression was bimodal and correlated moderately (r = 0.55) with disease activity. The results indicate that estradiol alters signaling pathways in activated SLE T cells that control T cell function. Differential expression of transcriptional coactivators could influence estrogen-dependent gene regulation in T cell signaling and contribute to SLE onset and disease pathogenesis.
SLE; estradiol; interferon-α; T cell signaling; microarray
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