The effects of PBMCs-derived exosomes of ankylosing spondylitis patients on T cell profiles

Ankylosing spondylitis (AS) as a progressive inflammatory disease, usually affects the articulation of the axial skeleton. The accumulation of data indicates that T lymphocytes possess a major part in the pathogenesis of AS. Herein, we assessed the effect of PBMC exosomes from AS patients on the function and expression profile of normal T cells. Blood was obtained from individuals and exosomes were isolated from PBMCs. T cells were cultured and treated with PBMC exosomes to evaluate the expression and concentration of transcription factors and cytokines. Data revealed an increased expression of RORγt (1.232 ± 0.3527 fold versus 0.9220 ± 0.1727) STAT3 (1.242 ± 0.5935 fold versus 0.9052 ± 0.2497) and T-bet (1.230 ± 0.4558 fold versus 0.8580 ± 0.3406) in the group that treated with PBMC exosomes from AS compared to PBMC exosomes from healthy individuals. Moreover, the concentration and expression levels of cytokines including IL-17, IL-23, TNF-α, and IFN-γ were significantly increased in group that treated with PBMC exosomes from patients with AS. The expression level of FOXP3 (0.7092 ± 0.1902 fold versus 1.158 ± 0.6027), TGF-β (0.8236 ± 0.2831 fold versus 1.166 ± 0.5085) and IL-10 (0.7584 ± 0.1989 fold versus 1.209 ± 0.5317) were significantly decreased in the group that treated with PBMC exosomes from AS patients compared to healthy PBMC exosomes group, respectively. PBMC exosomes from AS patients could alter the T cell profile and induce normal T cells towards an inflammatory state by Th1 and Th17 transcription factors and cytokines upregulation, as well as Treg cytokines and transcription factors downregulation. • Ankylosing spondylitis (AS) is a chronic inflammatory disease that influence the axial skeleton and peripheral joints. • T cell-derived exosomes from AS patients could alter cytokines and expression profiles of normal T cells. • Exosomes driven from T cells of AS patients induce normal T cells towards inflammatory state. • Exosomes driven from T cells of AS patients upregulate RORγt, STAT3, T-bet and also IL-17, IL-23, TNF-α, and IFN-γ.