Yokoi Hidetoshi, Streilein J Wayne
The Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.
Ocul Immunol Inflamm. 2004 Jun;12(2):101-14. doi: 10.1080/09273940490895317.
To identify the means by which in-vitro-generated regulatory T cells, similar to those in anterior chamber-associated immune deviation (ACAID), suppress antigen-specific T-cell responses.
T regulators (T regs), generated by stimulating ovalbumin (OVA)-specific Tcr transgenic DO11.10 T cells with OVA-pulsed, TGF-beta2-treated peritoneal exudates cells (PEC), or their supernatants were added to OVA-pulsed PEC that were used to activate DO11.10 T cells in vitro or to suppress OVA-specific delayed hypersensitivity (DH) induction in vivo.
OVA-pulsed PECs exposed in vitro to TGF-beta-producing T regs or their supernatants failed to activate DO11.10 T cells in vitro, and suppressed DH in mice immunized with OVA plus adjuvant.
T cells exposed to TGF-beta2-pretreated, antigen-pulsed PECs secrete soluble factors, including active TGF-beta that regulate OVA-specific responses by forcing antigen-presenting cells to promote deviant T-cell activation in vitro and in vivo.
确定体外产生的调节性T细胞(类似于前房相关免疫偏离(ACAID)中的调节性T细胞)抑制抗原特异性T细胞反应的方式。
用卵清蛋白(OVA)脉冲处理、经转化生长因子-β2(TGF-β2)处理的腹腔渗出细胞(PEC)或其上清液刺激OVA特异性T细胞受体转基因DO11.10 T细胞产生的调节性T细胞(Tregs),被添加到OVA脉冲处理的PEC中,这些PEC用于在体外激活DO11.10 T细胞或在体内抑制OVA特异性迟发型超敏反应(DH)的诱导。
体外暴露于产生TGF-β的Tregs或其上清液的OVA脉冲处理的PEC,在体外未能激活DO11.10 T细胞,并抑制了用OVA加佐剂免疫的小鼠的DH。
暴露于TGF-β2预处理、抗原脉冲处理的PEC的T细胞分泌可溶性因子,包括活性TGF-β,其通过迫使抗原呈递细胞在体外和体内促进异常T细胞活化来调节OVA特异性反应。