CD_4在成年鼠胸腺内前T细胞上的表达

T 细胞在成年胸腺内发育所必须的条件是缓慢而持续地输入干细胞或前胸腺细胞。本文研究胸腺内前T 细胞上CD_4的表达。C_(57)BL/Ka Thy1.2小鼠胸腺细胞经抗CD_8及CD_3抗体处理后,使其缺乏CD_4~+CD_8~+胸腺细胞及成熟T 细胞;再用抗IL-2受体(IL-2R)及CD_2抗体处理以除去CD_4~-CD_8~-前体细胞;亦用抗红细胞、单核细胞、巨噬细胞及B 细胞抗体处理以除去各种非T 细胞。经上述处理过的胸腺细胞用免疫荧光及流式细胞仪测定其表型,即以荧光标记的抗CD_4(GK1.5)及抗热稳定抗原HSA(M1/69)抗体染色,并通过FACS 分离;然后将这些细胞输入X 线照射的C_(57)BL/Ka     

淋巴细胞亚群与肿瘤免疫的初探

应用淋巴细胞单克隆抗体分离主要的淋巴细胞亚群,用间接免疫荧光法测定了癌病人外周血CD_4~+细胞的数量,显著少于正常人。分离了CD_4~+和CD_4~-细胞,分别用PHA激活及~3H-TdR掺入反映其功能变化,发现CD_4~+和CD_4~-细胞的掺入活性均比正常人显著降低。观察了正常人NK、CD_4~+、CD_8~+和B细胞对K_(562)肿瘤细胞的协同杀伤活性,以NK+CD_4~+细胞的活性最高。本文提示癌病人的CD_4~+细胞数量和功能下降,正常人CD_4~+细胞在协同杀伤肿瘤细胞中具有重要作用,说明CD_4~+细胞在肿瘤免疫中的重要意义。     

鼠IL-2依赖性细胞(C-702)的IL-4反应性和IL-2的受体分析

自IL-2做为T 细胞生长因子被发现以后,又有报道认为它可以诱导淋巴因子激活的杀伤细胞的生成以及IL-2依赖性细胞和IL-4有交差反应。本文首先证明C-702对于IL-2的依赖性,然后又对其它细胞分裂素的反应性及IL-2受体进行了研究。实验应用了该研究室培养的鼠IL-2依赖性细胞C-702,重组白细胞介素使用了人rIL-1α、人rIL-1β、人rIL-2、人rIL-4、人rIL-6、鼠rIL-2、鼠rIL-3及rIL-4。细胞表面抗原分析使用的鼠用抗体为抗IL-2R(IL-2受体)McAb3C7,Thy1.2,Lyt2.2,L_3T_4,B220,Mac1,Mac2,Mac3,Snlg 及抗asialoGM1抗体。人用抗体为CD_2、CD_3、CD_4、CD_8、CD_(19)、及CD_(25)。根据对~3H-TdR 的吸收程     

T淋巴细胞与结核免疫

关于T 细胞与结核免疫,近年来的研究表明,CD_4~+、CD_8~+T 细胞都参与抗结核的保护作用。CD_8~+ T 细胞的增殖和分化需要由CD_4~+T 细胞提供的IL-2。CD_4~+T 细胞可通过淋巴因子的分泌激活巨噬细胞,CD_4~+T 细胞还可过继转移DTH 反应,并能激活体内的抗结核防御机制。接受过BCG 预防注射的健康人的外周血单核细胞,在体外用BCG 刺激5天后可诱导产生抑制细胞,这种抑制细胞的抑制作用是特异性的,并表现为MHC 制约性,用单克隆抗体检测发现它是CD_4~+亚类。     

抗人T细胞及其主要功能亚群McAb的产生

本文报道用杂交瘤技术产生了一组抗全部T细胞、T辅助细胞及T抑制杀伤细胞抗体。 经用间接免疫荧光检测,抗体T1b、T1C识别所测试的8个T细胞株;与周血E~+细胞反应达77％,提示其识别全部T细胞;与部分B细胞慢淋的交叉反应性提示其为CD_5(即OKT_1或Lcu-1)类抗体。抗体T8b与部分T细胞反应;与周血E~+细胞为35％,与胸腺细胞为79％,提示其为CD8(OKT8、Leu-2a)类抗体。抗体T4a也与部分T细胞反应;与周血E~+细胞为     

转基因γδT细胞在胸腺内灭活后建立自身耐受

表达αβTcR 的T 淋巴细胞在胸腺内被分化为αβ~+与αβ~-,这种选择性作用有助于建立自身耐受性并保障成熟的CD_4~+、CD_8~+细胞群受自身MHC 约束;但有关γδT 细胞的发育所知不多。据此,本文开展这方面研究。将成年C_(57)BL/b(H-Z~b、TL~b)小鼠的CD_4~-、CD_8~-胸腺细胞和胸腺瘤BW5147融合后获得几株γδTcRT 杂交瘤。用杂交瘤生长抑制测定法鉴定一株转基因细胞特异的杂交瘤(KNb),它能识别TL~b 单型产物,后     

外周血干细胞采集物来源的巨细胞病毒特异性T细胞的体外培养和扩增

目的建立巨细胞病毒特异性细胞毒性T淋巴细胞(CMV CTL)体外扩增的方法。方法用1μg/mL全长巨细胞病毒pp65(CMV pp65)多肽体外多轮刺激由粒细胞-集落刺激因子(G-CSF)动员的外周血干细胞采集物中分离的单个核细胞(PBMC),同时加入白细胞介素2(IL-2)、 IL-15、 IL-21扩增20 d。在培养第7天,加入丝裂霉素处理的负载CMV pp65抗原肽的自体PBMC,第10天补充经γ射线辐照处理并负载CMV pp65抗原肽的PBMC和CD3(OKT3);对照组为未加入抗原肽进行扩增的PBMC组。采用多色流式细胞术分别对扩增前、扩增后的T淋巴细胞表型及细胞内肿瘤坏死因子α(TNF-α)和γ干扰素(IFN-γ)的分泌水平进行分析, ELISA检测供者血清中CMV IgM/IgG抗体滴度水平。结果培养后可以收集得到(165.26±6.14)×10~6个细胞,其中CD3~+ T细胞占89.21%, CD8~+ T细胞占CD3~+ T细胞的(43.54±28.03)%, CD4~+ T细胞占CD3~+ T细胞(34.23±26.18)%。获得的CD3~+ T细胞以效应记忆性T细胞(T_(EM))为主,且扩增培养后的CD8~+和CD4~+ T_(EM)比例较培养前显著增高。另外,培养后干细胞样记忆性T细胞(T_(SCM))和组织原位记忆T细胞(T_(RM))的比例均较培养前显著增加。在功能实验中,培养后得到的IFN-γ~+的分泌型CMV特异性CD8~+ T细胞群比例较扩增前明显增加, TNF-α~+ CMV特异性CD8~+ T细胞比例呈增长趋势;能够分别分泌IFN-γ和TNF-α的CMV特异性CD4~+ T细胞群比例与培养前无明显变化。此外,供者体内CMV IgG水平与供者年龄呈现正相关,且在该培养体系下, IFN-γ~+和TNF-α~+ CMV特异性T细胞扩增比例与供者年龄呈负相关。结论本研究成功建立了在体外有效的培养和扩增CMV CTL的方法。     

人对白细胞间介素-2的反应及其产生的细胞基础 用单克降抗体鉴定的自身玫瑰花形成细胞的作用

作者用自身玫瑰花形成T细胞(Tar)和花生凝集素(PNA)将T细胞亚群(T_4~+与T_8~+)进一步分成不同的组份,分析了这些不同组份产生白细胞间介素-2(IL-2)和对其反应的情况,同时提及了对IL-1的反应。用梯度离心及E玫瑰花法从健康人外周血中分离获取T细胞,以OKT_4和OKT_8单克隆抗体加补体的阴性选择法纯化分离T_4~+和     

慢性乙型肝炎患者T细胞功能的研究

本文以31例慢性乙型肝炎患者为研究对象,用CD系列单克隆抗体检测了患者外周T细胞亚群分型,观察ConA诱导的白细胞介素-2分泌功能,以及非特异性T细胞抑制功能(Ts)对B细胞抗体分泌的影响。结果表明,慢性乙肝患者体内存在T细胞免疫功能的异常,其外周血CD_4~+细胞比例低下,CD~+细胞比例增高,导致CD_4/CD_3比值下降,这种变化与HBV复制活跃的指标HBsAg~+密切相关。因此血清HBeAg~+是反映患者外周血T细胞亚群变化较敏感的指标。此外慢性乙肝患者T细胞产生IL-2的功能明显障碍,同时伴有ConA诱导的Ts功能低下,这种功能的异常与外周血CD_4~+与CD_8~+细胞亚群的变化无明显的统计相关性。     

CD_4影响CD_4~+、CD_8~+胸腺细胞TCR新转译后调节

以往已发现,抗CD_4单抗注入小鼠能使不成熟CD_4~+CD_8~+胸腺细胞表面TCR 数目增加3～4倍。这是因为抗CD_4单抗在体内作用于CD_4~+CD_8~+胸腺细胞后使其表面的各种TCR 亚单位(α、β、γ、δ、ζ2ε、)表达增加。作者为了分析此增加是由于受体总数增加,还是由于细胞内及其表面原有受体重分配的结果,故将对照小鼠及抗-CD_4单抗处理小鼠的CD_4~+CD_8~+细胞先以去污剂溶解,然后用抗-CO_(?)-δ抗体分离TCR,再用免疫印迹法(Immunohoting)测定CD_3-δ总量。结果     

Increasing circulating T-cell activation markers are linked to subsequent implantation failure after transfer of in vitro fertilized embryos

PROBLEM: Implantation determines success of in vitro fertilization (IVF) and embryo transfer (ET) cycles. Data are accumulating to support a role of the immune system in implantation. Most of the literature addresses the importance of natural killer (NK) cells in this process. The purpose of the current study is to examine the role of circulating T cells in implantation failure. METHOD OF STUDY: Blood from 22 women undergoing IVF/ET during November, 2001, was drawn on cycle day 9 and analyzed for the percentage of circulating T cells expressing the activation markers CD69+ and human leukocyte antigen (HLA)-DR and the suppressor marker CD11b using immunofluorescence and flow cytometry. These results were compared with total percentage circulating CD3, CD4 and CD8 cells as well as NK cells and pregnancy outcome that cycle. RESULTS: Infertile women had significantly greater expression of the activation marker of CD69+ among CD8+ and CD4+ T cells and HLA-DR among CD4 cells than fertile women. No difference in expression of T cell suppressor marker of CD11b was noted when infertile and fertile women were compared. No correlations were observed when activated T cells were compared with circulating CD3+, CD4+, CD8+, activated NK cells and NK cytotoxicity. CD3+ 4+ HLA-DR+ was expressed significantly less among successfully pregnant compared with unsuccessfully pregnant women. CONCLUSION: T-cell activation markers CD 69+ and HLA-DR+ are associated with increased implantation failure after IVF/ET.     

新辅助化疗对局部进展期乳腺癌患者T淋巴细胞亚群及NK细胞免疫功能的影响

目的:探讨局部进展期乳腺癌患者新辅助化疗前、后T淋巴细胞亚群及NK细胞免疫功能的变化。方法:采用流式细胞术检测54例局部进展期乳腺癌患者新辅助化疗前后的静脉血T淋巴细胞亚群及NK细胞免疫功能。美国癌症联合会(American Joint Commitree on Cancer,AJCC)肿瘤分期为Ⅱb期(仅T3N0M0)和Ⅲ期(不包括N3),静脉血于第1周期新辅助化疗治疗前及第3周期化疗后21日抽取,淋巴细胞亚群检测包括:T(CD3+,CD4+,CD8+),NK(CD56+,CD16+),经过3周期新辅助化疗CEF方案(表柔比星、环磷酰胺和5-氟尿嘧啶),根据新辅助化疗临床效果评价分为2组,化疗有效组38例(CR和PR),化疗无效组16例(SD和PD),并与正常体检健康者(40例)作比较。结果:乳腺癌患者治疗前CD4+、CD4+/CD8+明显低于对照组(P<0.01),NK细胞明显低于对照组(P<0.05),新辅助化疗后,有效组总CD3+、CD4+、CD4+/CD8+、NK细胞较治疗前均显著升高(P<0.05),CD8+降低(P<0.05);无效组CD3+、CD4+/CD8+及NK细胞较治疗前显著降低(P<0.05),而CD8+升高(P<0.05)。结论:局部进展期乳腺癌患者免疫功能低下,有效的辅助化疗能提高患者的免疫功能,定期监测免疫功能对指导临床治疗有意义。     

CD28 costimulation and CD28 expression in T lymphocyte subsets in HIV-1 infection with and without progression to AIDS

In a prospective study of 152 HIV-1 patients (with and without progression to AIDS) we examined CD28 MoAb costimulation and CD3 MoAb response using whole blood culture at baseline and up to either the time of AIDS diagnosis or the end of the observation period. CD28 antigen expression on both CD4+ and CD8+ T lymphocytes was also studied in both groups of patients. In patients who progressed to AIDS, CD28 MoAb costimulation was found to be decreased. Univariate time-dependent analysis showed that decreases in (i) absolute numbers of either CD4+, CD4+CD28+, CD8+CD28+ T cells, (ii) CD28 MoAb costimulation, and (iii) CD3 MoAb response, and an increase in CD8+CD28- %, are significant predictors for progression to AIDS. In addition, multivariate time-dependent analysis demonstrated that a decrease in CD28 MoAb costimulation (but not a decrease in CD3 MoAb response) was predictive for progression to AIDS, as were decreases in the percentage of CD4+ T cells and the absolute number of CD4+CD28+ T cells. Thus, CD28 MoAb costimulation can be considered a useful assay for monitoring HIV-1 infection. Furthermore, apart from the early increase in the percentage of CD8+CD28- T cells and an increase in the percentage of CD28- on CD8+ T cells in both groups of patients at baseline compared with normal controls, a negative correlation was found to exist between the percentages of CD4+ or CD4+CD28+ T cells and the percentage of CD8+CD28- T cells; this suggests that these cells are probably mutually regulated.     

Th1、Th2样细胞因子对CD158+细胞比率的调节作用

目的:观察Th1、Th2样细胞因子对外周血CD158+细胞比率的调节作用,为寻找干细胞移植免疫耐受的方法提供论理依据。方法:将Th1样细胞因子(IL-2、IFN-γ)和Th2样细胞因子(IL-4、IL-6),单独或联合与人外周血单个核细胞(PBMC)培养72h,用流式细胞法分析总CD158a+、CD158b+细胞及CD3+、CD4+、CD8+和CD16+ CD56+细胞亚群中CD158a+、CD158b+细胞的比率。结果:①细胞因子对CD3+、CD4+、CD8+细胞及CD16+ CD56+细胞的影响:IL-2和IFN-γ均可增加上述细胞的百分率(P<0.05),但IL-2的作用大于IFN-γ(P<0.05)。IL-2+IFN-γ联合处理的效应高于IFN-γ单独处理(P<0.05)。IL-4+IL-6可降低上述细胞的百分率(P<0.05)。IL-2+IL-4对上述细胞百分率的影响,高于IL-4(P<0.05)但低于IL-2(P<0.05)。②细胞因子对CD158a+/b+细胞的影响:IL-2可增加总的CD158a+/b+细胞及CD3+、CD4+、CD8+和CD16+ CD56+细胞中的CD158a+/b+细胞的百分比率(P<0.05);IL-2+IFN-γ可增加CD158a+/b+细胞的百分率(P<0.05),但与IL-2单独处理无明显区别,IL-4+IL-6可降低CD158a+/b+细胞的百分率(P<0.05)。IL-2+IL-4可增加总的CD158a+/b+细胞及各亚群中CD158a+/b+细胞的百分率(P<0.05),但低于IL-2单独处理(P<0.05)。结论:IL-2有促进CD158基因表达或使CD158a+、CD158b+     

Echinococcus granulosus: the potential use of specific radiolabelled antibodies in diagnosis by immunoscintigraphy.

In normal individuals, 80 +/- 5% of circulating CD8+ T cells express CD45RA, and 20 +/- 7% of these cells express CD45R0 antigens. After activation, CD8+ cells expressing CD45RA decrease to 56-67% while those expressing CD45R0 increase to 38-67%. Although precursors of alloantigen-specific cytotoxic T cells were found in both CD8+, CD45RA+ and CD8+, CD45R0+ subsets, the specific effector cells were exclusively CD8+, CD45R0. Allospecific cytotoxic CD8+ clones were also entirely CD45R0+. A lectin-dependent cytotoxic (LDC) assay unmasked a hierarchy of killing after alloactivation which was CD8+, CD45R0+ greater than CD8+, CD45RA+ greater than CD4+, CD45R0+ greater than CD4+, CD45RA+. The phenotype of CD8+ T cells in rejecting kidneys was similar to in vitro alloantigen-activated CD8+, CD45R0+ cells and cytotoxic CD8+ clones. Firstly there was an increase in the relative proportions of CD45R0+ (60 +/- 8%) and a decrease in CD45RA+ (35 +/- 10%) CD8+ cells relative to circulating CD8+ subsets. In the rejecting grafts, 34 +/- 9% of the CD8+ cells were also DR+ indicative of recent activation. Furthermore, 16% (range 4-35%) of rejecting CD8+ cells were Ki67+ suggesting that these cells were proliferating. Finally, 17% (range 4-53%) of T cells in rejecting kidneys simultaneously expressed both CD45RA and CD45R0 markers. These results show that in vitro alloantigen-activated CD8+, CD45R0+ cells represent a primed/memory cytotoxic population. In addition, they provide indirect evidence that a proportion of CD8+ cells in rejecting kidneys were actively switching from a naive to a memory phenotype in vivo in a manner analogous to that in vitro.     

Phenotypic identification of suppressor-effector, suppressor-amplifier and suppressor-inducer T cells of B cell differentiation in man

Using monoclonal anti-Leu8 antibody to isolate subpopulations of human helper/inducer (CD4+) and suppressor/cytotoxic (CD8+) T cells, we have investigated the role of these subpopulations in the regulation of B cell differentiation in the human autologous mixed leukocyte reaction (AMLR). Whereas AMLR-activated CD8+,Leu8- cells were capable of suppressing fresh AMLR cultures in the absence of fresh CD8+ cells, CD8+,Leu8+ cells suppressed only those cultures containing fresh CD8+ cells. On the other hand, CD8+,Leu8- cells became suppressor cells only when cultured in the presence of CD8+,Leu8+ cells. Finally, the development of CD8+ suppressor cells was dependent on the presence of CD4+,Leu8+ cells; CD4+,Leu8- cells were incapable of acting as suppressor-inducer cells, but have been shown previously to mediate T cell help for B cell differentiation. Thus, at least 3 phenotypically distinct subsets of T cells interact sequentially to generate suppression of B cell differentiation induced in the AMLR: CD4+,Leu8+ suppressor/inducer cells, CD8+,Leu8+ suppressor-amplifier cells and CD8+,Leu8- suppressor-effector cells.     

T cell malignancy in Richter's syndrome presenting as hyper IgM. Induction and characterization of a novel CD3+, CD4-, CD8+ T cell subset from phytohemagglutinin-stimulated patient's CD3+, CD4+, CD8+ leukemic T cells

A patient is described, having Richter's syndrome and immunodeficiency with hyper IgM, who developed suppressor T cell lymphoma (CD3+, CD4-, CD8+) following untreated helper-suppressor T cell chronic lymphocytic leukemia (CD3+, CD4+, CD8+). The neoplastic T cells in both malignancies expressed interleukin (IL) 2 receptors but were deficient in typical CD2+ and CD5+ pan T antigens. Additionally, a large percentage of malignant lymph node T cells expressed HLA-DR+ activation antigens. In vitro immunoglobulin-production experiments demonstrated that the patient's leukemic blood T cells had an excess helper function for IgM synthesis but a suppressor function for IgG and IgA synthesis by normal B and T cells. The leukemic blood T cells demonstrated a poor response to phytohemagglutinin (PHA). A defect in IL 2 receptor expression was evident in PHA-stimulated leukemic blood T cells. Of interest was the observation that PHA stimulated the induction of a novel CD3+, CD4-, CD8+ T cell subset from patient's CD3+, CD4+, CD8+ leukemic blood T cells. These PHA-induced CD3+, CD4-, CD8+ T cell subsets produced an elevated proliferative response to PHA and concanavalin A, had a helper cell function for IgM synthesis and produced highly elevated amounts of IL 2.     

L-selectin expression differentiates T cells isolated from different lymphoid tissues in cattle but does not correlate with memory.

L-selectin (LECAM-1, LAM-1) was expressed by a high proportion of CD4+ and CD8+ T cells, as well as almost all of the gamma delta T-cell receptor (TcR)+ (WC1+) T cells, isolated from blood, lymph nodes or tonsils. CD4+ T cells in the lamina propria of the gut villi and CD8+ T cells in the villous epithelium as well as the majority of WC1+ T cells in the gut mucosa were L-selectin-. The proportion of T cells from Peyer's patches that synthesized the molecule was intermediate between the value for blood and gut mucosa. Expression of L-selectin therefore marks T cells in cattle with a distinct tissue distribution that correlates with its function as the peripheral node homing receptor. The proportion of CD4+ and CD8+ T cells in the circulation that were L-selectin+ decreased with age. Unlike CD45R, expression of L-selectin was not related to CD4 T-cell memory as judged by proliferation in transformation assays to soluble antigen. Three-colour immunofluorescent staining demonstrated four subpopulations of CD4 and CD8 T lymphocytes in peripheral blood mononuclear cells (PBMC) that were CD45R+, L-selectin+; CD45R+, L-selectin-; CD45R-, L-selectin+; CD45R-, L-selectin-. CD4(4) memory cells were CD45R- and L-selectin+ or L-selectin-. Taken with earlier studies the reported observations demonstrated that only one of the four phenotypes of the CD4+ T cells in blood is present in the lamina propria of the gut villi and these are CD45R-, L-selectin-. Two of the four phenotypes of CD8+ T cells were present in the gut epithelium; these were CD45R+, L-selectin- or CD45R-, L-selectin-. Expression of the bovine molecule was not rapidly down-regulated on T cells following activation by exposure to phorbol myristate acetate.     

BHV-1-Specific CD4+, CD8+, and gammadelta T cells in calves vaccinated with one dose of a modified live BHV-1 vaccine

Expression of the high-affinity interleukin 2 receptor alpha chain (CD25) was used to monitor antigen-specific activation of T lymphocyte subsets (CD4+, CD8+, and gammadelta T cells) from cattle immunized with modified live bovine herpesvirus-1 (BHV-1). Calves seronegative for BHV-1 were either vaccinated with one dose of modified live vaccine containing BHV-1 or not vaccinated to serve as negative controls. Two animals vaccinated 7 and 5 weeks before the start of the experiment with two doses of modified live vaccine containing BHV-1 served as positive controls. Blood samples were taken from the nonvaccinate group, the positive control group, and the vaccinate group at 0, 21, 35, 60, and 90 days postinoculation (PI). Isolated peripheral blood mononuclear cells from immunized and control animals were incubated for 5 days with and without live BHV-1 ISU99. Compared to the nonvaccinates, a significant (p < 0.05) increase in expression of CD25 by CD4+, CD8+, and gammadelta T lymphocytes from the vaccinate group was detected following in vitro exposure to live BHV-1 after vaccination. This is apparently the first report using live BHV-1 to stimulate lymphocytes in vitro and showing CD8+ T cell activation. Peripheral blood from the positive control animals was depleted of CD4+, CD8+, or gammadelta T lymphocytes prior to incubation with BHV-1 to assess bystander activation in the CD25 expression assay. When incubated with live BHV-1, depletion of CD4+ T cells depressed the expression of CD25 by CD8+ T cells, but not gammadelta T cells. Depleting CD8+ or gammadelta T cells prior to in vitro culture with BHV-1 did not affect the expression of CD25 by the remaining T lymphocyte subsets. Vaccinates were protected from challenge with virulent BHV-1 at 110 days postvaccination compared to nonvaccinates. Expression of CD25 appears to be a useful marker for evaluating induction of antigen-specific T lymphocyte subset responses following vaccination.     

Immune biology of macaque lymphocyte populations during mycobacterial infection

Immune responses of lymphocyte populations during early phases of mycobacterial infection and reinfection have not been well characterized in humans. A non-human primate model of Mycobacterium bovis bacille Calmette-Guerin (BCG) infection was employed to characterize optimally the immune responses of mycobacteria-specific T cells. Primary BCG infection induced biphasic immune responses, characterized by initial lymphocytopenia and subsequent expansion of CD4+, CD8+ and gammadelta T cell populations in the blood, lymph nodes and the pulmonary compartment. The potency of detectable T cell immune responses appears to be influenced by the timing and route of infection as well as challenge doses of BCG organisms. Systemic BCG infection introduced by intravenous challenge induced a dose-dependent expansion of circulating CD4+, CD8+ and gammadelta T cells whereas, in the pulmonary compartment, the systemic infection resulted in a predominant increase in numbers of gammadelta T cells. In contrast, pulmonary exposure to BCG through the bronchial route induced detectable expansions of CD4+, CD8+ and gammadelta T cell populations in only the lung but not in the blood. A rapid recall expansion of these T cell populations was seen in the macaques reinfected intravenously and bronchially with BCG. The expanded alphabeta and gammadelta T cell populations exhibited their antigen specificity for mycobacterial peptides and non-peptide phospholigands, respectively. Finally, the major expansion of T cells was associated with a resolution of active BCG infection and reinfection. The patterns and kinetics of CD4+, CD8+ and gammadelta T cell immune responses during BCG infection might contribute to characterizing immune protection against tuberculosis and testing new tuberculosis vaccines in primates.