国际免疫学杂志
國際免疫學雜誌
국제면역학잡지
INTERNATIONAL JOURNAL OF IMMUNOLOGY
2008年
4期
279-283
,共1页
感染免疫%慢性病毒感染%PD-1
感染免疫%慢性病毒感染%PD-1
감염면역%만성병독감염%PD-1
Infection immunology%Chronic viral infection%Programmed-Death-1(PD-1)
杀伤性T细胞(CTL)是病毒感染过程中主要的效应细胞.在急性病毒性感染中,CTL细胞通过杀伤病毒感染的细胞,分泌抗病毒细胞因子从而有效清除病毒.而在慢性病毒感染过程中,病毒特异性CTL发生克隆耗竭,细胞数量少,细胞功能受损,分泌细胞因子能力下降.目前证明,CD28家族成员Programmed Death-1(PD-1)是一种重要的细胞表面分子,能够抑制CTL细胞功能,参与外周免疫耐受,维持T细胞克隆耗竭,保护机体不受免疫病理损伤.在慢性病毒性感染中,T细胞表面的PD-1与其受体PD-L1/2结合后,传递抑制性信号,下调外周T细胞功能.阻断PD-1通路,能够重建CD8+T细胞功能,抑制病毒复制,促进病毒清除.因此,通过干扰PD-1/PD-L1抑制途径进行免疫调节,可能是处理慢性病毒感染性疾病的一个新方法.
殺傷性T細胞(CTL)是病毒感染過程中主要的效應細胞.在急性病毒性感染中,CTL細胞通過殺傷病毒感染的細胞,分泌抗病毒細胞因子從而有效清除病毒.而在慢性病毒感染過程中,病毒特異性CTL髮生剋隆耗竭,細胞數量少,細胞功能受損,分泌細胞因子能力下降.目前證明,CD28傢族成員Programmed Death-1(PD-1)是一種重要的細胞錶麵分子,能夠抑製CTL細胞功能,參與外週免疫耐受,維持T細胞剋隆耗竭,保護機體不受免疫病理損傷.在慢性病毒性感染中,T細胞錶麵的PD-1與其受體PD-L1/2結閤後,傳遞抑製性信號,下調外週T細胞功能.阻斷PD-1通路,能夠重建CD8+T細胞功能,抑製病毒複製,促進病毒清除.因此,通過榦擾PD-1/PD-L1抑製途徑進行免疫調節,可能是處理慢性病毒感染性疾病的一箇新方法.
살상성T세포(CTL)시병독감염과정중주요적효응세포.재급성병독성감염중,CTL세포통과살상병독감염적세포,분비항병독세포인자종이유효청제병독.이재만성병독감염과정중,병독특이성CTL발생극륭모갈,세포수량소,세포공능수손,분비세포인자능력하강.목전증명,CD28가족성원Programmed Death-1(PD-1)시일충중요적세포표면분자,능구억제CTL세포공능,삼여외주면역내수,유지T세포극륭모갈,보호궤체불수면역병리손상.재만성병독성감염중,T세포표면적PD-1여기수체PD-L1/2결합후,전체억제성신호,하조외주T세포공능.조단PD-1통로,능구중건CD8+T세포공능,억제병독복제,촉진병독청제.인차,통과간우PD-1/PD-L1억제도경진행면역조절,가능시처리만성병독감염성질병적일개신방법.
Cytotoxic T lymphocyte(CTL)is the most important effector cell type for the control of viral in-fection.In acute infection.specific CTLs effectively contribute to the viral clearance by destruction of virus infected ceUs and producton of antiviral cytokines.However,specific CTLs may be exhausted daring chronic viral infections with impaired functions like suppressed cytokine predutions.Recent studies demonstrated that Programmed Death-1(PD-1),a member of CD28 family,is an important factor that inhibits the function of CTLs and plays a role in the peripheral immunological tolerance.It takes part in the maintenance of T cell exhaustion and protects the host against immunopathegenesis.T-cells receive a negative signal when engaged with the PD-L1 ligand on the APC.This mechanism is responsible for the down-regulation of T-cell functions in the periphery during chronic viral infections.By blocking the PD-1/PD-L1 pathway.the function of CD8+ T cell could be restored,leading to the suppression of viral replication in chronically infected hosts.Thus,the immunomodulation by interfering with PD-1/PD-L1 pathway represents a new way to treat chronic viral infections.