In particular, with the exception of IL-2, IL-4, and TGF-β1, the levels of Th1, Th2, and Th17 cytokines are increased in SLE patients associated with disease severity.
MicroRNA-663 induces immune dysregulation by inhibiting TGF-β1 production in bone marrow-derived mesenchymal stem cells in patients with systemic lupus erythematosus.
PC1 changes from controls to SLE-HDA patients, included: the increased impact of IL-1β (from 0.58 to >0.95); increased impact of IL-6 in HDA (0.76); increased influence of MIP-1α (0.60) and MIP-1β (0.85); and the uncoupling of TGF-β1 (0.14).
miR-125a-3p decreases levels of interlukin-17 and suppresses renal fibrosis via down-regulating TGF-β1 in systemic lupus erythematosus mediated Lupus nephritic mice.
MicroRNA-663 induces immune dysregulation by inhibiting TGF-β1 production in bone marrow-derived mesenchymal stem cells in patients with systemic lupus erythematosus.
An impaired transcription of TGF-β1 target genes was demonstrated in the CD3+ lymphocytes of active SLE patients confirming that the defect involves T cells and pointing to its extrinsic nature.
Association between circulating transforming growth factor-β1 level and polymorphisms in systemic lupus erythematosus and rheumatoid arthritis: A meta-analysis.
Our data demonstrate the presence of an impaired response of peripheral cells to TGF-β1 in patients with active SLE that may participate to the pathogenesis of the disease.
However, in more than 50% of SLE patients the isolated T cell population showed no TGFbeta1 mRNA expression and at least one member of the TGFbeta1 pathway was also missing (TGFbeta-RI, Smad2 and Smad3) in more than half of the patients.
Moreover, the increments in the percentage of CD4+CD25+ cells and intracellular TGF-beta1 expression by TGF-beta1 stimulation were comparable in SLE and controls, and were not significantly influenced by disease activity or renal involvement in SLE.
However, the expression of TIM-3 ligand, galectin-9 increased in SLE patients indicating an enhanced engagement of TIM-3 with its ligand in SLE, which may result in a decreased regulatory T-cell function as shown by the decreased expression of FoxP3 and TGF-beta1 in SLE.
We conclude that the TGF-beta signaling pathway can be altered in circulating leukocytes derived from treated patients with SLE and that the assumed forms of the applied therapy in the group of patients under consideration are accompanied by similarity in the expression level of transcripts for TGF-beta1 and TGF-beta Rs determined in whole blood.
The intrinsic capability of immunoregulation for spontaneous B cell hyperactivity through PBMC TGF-beta1 production was presumed to be intact in clinically stable SLE in Taiwanese.
One major subgroup of the samples expressed fibrosis-related genes that correlated with pathological evidence of glomerulosclerosis; however, decreased expression of TGF-beta1 argued against its role in lupus renal fibrosis.
Further studies are needed to corroborate the pathogenic role of TGF-beta1 in SLE patients and to identify the precise genetic elements controlling its production.