Stem cell-like memory T cells:Role in viral infections and autoimmunity

Stem cell-like memory T(TSCM)cells possess stem cell properties including multipotency and self-renewal and are being recognized as emerging players in various human diseases.Advanced technologies such as multiparametric flowcytometry and single cell sequencing have enabled their identification and molecular characterization.In case of chronic viral diseases such as human immunodeficiency virus-1,CD4+T_(SCM) cells,serve as major reservoirs of the latent virus.However,during immune activation and functional exhaustion of effector T cells,these cells also possess the potential to replenish the pool of functional effector cells to curtail the infection.More recently,these cells are speculated to play important role in protective immunity following acute viral infections such as coronavirus disease 2019 and might be amenable for therapeutics by ex vivo expansion.Similarly,studies are also investigating their pathological role in driving autoimmune responses.However,there are several gaps in the understanding of the role of T_(SCM) cells in viral and autoimmune diseases to make them potential therapeutic targets.In this minireview,we have attempted an updated compilation of the dyadic role of these complex T_(SCM) cells during such human diseases along with their biology and transcriptional programs.

吉兰-巴雷综合征患者外周血记忆性T细胞和记忆性B细胞亚群的变化及其临床意义

目的探讨吉兰-巴雷综合征(Guillain-Barrésyndrome,GBS)患者外周血记忆性T细胞和记忆性B细胞亚群的变化及其临床意义。方法选取2018年6月至2020年12月于徐州医科大学附属医院神经内科住院的16例GBS患者作为研究组,并选取同期16名来院的健康体检者作为对照组。流式细胞术检测两组入选者的外周血T细胞亚群,包括CD4^(+)初始T细胞(naive T cells,TN)、CD4^(+)中央记忆性T细胞(central memory T cells,TCM)、CD4^(+)效应记忆性T细胞(effector memory T cells,TEM)和CD4^(+)终末分化效应记忆性T细胞(terminally differentiated effector memory T cells,TEMRA)及记忆性B细胞、浆母细胞的占比并分析其临床价值。结果与对照组相比,研究组患者的CD4^(+)TN及CD8^(+)TN均明显下降(P<0.05),CD4^(+)TEM及CD8^(+)TEM均明显升高(P<0.05),TCM及TEMRA在CD4和CD8上的比例比较,差异无统计学意义(P>0.05)。与对照组相比,研究组记忆性B细胞比例明显升高(P<0.05),两组患者间浆母细胞占比比较,差异无统计学意义(P>0.05)。GBS患者外周血CD4^(+)TEM及CD8^(+)TEM占比与Hughes残疾评分、脑脊液蛋白、脑脊液免疫球蛋白G及记忆性B细胞占比均呈正相关(P<0.05)。结论GBS患者存在记忆性T细胞和记忆性B细胞亚群免疫紊乱,CD4^(+)TEM细胞、CD8^(+)TEM细胞及记忆性B细胞占比升高,这很可能是GBS发病过程中重要的外周免疫机制。

人外周血卡介苗(BCG)特异性中央型和效应型记忆CD4^+ T细胞的特征

目的:探讨正常人外周血BCG特异性记忆T细胞的特征。方法:分离PPD-和PPD+正常人PBMCs,与BCG进行培养,采用ELISA法检测细胞培养上清液中IFN-γ的水平,ELISPOT法检测分泌IFN-γ的细胞数,利用流式细胞仪在单个细胞水平上检测细胞表面分子及细胞内因子IFN-γ和IL-2的表达及其关系。结果:当BCG刺激后,PPD-正常人PBMCs不产生或只产生少量的IFN-γ,而PPD+者IFN-γ产生的量和细胞数均明显增加(P<0·05)。流式细胞检测分析的结果表明,当BCG刺激后,主要是CD4+而非CD8+T细胞表达IFN-γ和IL-2,两者相比具有显著差异。在CD4+T细胞中单独产生IFN-γ的细胞占大多数,其次为IFN-γ和IL-2双阳性细胞,只产生IL-2的细胞占少数。此外,85%~95%以上的CD4+IFN-γ+T细胞为CD45RO+,其中60%以上的细胞为CCR7+,其余的为CCR7-。同样地,80%~95%左右的细胞为CD62L-。结论:BCG可以诱导抗原特异性记忆CD4+T细胞的产生,其中大多数为中央型记忆CD4+T细胞,少数为效应记忆CD4+T细胞,提示其在预防和控制结核分枝杆菌感染中发挥重要作用。

初始CD4^+T和记忆性Th1细胞在淋巴器官的分布和IFN-γ的表达

目的比较观察抗原特异性初始CD4+T细胞和效应性/记忆性Th1细胞在体内外IFN-γ的产生和在淋巴组织的分布。方法将标记相同数量的OVA-抗原受体转基因小鼠(OVA-TCR-Tg)的初始CD4+T细胞和Th1细胞被动输给正常小鼠后,利用流式细胞仪在单个细胞水平上观察初始CD4+T细胞和Th1细胞在体内淋巴组织器官的分布和IFN-γ的产生。结果体外经抗原刺激后,大于98%的Th1细胞和4.1%的初始CD4+T细胞表达IFN-γ。当被动输入机体后,初始CD4+T细胞主要分布于淋巴结,而Th1细胞主要分布于脾脏。当再次受到抗原的刺激后,记忆性Th1细胞能迅速产生IFN-γ。初始CD4+T细胞与效应/记忆Th1细胞在淋巴结和脾脏不同的分布,可能与CD62L的表达有关。结论本研究在我们以前研究的基础上进一步探讨了CD4+T细胞和记忆性Th1细胞的差异。此结果为进一步揭示初始CD4+T细胞与Th1细胞的差异提供了实验和理论依据。

CD4＋CD25＋调节性T细胞与衰老关系的研究进展

衰老伴随着免疫系统多种功能和表型的改变，使机体免疫力下降。CD4＋CD25＋调节性T细胞址体内具有免疫抑制活性的一群细胞，它在维持自身内环境稳定、抑制移植排斥反应以及防止自身免疫忤疾病的发生等方面发挥重要的保护作用，同时也是免疫力衰退的重要因素之一。调节性T细胞在机体衰老过程中发生变化，并发挥重要的作用。现将衰老过程中调节性T细胞的数量、功能、表型等的变化，以及调节性T细胞与老年相关性疾病的关系进行综述。

记忆性T细胞和HIV疫苗

HIV疫苗被认为是预防艾滋病的最有效工具。以前研制的HIV疫苗,大多数能诱导机体产生记忆性B淋巴细胞和持久的抗体,但并不能保护机体免受HIV的感染。记忆性T细胞的研究给研究HIV疫苗提供了新思路。本文着重描述了记忆性T细胞的分群、分化、形成和维持的一般规律及其在HIV疫苗研制中的意义。

慢性乙型肝炎患者外周血中记忆T细胞亚群分布研究

目的了解慢性乙型病毒性肝炎患者外周血中CD4+、CD8+T细胞的分布,以及相应记忆细胞亚群的表达水平,为研究记忆T淋巴细胞在抗乙肝病毒感染中的作用提供基础。方法采用多色流式细胞仪检测技术,检测慢性乙肝病例和健康对照外周血单个核细胞(PBMC)中T淋巴细胞表面标志CD3、CD4、CD8、CD45RO、CD62L、CCR7的表达情况。结果乙肝组CD4+、CD8+T淋巴细胞分别占外周血PBMC的(11.56±5.78)%、(13.11±6.64)%,均低于对照组,差异均有统计学意义(P值均<0.05)。乙肝组和对照组外周血PBMC中,CD4+TEM的表达水平高于CD4+TCM,CD8+TEM的表达水平高于CD8+TCM,差异均有统计学意义(P值均<0.05);CD4+TEM、CD4+TCM所占CD4+Tm的比例,差异均无统计学意义(P值均>0.05);CD8+TEM、CD8+TCM所占CD8+Tm的比例差异无统计学意义(P值均>0.05)。结论慢性乙肝病例外周血PBMC中,CD4+、CD8+T淋巴细胞均减少。对照组和乙肝组外周血PBMC中,CD4+、CD8+T记忆淋巴细胞均以TEM为主。

维生素C对CD4＋效应记忆性T细胞体外扩增的影响

目的:探讨小分子药物维生素C(VC)对CD4+效应记忆性T细胞(TEM)体外扩增的影响从而改善过继免疫治疗的效果。方法:体外分离正常人的外周血CD4+T淋巴细胞,将细胞分为2组(实验组和对照组)进行细胞培养。实验组加入VC后,通过细胞计数仪和流式细胞仪对2组细胞中TEM的扩增情况进行检测。结果:(1)在CD4+T细胞体外扩增实验中,VC对CD4+T细胞的总数无显著影响。(2)VC使TEM在CD4+T细胞中的比例显著升高,100 mg/L为扩增的最佳浓度。(3)在CD4+T细胞扩增的第10天检测其中TEM的细胞数量,对照组TEM的数量为(1.22±0.15)×106,实验组TEM的数量为(3.56±0.35)×106,两者的差异有统计学意义(P<0.01)。结论:VC可有效地促进CD4+TEM的体外扩增,为过继免疫治疗提供简单、安全及有效的体外扩增方法。

CD8^+ T细胞活化与分化的分子机制

CD8^+ T细胞识别由MHCⅠ分子递呈的抗原肽,由于大多数有核细胞都表达MHCⅠ分子,因此CD8^+ T细胞在清除被病毒、胞内菌、寄生虫等感染的细胞或突变的肿瘤细胞中发挥着重要作用。识别病原微生物等抗原后,CD8^+ T细胞活化并分化形成多种类型的效应和记忆细胞,不仅能及时清除被感染的细胞,也能形成长期保护。各亚群CD8^+ T细胞的表面分子、功能和定位不同,细胞存活的时间、再次感染时的增殖能力和效应功能也有所差别。本文主要讨论CD8^+ T细胞如何受到多条信号通路和转录因子调控,活化和分化成不同类型的效应和记忆细胞,并对临床应用T细胞抵御肿瘤和病原微生物的进展作一简单概述。

IL-15 increases the frequency of effectormemory CD8^(+) T cells in rhesus monkeys immunized with HIV vaccine

Several studies have suggested that interleukin(IL)-15 is a promising adjuvant that promotes cellular immunity when administered with human immunodeficiency virus(HIV)vaccine.Here we evaluated the effect of IL-15 plasmid on HIV-specific immune responses,especially cellular immunity,in eight rhesus monkeys.These monkeys were immunized three times with HIV DNA vaccine with or without IL-15 plasmid and boosted with recombinant Tiantan strain vaccinia virus-based HIV vaccine(rTV)22 weeks after the first immunization.Although we did not detect any significant differences in the HIV-specific CD81 T-cell response between monkeys with IL-15 coimmunization and monkeys with HIV vaccine alone,our results showed that the frequency of effector CD8^(+) memory T cells in the peripheral blood was significantly higher in monkeys with IL-15 coimmunization than those with HIV vaccine alone at almost all of the time points examined.Furthermore,the titers of anti-HIV antibodies were higher in Group T than those in Group C after rTV boosting.These findings in rhesus monkeys suggest that IL-15 may be useful as a cytokine adjuvant for HIV vaccine.

Origin of CD8^+ Effector and Memory T Cell Subsets

It is well accepted that CD8＋ T cells play a pivotal role in providing protection against infection with intracellular pathogens and some tumors. In many cases protective immunity is maintained for long periods of time （immunological memory）. Over the past years, it has become evident that in order to fulfill these multiple tasks, distinct subsets of effector and memory T cells have to be generated. Until today, however, little is known about the underlying mechanisms of subset differentiation and the timing of lineage fate decisions. In this context, it is of special importance to determine at which level of clonal expansion functional and phenotypical heterogeneity is achieved. Different models for T cell subset diversification have been proposed; these differ mainly in the time point during priming and clonal expansion （prior, during, or beyond the first cell division） when differentiation programs are induced. Recently developed single-cell adoptive transfer technology has allowed us to demonstrate that individual precursor cell still bears the full plasticity to develop into a plethora different T cell subsets. This observation targets the shaping of T cell subset differentiation towards factors that are still operative beyond the first cell division. These findings have important implications for vaccine development, as the modulation of differentiation patterns towards distinct subsets could become a powerful strategy to enhance the efficacy and quality of vaccines. Cellular ＆ Molecular Immunology.

TRAF2 regulates T cell immunity by maintaining a Tpl2-ERK survival signaling axis in effector and memory CD8 T cells

Generation and maintenance of antigen-specific effector and memory T cells are central events in immune responses against infections.We show that TNF receptor-associated factor 2(TRAF2)maintains a survival signaling axis in effector and memory CD8 T cells required for immune responses against infections.This signaling axis involves activation of Tpl2 and its downstream kinase ERK by NF-κB-inducing kinase(NIK)and degradation of the proapoptotic factor Bim.NIK mediates Tpl2 activation by stimulating the phosphorylation and degradation of the Tpl2 inhibitor p105.Interestingly,while NIK is required for Tpl2-ERK signaling under normal conditions,uncontrolled NIK activation due to loss of its negative regulator,TRAF2,causes constitutive degradation of p105 and Tpl2,leading to severe defects in ERK activation and effector/memory CD8 T cell survival.Thus,TRAF2 controls a previously unappreciated signaling axis mediating effector/memory CD8 T cell survival and protective immunity.

中央记忆T细胞和效应记忆T细胞亚群在肝癌患者外周血中分布特点分析

目的研究肝癌患者外周血中CD45RO^+记忆T细胞(memory T cells,Tm)表面标志CD45RO、CD62L和CCR7的表达,以了解CD45RO^+CD62L~^+CCR7^+T细胞(中央型记忆T细胞,central memory T cells,TCM)和CD45RO^+CD62L^-CCR7^-T细胞(效应型记忆T细胞,effector memory T cells,TEM)亚群在肝癌患者外周血中的分布特点。方法获取正常人健康志愿者(正常对照组)28例和2011年8月至2013年8月的初诊慢性乙型病毒性肝炎患者(乙肝对照组)28例以及同期患有乙肝的肝癌患者(乙肝肝癌组)30例的外周静脉血,分离外周血单个核细胞(PBMC)。用多色流式细胞仪检测技术(polychromatic flow cytometry,PFC)检测外周血PBMC中记忆T淋巴细胞表面标志CD3、CD4、CD8、CD45RO、CD62L、CCR7的表达情况。结果乙肝肝癌组外周血PBMC中,CD4^+T淋巴细胞和CD8^+T淋巴细胞分别占外周血PBMC的比例显著高于乙肝对照组(28.15±12.32 VS 11.56±5.78,29.33±15.54 VS 13.11±6.64)(P<0.001,P=0.019);而较正常对照组无明显差异。乙肝肝癌组外周血PBMC的T淋巴细胞中CD4^+T_(EM)占CD4^+T记忆淋巴细胞比例显著高于乙肝对照组、正常对照组(93.78±5.63 VS 75.82±19.74,93.78±5.63 VS 68.25±15.65)(P=0.001,P=0.018),而CD4+TCM则显著低于乙肝对照组、正常对照组(0.55±1.02 VS 4.87±6.28,0.55±1.02VS 4.16±3.49)(P均小于<0.001)。三组的CD4^+TEM记忆细胞占外周血PBMC中CD4^+T记忆淋巴细胞的比例显著高于CD4^+T_(CM)记忆细胞占外周血PBMC中CD4^+T记忆淋巴细胞的比例(91.78±5.63 VS 0.55±1.02,75.82±19.74 VS 4.87±6.28,68.25±15.65 VS 4.16±3.49)(P值均小于0.001)。乙肝肝癌组外周血PBMC的T淋巴细胞中CD8^+TEM和CD8^+TCM占CD8^+T记忆淋巴细胞比例与乙肝对照组、正常对照组相比,差异均无显著意义。三组的CD8+TEM记忆细胞占外周血PBMC中CD8^+T记忆淋巴细胞的比例显著高于CD8^+TCM记忆细胞占外周血PBMC中CD8^+T记忆淋巴细胞的比例(80.12±13.56 VS 3.25±2.47,79.21±11.34 VS 4.44±7.19,73.33±16.88 VS 2.66±3.10)(P值均小于0.001)。结论在乙肝肝癌组、乙肝对照组和正常对照组中,无论是CD4^+T记忆淋巴细胞,还是CD8^+T记忆淋巴细胞,均以TEM占绝大多数,而TCM比例很小。乙肝肝癌组中,CD4^+TEM显著高于乙肝对照组和正常对照组,CD4^+TCM显著低于乙肝对照组和正常对照组,而CD8^+TEM和CD8^+TCM则与乙肝对照组、正常对照组均无明显差异。

Defect of CD8^+ Memory T Cells Developed in Absence of IL-12 Priming for Secondary Expansion

IL-12 priming plays an important role in stimulation of CD8^＋ effector T cells and development of CD8^＋ memory T （Tm） cells. However, the functional alteration of CD8^＋ Tm cells developed in the absence of IL-12 priming is elusive. In this study, we investigated the capacity of secondary expansion of CD8~ Tm cells developed from transgenic OT I CD8^＋ T cells. The latter cells were in vitro and in vivo stimulated by ovalbumin （OVA）-pulsed dendritic cells [DCovA and （IL-12^-/-）DCovA] derived from wild-type C57BL/6 and IL-12 gene knockout mice, respectively. We demonstrated that IL-12 priming is important not only in CD8^＋ T cell clonal expansion, but also in generation of CD8^＋ Tm cells with the capacity of secondary expansion upon antigen re-encounter. However, IL-12 signaling is not involved in CD8^＋ Tm cell survival and recall responses. Therefore, this study provides useful information for vaccine design and development. Cellular ＆ Molecular Immunology.

Mettl3依赖的m^(6)A甲基化调控CD8^(+)T细胞效应分化和记忆形成

Efficient immune responses rely on the proper differentiation of CD8^(+)T cells into effector and memory cells.Here,we show a critical requirement of N^6-Methyladenosine(m^(6)A)methyltransferase Mettl3 during CD8^(+)T cell responses upon acute viral infection.Conditional deletion of Mettl3 in CD8^(+)T cells impairs effector expansion and terminal differentiation in an m^(6)A-dependent manner,subsequently affecting memory formation and the secondary response of CD8^(+)T cells.Our combined RNA-seq and m^(6)AmiCLIP-seq analyses reveal that Mettl3 deficiency broadly impacts the expression of cell cycle and transcriptional regulators.Remarkably,Mettl3 binds to the Tbx21 transcript and stabilizes it,promoting effector differentiation of CD8^(+)T cells.Moreover,ectopic expression of T-bet partially restores the defects in CD8^(+)T cell differentiation in the absence of Mettl3.Thus,our study highlights the role of Mettl3 in regulating multiple target genes in an m^(6)A-dependent manner and underscores the importance of m^(6)A modification during CD8^(+)T cell response.

Role of Triggering Receptor Expressed on Myeloid Cell-1 Expression in Mammalian Target of Rapamycin Modulation of CD8＋ T-cell Differentiation during the Immune Response to Invasive Pulmonary Aspergillosis

Background： Triggering receptor expressed on myeloid cell- 1 （TREM- 1） may play a vital role in mammalian target ofrapamycin （mTOR） modulation ofCD8＋ T-cell differentiation through the transcription factors T-box expressed in T-cells and eomesodermin during the immune response to invasive pulmonary aspergillosis （IPA）. This study aimed to investigate whether the roTOR signaling pathway modulates the proliferation and differentiation of CD8＋ T-cells during the immune response to I PA and the role TREM-1 plays in this process. Methods： Cyclophosphamide （CTX） was injected intraperitoneally, and Asl？e;gillus.[mnigams spore suspension was inoculated intranasally to establish the immunosuppressed IPA mouse model. After inoculation, rapamycin （2 mg-kg ·d -1） or interleukin （IL）-12 （5 μg/kg every other day） was given for 7 days. The number of CD8＋ effector memory T-cells （Tern）, expression of interferon （IFN）-y, roTOR, and ribosomal protein $6 kinase （S6K）, and the levels of IL-6, IL- 10, galactomannan （GM）, and soluble TREM- 1 （sTREM-I） were measured. Results： Viable A. fumigatus was cultured from the lung tissue of the inoculated mice. Histological examination indicated greater inflammation, hemorrhage, and lung tissue injury in both IPA and CTX ＋ IPA mice groups. The expression of mTOR and S6K was significantly increased in the CTX ＋ IPA ＋ I L- 12 group compared with the control, I PA （P = 0.01 ; P - 0.001 ）, and CTX ＋ 1PA （P = 0.034; P = 0.032） groups, but significantly decreased in the CTX ＋ IPA ＋ RAPA group （P 〈 0.001 ）. Compared with the CTX ＋ IPA group, the proportion of Tern, expression of IFN-y, and the level ofsTREM-I were significantly higher after IL-12 treatment （P = 0.024, P = 0.032, and P = 0.017, respectively）, and the opposite results were observed when the roTOR pathway was blocked by rapamycin （P 〈 0.001）. Compared with the CTX ＋ I PA and CTX ＋ I PA ＋ RAPA groups, IL-12 treatment increased IL-6 and downregulated IL- 10 as well as G M, which strengthened the immune response to the IPA infection. Conclusions： mTOR modulates CD8＋ T-cell differentiation during the immune response to IPA. TREM-1 may play a vital role in signal transduction between mTOR and the downstream immune response.

Mechanisms underlying lineage commitment and plasticity of human yo T cells

Phenotypic and functional heterogeneity are the hallmarks of effector and memory T cells. Upon antigen stimulation, y T cells differentiate into two major types of memory T cells： central memory cells, which patrol the blood and secondary lymphoid organs, and effector memory cells, which migrate to peripheral tissues, y T cells display in vitroa certain degree of plasticity in their function that is reminiscent of that which is observed in conventional CD4 T cells. Similar to CD4 T cells, in which a plethora of specialized subsets affect the host response, y8 T cells may readily and rapidly assume distinct Thl-, Th2-, Th17-, TFH and T regulatory-like effector functions, suggesting that they profoundly influence cell-mediated and humoral immune responses. In addition to differences in cytokine repertoire, y~ T cells exhibit diversity in homing, such as migration to lymph node follicles, to help B cells versus migration to inflamed tissues. Here, we review our current understanding of y T-cell lineage heterogeneity and flexibility, with an emphasis on the human system, and propose a classification of effector y T cells based on distinct functional phenotypes.

Enhancement of antitumor immunity by low-dose total body irradiation is associated with selectively decreasing the proportion and number of T regulatory cells

Low-dose total body irradiation （LTBI） is used in the treatment of some cancers mainly for immune enhancement rather than cell killing. However, the mechanism underlying LTBI remains unknown. In this study, by analyzing the immune patterns of lymphocytes, we found that the percentage and absolute number of CD4^＋CD25^＋Foxp3^＋ regulatory T cells are markedly decreased in naive mice following treatment with LTBI. On the contrary, the CD4^＋CD44^＋/CD8^＋CD44^＋ effector-memory T cells are greatly increased. Importantly, naive mice treated with dendritic cell-gp100 tumor vaccines under LTBI induced an enhancement of antigen-specific proliferation and cytotoxicity as well as interferon-γ, （IFN-γ） secretion against FIO melanoma tumor challenge, compared to treatment with either the tumor vaccine or LTBI alone. Consequently, the treatment resulted in a reduced tumor burden and prolonged mouse survival. Our data demonstrate that LTBI＇s enhancement of antitumor immunity was mainly associated with selectively decreasing the proportion and number of T regulatory cells, implying the potential application of the combination of LTBI and a tumor vaccine in antitumor therapy.

肿瘤特异性CD8^(+)T细胞分化及调控机制的研究进展

肿瘤特异性CD8^(+)T细胞是抗肿瘤免疫应答的主要效应细胞之一,其分化状态与免疫应答强度、对免疫疗法的响应程度密切相关。在肿瘤病程中,CD8^(+)T细胞往往呈现耗竭状态,主要表现为效应功能降低和增殖能力下降。近几年,耗竭CD8^(+)T细胞的高度异质性特征备受关注,其中记忆、效应和终末耗竭表型是当下考察肿瘤特异性CD8^(+)T细胞分化状态的3个重要维度。伴随肿瘤进展,肿瘤特异性CD8^(+)T细胞的干性、效应表型逐渐丢失,最终分化为终末耗竭细胞,表观遗传学变化和代谢重编程参与调控这一过程,另外肿瘤微环境中复杂多样的免疫抑制性信号加速了这一过程的发生。本文综述了肿瘤特异性CD8^(+)T细胞激活后的命运以及不同分化状态的分子标志物和转录调控分子、影响分化状态的因素、与免疫疗法响应相关的标志物、调控CD8^(+)T细胞增强抗肿瘤作用的应用等方面近年来的研究进展,以期为更加精准地调控CD8^(+)T细胞表型,增强抗肿瘤免疫应答等研究提供参考。

记忆性T细胞亚类的研究进展

T细胞免疫对于调节抗体的生成及清除受感染的细胞均发挥相当重要的作用。记忆性T细胞的特点是在初次免疫反应完成后仍能长期存活,并形成不同的亚类,每一亚类细胞又分为中枢记忆性T细胞和效应记忆性T细胞。这些记忆性T细胞在宿主体内长期存在,当宿主受到再次感染时可提供有效的保护作用。本文结合最新研究进展,对主要的记忆性T细胞(如CD8+和CD4+记忆性细胞)类型及其功能作一综述。