Our results suggest that low levels of CR1 on erythrocytes in SLE patients are required during the course of the disease and that the 6.9 kb restriction fragment does not play a role in causing susceptibility to the disease.
3H - TdR incorporation of SLE B cells without stimuli (P<0.001) and with CD40L-LZ stimulation (P<0.05) were significantly lower in SLE patients compared with normal controls.
On the other hand, CR1 levels of PMN stimulated by FMLP were also found to be decreased in SLE patients, while both the expression of circulating PMN (cells isolated at 4 degrees C) and the total cellular CR1 content were normal.
SLE and normal T cells pretreated with estradiol and cultured with ionomycin for 2 h to activate calcineurin showed no significant differences in CD40L mRNA.
Expressions of IL-6 and ds-DNA antibody were high in SLE patients serum and were positively correlated with TLR9 level in SLE patients (IL-6, R(2) = 0.768; ds-DNA antibody, R(2) = 0.730).
Increased expression of TLR2 in CD4(+) T cells from SLE patients enhances immune reactivity and promotes IL-17 expression through histone modifications.
G-MDSCs produce high levels of ROS (reactive oxygen species) through increasing gp91(phox) expression, and activated TLR2 (Toll-like receptor 2) and AIM2 (absent in melanoma 2) inflammasome in M-MDSCs lead to IL-1β (interleukin 1β) expression in diseased MRL/lpr mice and high-disease-activity SLE patients.
The increase of miR-326 expression in Treg cells from SLE patients may inhibit the expression of Ets-1 to participate in the pathological process of SLE.
Elevated transcription of the hsp90 beta gene in SLE patients is not in general paralleled by enhanced transcription of the hsp70 or ubiquitin genes indicating that the hsp90 beta gene is specifically activated in some SLE patients.
The higher CD48 mRNA levels observed in CD4⁺ T cells from SLE patients and the positive correlation found with SLEDAI lead us to infer that an overexpression of the protein coded by this gene may have important consequences on the development of SLE.