| BackgroundPercutaneous carotid angioplasty and stenting (CAS) is being evaluated as a primaryalternative to the artery stenosis because of the potential of being minimally invasive, lesstraumatic. However, the procedure may inescapably damage the vascular wall whileenlarging the minimal lumen diameter. Several experimental studies have demonstrated thatlocal and systemic inflammation plays a pivotal role in the pathogenesis of ISR, promotingneointimal proliferation through the stent struts.Atherosclerosis is a chronic inflammatory disease of the arterial wall where both innateand adaptive immune responses contribute to disease initiation and progression. CD4~+Tcells play important roles in mediating inflammatory response, which can be classified intoTh1, Th2, Th17and regulatory T (Treg) cells, based on their distinct cytokine repertoire.Different CD4~+T cell subtypes have different roles in immune system, but they haveinteractions in maturation and functions, forming a network and maintaining a dynamicbalance.There have imbalance of the pro-and anti-inflammatory cytokines in the pathogenesisof intracranial atherosclerosis in patients with ICAS. Meanwhile, inflammation reactionexists after the stent implantation. Is the subset of the CD4~+T cells participated theinflammation after stenting, and can the severity of clinical symptoms influence theproportion of the CD4~+T cells. So we investigate the effects of CD4~+T cells on theinflammation after the stent implantation. Early intervention may be conducive to preventrestenosis and the secondary prevention.There are researches showed that the inflammation is increased after the coronary stentimplantation. What’s more, in patients with the coronary stent implantation, the Treg levelswere found to be significantly decreased. However, all the study are limited in the Tregsand to large extent from coronary stents, and the longest follow-up time is one month only. There are little known reffering to the CD4~+T cells subset after the intracranial and carotidatery stenting. In our study, periprocedural frequency of the CD4~+T cell subsets and theirprimary transcription factors and correlated cytokines were analyzed during clinicallong-term (3month) follow-up.PurposeTo investigate the expression of Treg cells, IL-17A and IFN-γ in the perepherial bloodcells of patients with cerebral stent implantation. In this study, we aimed to investigate theeffects of Treg cells，IL-17A and IFN-γ on the pathogenesis of the imflammation responseafter stent implantation.MethodsWe studied fifty patients with cerebral stent implantation were enrolled as theinvestigate subjects,30age-matched volunteers were selected as the control group. Flowcytometry was used to analyze the frequency of Treg cells and phenotype ofIL-17-producing and IFN-γ-producing T cells in the peripheral blood. Quantitative-PCRwas used to determine the expression of FOXP3, RORγt and T-bet in peripheral bloodmononuclear cell. The plasma levels of TGF-β, IL-17A, TNF-γ were measured by ELISA.ResultsThe frequency and signature transcriptional factors/cytokine production of Treg wasdecreased on the first week and returned to the control level3month after stentimplantation.However, we observed the opposite trends for Th17cells, which increased in acutephase and restored to the control level at3months. No significant difference of frequencyand signature transcriptional factors/cytokine for Th1cells was observed in patients beforeand after stent implantation.ConclusionWe speculate that the maintenance of the frequency and function of Treg is involved incontrolling the inflammation response, which otherwise causes the acute inflammation afterstent implantation. |
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