The peripheral blood FOXP3+ T-cell frequency among CD4+ T cells is altered in SLE patients with the active disease activity. Therefore, the analysis on peripheral blood FOXP3+ T cells may be useful for the evaluation of lupus disease activity.

No abstract

B and T lymphocyte attenuator (BTLA) is an immuno-inhibitory receptor with the ability to deliver inhibitory signal for suppressing lymphocyte activation. To test the potential association of the human BTLA gene with the development of rheumatoid arthritis (RA), a genetic case-control association study was conducted, by using a single nucleotide polymorphism (SNP), C+800T SNP, in the exon 5 of the human BTLA gene for genotyping 93 RA patients and 294 normal control individuals. The results showed that there is statistically significant difference in the genotype distributions between RA and control groups (p = 0.022). When compared with the heterozygous genotype (C/T genotype), the homozygous genotype (C/C or T/T genotype) appears to confer the increased risk of the RA susceptibility with the odds ratio of 1.88 (p = 0.015). These data indicate the significant association between the C+800T SNP in the BTLA gene with the RA susceptibility.

The expression of IL-28, a T-cell autocrine factor, is dysregulated in patients with SLE, supporting the possibility that IL-28 may contribute to some of the SLE pathogenesis.

Being expressed in immune cells, cytokine-inducible SH2 protein (CIS) and suppressors of cytokine signaling proteins, SOCS1, SOCS2 and SOCS3, can regulate cytokine signaling and immune responses. To evaluate the possible expressional dysregulation of CIS, SOCS1, SOCS2 and SOCS3 in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients, the transcript levels of these genes in peripheral blood mononuclear cells (PBMCs) from SLE and RA patients were determined and statistically compared with those in PBMCs from normal individuals. It was found that SLE patients with the active disease activity significantly express higher CIS transcript levels than normal individuals and SLE patients with the inactive disease activity, whereas the difference in SOCS1, SOCS2 and SOCS3 transcript levels between normal individuals and SLE patients is not statistically significant. However, transcript levels of these CIS/SOCS genes in RA patients were not significantly different from those in normal individuals, except that treatment with a TNF-alpha-blocking agent in RA patients appears to enhance the CIS transcript expression, but down-regulates the SOCS2 transcript expression in PBMCs. These data suggest that CIS can serve as an SLE disease marker and may be involved in the pathogenesis of SLE, and that TNF-alpha may play an important role in the regulation of CIS and SOCS2 gene expression in PBMCs in vivo.