移植耐受

摘要： 记忆性T细胞(Tm)是获得性免疫反应的产物,是抵御病原体入侵的重要效应成分,能为机体提供长期免疫保护.但对于移植患者来说,其存在可能对移植物存活产生负面影响.最近有关Tm在产生机制、稳态调控、亚群异质性、细胞耗竭等方面的研究取得了重大进展,使以Tm为靶点的免疫治疗成为移植领域中一项具有挑战性的任务.本文综述了Tm的生物学特征及其对移植耐受的影响.

摘要： 心脏移植是心脏疾病终末阶段最有效的治疗方法,心脏移植后能否长期存活依然是一个挑战,移植排斥是影响移植物存活的主要障碍,早期发现亚临床排斥可显著提高移植排斥的诊断并对及时指导调整排斥药物治疗剂量有重要意义.长链非编码RNAs(lncRNAs)是长度>200个氨基酸的非编码RNAs,调节基因表达分化和发育过程.LncRNAs在心脏移植中存在差异表达并可能参与调节免疫反应和移植结果,有可能成为心脏移植状态标志物和改善移植结果的新治疗目标.现就近年来lncRNAs在心脏移植中研究进展做简要综述.

摘要： 目的:研究体外模拟异基因移植环境下,碳二亚胺(ECDI)偶联的供者抗原提呈细胞(ECDI-APCs)诱导受者T细胞针对供者抗原特异性耐受的效果.方法:每组以HLA-A、-B、-DR完全错配的3名志愿者外周血淋巴细胞建立混合淋巴细胞培养体系,模拟异基因移植环境.在-6 d将受者外周血单个核细胞(PBMCs)与供者ECDI-APCs共培养,第0天再次加入新鲜分离的原供者APCs或无关供者APCs模拟移植,第8天以流式细胞术检测受者T细胞的增殖情况.结果:ECDI偶联浓度为150 mg/ml,供、受者细胞共培养比例为0.1:1时,ECDI-APCs可诱导出受者T细胞对原供者抗原刺激的耐受状态(P0.05).结论:ECDI-APCs能诱导CD8+T细胞对同种异体抗原刺激的耐受状态,并且具有供者抗原特异性,可为临床器官移植术后供者抗原特异性耐受的建立提供实验依据.

摘要： 芳香烃受体(AhR)是一种配体依赖性胞内受体,配体种类多样,根据来源可分为外源性和内源性配体.不同配体结合并激活AhR,可使AhR转位至核上,调节下游基因如细胞色素P450家族基因CYP1转录活动,在介导病理过程和维持机体正常发育与生理功能中发挥着重要作用.色氨酸(Trp)代谢产物是一类主要的内源性配体.犬尿氨酸(Kyn)作为Trp代谢的主要产物,与AhR相互作用后可影响免疫细胞分化与活性,调节机体适应性免疫应答,发挥抑制抗肿瘤免疫的作用.近年来Kyn在移植免疫中的作用也越来越引人瞩目.本文将对AhR在Trp代谢调节免疫中作用的研究进展进行综述.%Aromatic hydrocarbon receptor (AhR),an intracellular receptor,contains multiple ligand binding sites.Various ligands of AhR are divided into exogenous and endogenous ligands according to the origination.Different ligands bind and activate AhR,regulating the transcription of downstream target genes,especially CYP1 from Cypcytochrome P450 gene family,which plays an essential role in different pathological problems,as well as in the normal development and function of organism.Kynurenine(Kyn),a key metabolic product of tryptophan (Trp),metabolic products of which are major types of endogenous ligands of AhR,has an impact on adaptive immune by manipulating the polarization and activity of immunocytes.Kyn has been focus for its supressive effect in anti-tumor immunity and raised concern recently for its intriguing role in allograft immunoregulation.Research advances in the role of AhR in immunoregulation related to tryptophan metabolism will be illustrated in this review in detail.

摘要： 目的 探讨在联合抗Tim-1/抗CD45RB抗体诱导的移植耐受中调节性B细胞(Bregs)与调节性T细胞(Tregs)的关系.方法 建立BALB/c小鼠到C57BL/6小鼠的同种胰岛移植长期耐受模型,将长期耐受小鼠(LTS)的B细胞过继输注至接受胰岛移植的B细胞缺陷小鼠(μMT-/-)体内,或加用抗CD25抗体(PC61)去除CD25+ Treg细胞,观察移植物的存活时间,用流式细胞仪检测Foxp3+ Treg数量变化.将CD4+ Foxp3-GFP-T细胞与Bregs细胞联合过继输注RAG小鼠体内,检测Foxp3+GFP+T细胞的扩增情况.建立小鼠皮肤移植模型,在双抗体治疗的同时加用抗CD20抗体祛除B细胞,观察对Tregs数量的影响.结果 继承性转移长期耐受小鼠的Bregs可诱导83.3％的小鼠长期耐受,但加用抗CD25单抗后,胰岛移植物在较短时间(MST=20 d)内全部被排斥;继承性转移长期耐受小鼠Bregs可使Tregs数量明显增加(P＜0.01),并且可诱导CD4+ Foxp-T细胞表达Foxp3;用抗CD20抗体祛除B细胞后,双抗体诱导的皮肤移植受体小鼠体内Tregs数量明显减少(P＜0.01).结论 在双抗体诱导的移植耐受中,Bregs可能通过促进Tregs生成而延长移植物的存活.%Objective To investigate the relationship between regulatory B cells (Bregs) and regulatory T cells(Tregs) in transplantation tolerance induced by dual anti-CD45RB/anti-TIM-1 antibody.Methods The longterm murine islet allograft transplant models from BALB/c to C57BL/6 were established.B cells purified from longterm survivors (LTS)were adoptively transferred to grafted B cell-deficient μMT-/-B6 recipients and treated with or without PC61.The allograft survival time was analyzed and the number of Foxp3+ Treg cells was examined by flow cytometry.Murine skin allograft transplant models was established and treated with dual antibody.The change of the percentage of Treg cells was observed after B-cell depletion using anti-CD20 antibody.Results Adoptive transfer of Bregs in longterm tolerated murines could induce longterm tolerance in 83.3 ％ of murines.But after adding CD25m monoclonal antibody,islet grafts were completely rejected in a short time(MST=20 d);adoptive transfer of Bregs in longterm tolerated murines could increase the Tregs number(P＜0.01),moreover could induce CD4+ Foxp-T cell to express Foxp3;after deleting B cells with CD20 antobody,Tregs cells number in the skin transplant recipient murine induced by dual antibody was remarkably reduced (P＜0.01).Conclusion In transplantation tolerance induced by dual antibody,Breg cells may prolong the graft survival time possibly through promoting Treg generation.

摘要： 目的 探讨诱导CD4+Foxp3+调节性T细胞(regulatory T cells,Tregs)表达的机制及其在移植耐受中可能的作用.方法 构建新生移植耐受小鼠动物模型,分析移植耐受与同种异体反应性T细胞、Tregs表达及嵌合体的关系;运用过继转移实验、EGFP转基因小鼠,研究移植排斥过程中Tregs表达及抗原特异性.结果 新生耐受小鼠形成嵌合体,同种异体反应性T细胞被克隆清除,但Tregs表达与初始小鼠相同;同种异体反应性T细胞识别抗原诱导免疫反应,Tregs在移植排斥反应中表达升高,且不仅同种异体反应性Tregs表达升高,非同种异体反应性Tregs表达也升高.结论 Tregs在移植排斥中非特异性诱导产生,可能为一种负反馈免疫调控机制.

摘要： Objective:To investigate the role of alloreactive T cell in clonal deletion and regulatory T cells ( Treg) in transplant tolerance.Methods:F1 mice were bred by crossing female BALB/c mice and male C57BL/6 mice.Within 24 h,newborn C57BL/6 mice were inoculated with F1 spleen cells via the orbital branch of the anterior facial vein.Six weeks later,the mice were subjected to F1 skin grafting to evaluate their tolerance.Proliferation,flow cytometry and adoptive transfer assay were used to analyze clonal deletion of alloreactive T cells and the expression of CD4+Foxp3+T cells in neonatal treated mice.Results: Newborn C57BL/6 mice injected with F1 splenic cells could induce transplantation tolerance,the level of tolerance was associated with the dose of splenic cells.3×107 splenic cells from F1 mice could induce long-term skin graft acceptance in C57BL/6 mice ,1×107splenic cells significantly prolonged the survival of F1 skin grafts,but the grafts completely rejected within 50 days.The mixed lymphocyte reaction ( MLR) experiment in vivo showed that alloreactive T cell in long-term tolerant mice was deleted completely,but a certain amount of reactive T cells existed in the low-dose group mice.Flow cytometry ( FCM) analysis showed that the expression of CD4+Foxp3+T cell in the high-dose group and low-dose group mice had no obvious difference compared with the naive mice.When alloreactive T-cells were injected into tolerant mice,the skin graft rejection was observed,and Treg cells upregulated in graft-rejected mice.Conclusion:The degree of transplantation tolerance depended on the clonal deletion of alloreactive T cells,instead of on the expression of CD4+Foxp3+Treg cells.CD4+Foxp3+regulatory T cells upregulated in graft rejected mice,which may be served as a negative feedback mechanism to control the intensity of rejection.%目的：初步探讨同种异体反应性T细胞克隆清除与调节性T细胞在小鼠移植耐受中的作用。方法：雌性BALB／c小鼠与雄性C57BL／6小鼠杂交一代获得F1小鼠，不同剂量的F1小鼠脾脏细胞经眶静脉输注给新生24 h C57BL／6小鼠体内诱导耐受，成年后移植F1小鼠来源的皮肤，建立不同耐受程度的小鼠移植耐受模型；耐受小鼠脾脏细胞经CFSE标记后注射到F1小鼠体内，分析耐受小鼠来源的T细胞在体内对F1抗原的增殖能力；流式细胞术、过继转移实验分析CD4＋Foxp3＋调节性T细胞在移植耐受和移植排斥过程中的表达。结果：C57BL／6小鼠在新生期输注F1小鼠脾脏细胞可诱导移植耐受，耐受程度与输注的脾脏细胞剂量有关，3×107个F1小鼠脾脏细胞可诱导C57BL／76小鼠长期皮肤移植耐受，1×107个细胞诱导可使移植皮肤生存时间显著延长，但在50 d内完全排斥；体内混合淋巴细胞反应实验证明，长期耐受小鼠体内的同种异体反应性T细胞被完全克隆清除，但低剂量组小鼠体内仍存在一定数量的反应性T细胞；流式细胞分析发现，高剂量和低剂量组小鼠体内的CD4＋Foxp3＋调节性T细胞表达与初始小鼠相比没有显著差异；同种异体反应性T细胞过继转移给耐受小鼠，移植耐受的皮肤发生排斥反应，小鼠体内的调节性T细胞表达升高。结论：小鼠的移植耐受程度与小鼠体内的同种异体反应性T细胞的克隆清除程度有关，与CD4＋Foxp3＋调节性T细胞的表达没有直接关系；调节细胞在移植排斥过程中表达升高，可能作为一种反馈机制参与耐受的形成。

摘要： Objective:To study if embryonic stem cell derived dendritic cells(esDCs) could induce transplant tolerance to syngeneic neural progenitor cells ( NPCs) in ischemic rat brain.Methods:Neural progenitor cells ( NPCs) were differentiated from 129/svj pCX-eGFP ES-D3 embryonic stem cells and dendritic cells were directly differentiated from 129/svj ES-D3 respectively.All of SD rats were accepted MCAo surgery and subdivided in two groups based on pretreatment with or without esDCs through tail vein injection 1 week after MCAo.pCX-eGFP NPCs were then injected into the lateral ventricle of animals 2 weeks after MCAo.A proliferation assay of lymphocytes dissociated from cervical lymph nodes by MTT method,counting of the survival of the grafted cells, histological evaluation of CD4,CD8 and ED1 positive cells in brain and detection of mRNA level of IL-10 and IFN-γin ischemic lesions by reverse transcriptase-polymerase chain reaction(RT-PCR) were performed 2 weeks after graft (4 weeks after MCAo).Results:Pre-treatment with esDCs decreased CD4 positive cells infiltration (134.7 ±36.2 vs.198.8 ±59.6,P0.05).There was also no difference in lymphocytes proliferation (PI,1.245 ±0.211 vs.1.331 ±0.235) or mRNA expression level of IL-10 ( 1.147 ±0.260 vs.1.264 ±0.119 ) and IFN-γ( 1.697 ±0.273 vs.1.829 ±0.250 ) between two groups ( P>0.05).Conclusion:The results indicate that pretreatment with esDCs may prolong syngeneic NPCs survival though reducing CD4 positive cells reaction in ischemic striatum,which provides some evidence for the tolerogenic function of esDCs.However,there was lack of evidence for cytokine-dependent routine involving in this mode and further investigation was needed to make certain the cardinal principle.%目的：观察脑缺血环境下胚胎干细胞源性树突状细胞（esDCs）能否诱导同源性神经前体细胞（NPCs）的移植耐受。方法：分别自129／svj pCX-eGFP ES-D3诱生NPCs及129／svj ES-D3诱生esDCs。线栓法制作MCAo模型SD大鼠并相应分为预处理组及对照组，术后1周预处理组经尾静脉注射esDCs而对照组注射PBS，两组动物在预处理1周后侧脑室注射NPCs，2周后（MCAo术后4周）免疫组化观察纹状区CD4＋、CD8＋、ED1＋细胞的分布差异，MTT法观察颈部淋巴细胞增殖性（ PI），逆转录PCR（ RT-PCR）半定量局部IL-10、IFN-γmRNA表达差异，荧光显微镜观察GFP标记NPCs海马存活率。结果：预处理组大鼠，CD4＋细胞浸润显著低于对照组（134.7±36.2 vs 198.8±59.6，P＜0.05），NPCs存活率显著高于对照组（P＜0.05），但预处理组对ED1＋（298.8±75.9 vs 302.2±88.5）、CD8＋（145.8±45.4 vs 134.3±39.0）细胞浸润、局部细胞因子mRNA IFN-γ（1.697±0.273 vs 1.829±0.250）、IL-10（1.147±0.260 vs 1.264±0.119）及外周淋巴细胞增长率（ PI，1.245±0.211 vs 1.331±0.235）无明显影响。结论：esDC可能通过降低局部CD4＋细胞反应诱导针对同源性NPCs免疫耐受，尚无确切证据表明细胞因子途径参与该过程，确切的机理尚需更深入研究。

摘要： Objective To investigate the effect of tolerogenic dendritic cells (Tol-DC) generated by Rapamycin (Rapa) on the differentiation of Treg/Thl7 cells and explore the possible mechanism of tolerance induction.Methods DC progenitors from mouse bone marrow were propagated with granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin (IL)-4 stimulation for 6 days in the presence or absence of Rapa (20 ng/ml).During DC culture,morphology of cell was observed under electron microscope.Cell surface expression of CD11c,CD40 and CD80 was analyzed by flow cytometry.The antigen-presenting function of DC was determined by one-way mixed leukocyte reactions.In vivo,the recipient BALB/c mice receiving transplantation of skin allograft from C57BL/6 mice were divided into control,Rapa,immature DC (imDC) and Tol-DC group.The survival time of the skin allograft was observed and Treg/Th17 cells were analyzed by flow cytometry in each group.Results The immunephenotypic analysis showed that in comparison with those in the control group and the LPS group the expression of the co-stimulatory molecules CD40 and CD80 were significantly lower in the Rapa-group and Rapa + LPS group.The ability to stimulate proliferation of T cells of the same genotype in the Rapa-group was significantly inhibited (P ＜ 0.01).In the in vivo experiment,the mice' s survival time remarkably prolonged,the percentage of Treg cells was enhanced and Th17 cells was reduced in the mice's spleen in Tol-DC group.Conclusions Tol-DC generated by Rapamycin can significantly induce immune tolerance through up-regulate Tregs and down-regulate Th17 cells.The present study highlights the therapeutic potential of preventing allograft rejection using in vitro-generated Tol-DCs,which can be loaded with donor antigen,and potentially used to promote organ transplant tolerance.%目的 应用雷帕霉素体外预处理小鼠树突细胞(DC),制备耐受树突细胞(Tol-DC),并建立同种异基因小鼠皮肤移植模型,Tol-DC过继性输注到小鼠体内,观察移植皮片存活时间及Treg/Th17细胞表达,探讨其诱导移植免疫耐受的可能机制.方法 在小鼠骨髓来源的DC前体培养过程中加入粒细胞-巨噬细胞集落刺激因子(GM-CSF),白细胞介素4(IL-4)和雷帕霉素,用流式细胞仪检测各组DC表面CD11c、CD40和CD80的表达;MTT比色法行体外混合淋巴细胞反应(MLR)观察每组对同种T细胞的刺激增殖能力;同时建立皮肤移植模型,观察皮肤移植前7d经尾静脉注射Tol-DC的受者移植物存活情况;第9天取其脾脏,检测Treg/Th17细胞变化,取移植皮肤HE染色观察炎性细胞的浸润情况.结果 Tol-DC组显著抑制了外源刺激下DC的成熟过程和表面共刺激分子(CD40、CD80)的表达,并显著抑制其同种T细胞激活能力(P＜0.01);而且Treg比例升高,Th17下降,小鼠皮肤存活时间延长,炎症反应减轻.结论 应用雷帕霉素能够制备耐受性树突细胞,并诱导小鼠移植免疫耐受,这种作用是通过扩增Treg细胞,抑制Th17细胞而实现的,从而为在临床应用Tol-DC诱导供者特异性免疫耐受提供新的策略.

摘要： Objective To explore the differentiation of allogeneic naive T cells to regulatory T cells (Tregs) and T helper (TH) 1/2/17 cells by coculture with bone marrow-derivedimmature dendritic cells (irnDC).Method Bone marrow-derived imDC were cultivated from Balb/c mice.Lipopolysaccharide-stimulated DC were harvested as mature dendritic cells (mDC) and unstimulated cells were collected as imDC.Then irnDC or mDC were cocultured with allogeniec naive T cells,respectively.TH1 cytokines [interferon-γ (IFN-γ) and interleukin (IL)-2],TH2 cytokines (IL-4 and IL-10),and TH17 cytokine (IL-17) of co-cultured cells were detected by enzyme linked immunospot assay.CD4+ Forkhead box p3 (FoxP3) + Treg proportion in CD4+ cells in the co-cultured system with IL-2 and transforming growth factor-β1 (TGF-β1) was analyzed by flow cytometry.Result As compared with mDC,na(i)ve T cells cocultured with imDC secreted much less IFN-γ (11.67 ± 2.18 vs.182.00±23.71,P＜0.01),IL-2 (26.67±2.96 vs.318.30± 18.62,P＜0.01),IL-4 (17.00±3.78 vs.45.33±3.48,P＜0.01),IL-10(7.00±1.00vs.158.70±10.90,P＜0.001) and IL-17 (0.66 ± 0.33 vs.238.30 ± 24.39,P＜0.001).Furthermore,imDC induced more CD4+ FoxP3+ Tregs than mDC after adding IL-2 and TGF-β1 in the coculture system for 7 days (22.70 ± 1.53 ％ vs.5.42 ± 1.27％,P＜0.01).Conclusion imDC are more effective to induce na ve T cells to Tregs,but not differentiate to TH 1/TH 2/TH 17 cells.These findings provide in vitro experimental evidence for induction of transplant tolerance by adoptive transfer of imDC.%目的 研究小鼠骨髓来源未成熟树突状细胞(imDC)诱导同种幼稚T淋巴细胞分化为调节性T淋巴细胞(Treg细胞)及辅助性T淋巴细胞(TH)1、TH2和TH 17的能力.方法 培养Balb/c小鼠骨髓来源树突状细胞(DC),加入脂多糖刺激DC成熟.分别将imDC与成熟DC(mDC)与同种C57BL/6小鼠幼稚T淋巴细胞共同培养,用酶联免疫斑点法检测TH 1类细胞因子[γ干扰素(IFN-γ)和白细胞介素(IL)-2]、TH2类细胞因子(IL-4和IL-10)、TH17类细胞因子(IL-17)的分泌情况.imDC和mDC分别与同种幼稚T淋巴细胞在加入IL-2及转化生长因子β1的条件下共同培养,用流式细胞术检测T淋巴细胞中Treg细胞比例.结果 分别与imDC或mDC共同培养后,T淋巴细胞中分泌IFN-γ细胞的数量分别为(11.67±2.18)/2×105个细胞和(182.00±23.71)/2×105个细胞(P＜0.01),分泌.IL-2细胞的数量分别为(26.67±2.96)/2×105个细胞和(318.30±18.62)/2×105个细胞(P＜0.01),分泌IL-4细胞的数量分别为(17.00±3.78)/2×105个细胞和(45.33±3.48)/2×105个细胞(P＜0.01),分泌IL-10细胞的数量分别为(7.00±1.00)/2×105个细胞和(158.70±10.90)/2×105个细胞和(P＜0.001),分泌IL-17细胞的数量为(0.66±0.33)/2×105个细胞和(238.30±24.39)/2×105个细胞(P＜0.001).imDC诱导产生的Treg细胞占(22.70±1.53)％,高于mDC诱导产生的(5.42±1.27)％ (P＜0.001).结论 imDC诱导同种幼稚T淋巴细胞较多分化为Treg细胞,而较少分化为TH1、TH2和TH17细胞.

摘要： 本发明公开了模式识别受体Dectin‑1抑制剂对受体移植物的免疫保护及诱导免疫耐受的应用，包括昆布多糖在抑制小鼠移植物排斥反应及诱导免疫耐受中的应用。本发明首次提出昆布多糖可抑制器官移植后排斥反应，明显延长移植物的存活时间，并且在他克莫司的协同作用下诱导免疫耐受，联用效果更佳；同时提出昆布多糖抑制移植物排斥反应及诱导免疫耐受是通过抑制dectin‑1而实现的。本发明首次将dectin‑1抑制剂昆布多糖和低剂量的他克莫司联合使用，诱导免疫耐受，可减少他克莫司的使用剂量，减少单独使用全剂量他克莫司的副作用，也减少患者的经济负担，提高器官移植患者的生存质量，应用前景好，同时为调控受体对移植器官排斥反应及诱导免疫耐受提供了新的靶点和途径。

摘要： 本公开内容涉及用于在移植物受者中诱导对移植的细胞、器官或组织的免疫耐受的组合物和系统。本文还提供了耐受性疫苗/方案或预备性方案的制备方法和施用方法。

摘要： 提供了用于向受者联合移植实体器官和造血细胞的方法和组合物，其中对移植物的耐受通过产生持久的混合嵌合状态而确立。具有持久的混合嵌合状态，通常持续至少六个月的时间段的个体能够在足以确立耐受的一段时间后撤去免疫抑制药物的使用。

摘要： 用于促进对实体器官移植受体的供体特异性耐受性和免疫活性的方法和组合物，所述方法通过在需要实体器官移植的受体中移植同种异体实体器官来进行并且进一步包括在接受来自供体的实体器官的受体中通过外科手术植入组织工程化的同种异体经培养的出生后胸腺组织产品。

摘要： 提供了用于向受者联合移植实体器官和造血细胞的方法和组合物，其中对移植物的耐受通过产生持久的混合嵌合状态而确立。具有持久的混合嵌合状态，通常持续至少六个月的时间段的个体能够在足以确立耐受的一段时间后撤去免疫抑制药物的使用。

摘要： 本公开文本涉及具有一个或多个用于增强异种移植物存活和/或耐受性的经修饰基因的细胞、组织、器官和/或动物。此外，本公开文本涉及制备和使用具有一个或多个所述经修饰基因的所述细胞、组织、器官和/或动物的方法。

摘要： 本发明公开一种原位肝移植免疫耐受方案及其动物模型的构建方法。其所述动物模型设计巧妙、合理、重复性好，符合大鼠原位肝移植术要求，和人肝移植相似。术后存活率高，重复性好，耐受率高达100％，在术后经肝功能检测，病理分析证实。能有效解决研究目标和肝移植完整复制过程所涉及时间久、死亡率高、人员和显微技术要求高等问题。同时可延伸到其他供‑受体不同组合的耐受诱导的基础研究。

摘要： 本发明提供细胞组合物，这些细胞组合物含有源自死亡供体的骨髓的CD34+细胞和源自该死亡供体的非骨髓的CD3+细胞。这些组合物可用于促进实体器官移植接受者中的混合嵌合。本发明还提供制备和使用此类组合物的方法。在某些实施例中，本发明进一步提供分析和制备来自死亡供体的血液和血液组分以在本发明的组合物中用于促进实体器官移植接受者中的混合嵌合。

摘要： 本公开涉及制备杂交猪‑人胸腺组织以及使用所述杂交胸腺组织在异种移植中诱导耐受性。所述杂交胸腺组织还可用于恢复或诱导受体的免疫能力，以及恢复或促进T细胞祖细胞在受体中发育成成熟功能性T细胞的胸腺依赖性能力。

摘要： 在某些实施方案中，本发明提供了鉴定和治疗具有由在瞬时免疫疗法的掩护下输注的凋亡供体白细胞诱导的移植耐受性的移植受体患者的方法。