PubMed · 2011 · 19 citations · 0 references
T-regulatory CellImmunologyPathologyRegulatory T CellsImmunotherapyHelper T-cell InvolvementImmune DysregulationInflammationRheumatoid DisorderInflammatory Rheumatic DiseaseRheumatoid ArthritisRheumatologySystemic Autoimmune DiseasesAllergyAutoimmune DiseaseSystemic Lupus ErythematosusSelf-toleranceAutoimmunityImmunologic DiseaseTh1/th2 CytokinesRegulatory T Cell TherapiesLupusCellular Immune ResponseMedicine
The study aimed to evaluate the T‑CD4⁺/T‑CD8⁺ ratio, regulatory T‑cell status, and TH1/TH2 cytokine profiles (IFN‑γ, IL‑2, IL‑4, IL‑6) in systemic autoimmune diseases. The authors quantified helper T‑cell responses in 14 SLE and 7 RA patients to assess cell‑based immune activity in SAID. SLE patients exhibited markedly reduced Treg levels compared to RA and controls, while T‑CD4⁺/T‑CD8⁺ ratios were similar across groups; SAID patients showed low IFN‑γ, elevated IL‑2 and IL‑6, and the data suggest Treg percentage is the sole reliable cellular marker, with TH2 dominance in SLE and TH1 in RA.
We assessed Helper T-cell involvement and possibilities to quantify the cell-based immune response in systemic autoimmune diseases (SAID) in 14 systemic lupus erythematosus (SLE) and 7 rheumatoid arthritis (RA) patients. The goals of investigation were T-CD4+/T-CD8+ ratio, regulatory T cells (Treg) status and TH1/TH2 serum cytokine profiles (IFN-gamma and IL-2, respectively IL-4 and IL-6). SLE group proved significant decreased average Treg value as compared to RA group and controls and showed significant low Treg incidence (86% patients). The distribution of high T-CD4+/T-CD8+ ratio registered no significant distinction among LES and RA groups. SAID patients presented low serum IFN-gamma (86% RA, 60% SLE), high IL-2 (57% RA) and high IL-6 (53% LES), but no significant IL-4 modification. We conclude that Treg percentage remains the only cellular criterion for SAID immune evaluation. In the same time, different secretion mechanisms seem to be involved in SAID, i.e. TH2 in SLE and TH1 in RA.