胶原蛋白肽改善模拟失重小鼠外周血淋巴细胞分布及脾脏T淋巴细胞增殖能力

目的:探讨胶原蛋白肽能否改善模拟失重小鼠的免疫功能。方法:采用尾吊法模拟失重小鼠模型,模拟失重小鼠每天1次腹腔注射600 mg/kg体重的胶原蛋白肽,10 d后处死小鼠,应用MTT法检测外周血白细胞分类和淋巴细胞亚群以及脾脏T淋巴细胞增殖能力。结果:与正常对照组相比,模拟失重组小鼠白细胞总数、淋巴细胞绝对值、T细胞、CD4+和CD8+T细胞、B细胞、NK细胞数量均明显降低(P0.05),脾脏T淋巴细胞增殖能力也明显降低(P0.05);模拟失重小鼠给予胶原蛋白肽后,除NK细胞外上述其他指标均有明显提高(P0.05),且部分指标恢复至正常对照组水平。结论:胶原蛋白肽能够有效改善模拟失重小鼠的外周血淋巴细胞分布及脾脏T淋巴细胞增殖能力。     

青蒿琥酯对迟发型超敏反应小鼠脾脏T淋巴细胞的免疫调节作用

背景：青蒿琥酯是青蒿素低毒、高效的衍生物,具有免疫调节功能,但其具体机制仍需研究阐明。目的：初步探讨青蒿琥酯对迟发型超敏反应小鼠脾脏T淋巴细胞的免疫调节作用。方法：建立迟发型超敏反应小鼠模型,40只小鼠随机数字表法均分正常对照组、青蒿琥酯干预组、p-38 MAPK抑制剂组、基质对照组进行实验观察。T淋巴细胞转化实验检测小鼠T淋巴细胞增殖水平;Western blot方法检测p38丝裂酶原激活蛋白激酶（p38 MAPK）蛋白的活性表达。结果与结论：局部给药后青蒿琥酯明显减轻迟发型超敏反应小鼠耳肿胀、降低脾指数、抑制刀豆蛋白A诱导的T淋巴细胞增殖;同时减弱p38MAPK的磷酸化活性表达。提示青蒿琥酯可以有效抑制小鼠迟发型超敏反应,其作用途径可能与抑制p38MAPK信号通路有关。     

青蒿琥酯对迟发型超敏反应小鼠脾脏T淋巴细胞的免疫调节作用

背景:青蒿琥酯是青蒿素低毒、高效的衍生物,具有免疫调节功能,但其具体机制仍需研究阐明。目的:初步探讨青蒿琥酯对迟发型超敏反应小鼠脾脏T淋巴细胞的免疫调节作用。方法:建立迟发型超敏反应小鼠模型,40只小鼠随机数字表法均分正常对照组、青蒿琥酯干预组、p-38 MAPK抑制剂组、基质对照组进行实验观察。T淋巴细胞转化实验检测小鼠T淋巴细胞增殖水平;Western blot方法检测p38丝裂酶原激活蛋白激酶(p38 MAPK)蛋白的活性表达。结果与结论:局部给药后青蒿琥酯明显减轻迟发型超敏反应小鼠耳肿胀、降低脾指数、抑制刀豆蛋白A诱导的T淋巴细胞增殖;同时减弱p38MAPK的磷酸化活性表达。提示青蒿琥酯可以有效抑制小鼠迟发型超敏反应,其作用途径可能与抑制p38MAPK信号通路有关。     

低剂量碳离子全身辐射对小鼠淋巴细胞增殖及血清干扰素的影响

目的:观察小于0.1Gy剂量碳离子全身辐射引起的小鼠脾淋巴细胞增殖及血清干扰素的变化。方法:实验于2006-11在中国科学院近代物理研究所医学物理实验室进行。①实验过程:取昆明系小鼠30只,采用完全随机设计方法分为5组,每组6只,采用离子束进行全身照射。12C6 离子照射在兰州重离子研究装置(HIRFL)辐照终端进行,照射剂量为0,0.01,0.03,0.05,0.10Gy。麻醉照射后24h,小鼠摘眼球取血。②实验评估:采用ELISA法测定血清γ-干扰素含量,操作严格按试剂盒说明进行。将眼球取血后的小鼠脱颈处死,无菌条件下取出脾脏,常规制备单细胞悬液,采用MTT法检测刀豆蛋白A和脂多糖对脾淋巴细胞的增殖作用。结果:30只小鼠均进入结果分析。①辐射对小鼠血清干扰素的影响:与未照射正常小鼠比较,0.01Gy和0.03Gy碳离子束照射后,小鼠血清中γ-干扰素含量明显增高(P<0.05)。照射剂量继续增大至0.05Gy和0.10Gy时,血清γ-干扰素含量下降。②辐射对小鼠脾淋巴细胞增殖的影响:与未照射组比较,0.01Gy碳离子束照射可明显促进刀豆蛋白A诱导的T淋巴细胞增殖和脂多糖诱导的B淋巴细胞增殖(P<0.001,P<0.001),其促进作用与0.03Gy组比较,差异有显著性意义(P<0.01)。0.05Gy照射开始抑制脾淋巴细胞增殖指数,当照射剂量增大为0.10Gy时显示出明显的抑制作用。结论:0.01Gy和0.03Gy碳离子束照射能刺激淋巴细胞增殖,并能诱导γ-干扰素活性以增强机体免疫力。     

桑色素对二硝基氟苯诱导的迟发型超敏反应的影响

目的研究桑色素（morin）对二硝基氟苯诱导迟发型超敏反应的影响。方法建立二硝基氟苯（dinitroflu-orobenzene,DNFB）诱导迟发型超敏反应（delayed type hypersensitivity,DTH）模型,观察morin对DTH模型小鼠耳组织肿胀、炎性细胞浸润程度和胸腺指数、脾指数的影响,光学显微镜下观察小鼠耳廓组织学变化,噻唑兰（methyl thia-zolyl tetrazolium,MTT）法检测淋巴结细胞和脾脏淋巴细胞增殖情况。结果双耳称重的结果显示,morin（70mg/ml）处理组与DTH组具有显著的差异（P〈0.05）,能明显抑制DNFB引起的炎症反应;耳廓局部组织学检测也表明,morin能够抑制DNFB诱导的DTH,明显减少淋巴细胞的浸润。morin能降低DTH小鼠胸腺指数和脾脏指数,抑制淋巴结淋巴细胞（P〈0.01）和脾脏淋巴细胞的增殖（P〈0.05）。结论 morin可显著抑制DTH小鼠耳组织肿胀和淋巴细胞浸润程度,降低胸腺和脾脏指数,抑制淋巴细胞的增殖可能是其作用机制之一。     

龙眼多糖抗肿瘤及免疫增强活性的实验研究

目的:探讨龙眼多糖对小鼠移植性肿瘤抑制作用及免疫增强作用。方法:观察龙眼多糖对小鼠肉瘤(S180)抑制作用;ConA刺激T淋巴细胞增殖转化法;小鼠腹腔巨噬细胞吞噬鸡红细胞(CRBC)实验;迟发型变态反应(DTH);观察分析LP免疫增强作用。结果:S180小鼠口服龙眼多糖200、400mg/kg剂量组可明显抑制肿瘤生长;可提高T淋巴细胞介导的细胞免疫;增强B淋巴细胞介导的体液免疫;提高了小鼠巨噬细胞吞噬能力。结论:龙眼多糖对小鼠肉瘤有明显抑制作用,其体内抑制肿瘤的生长可能与提升小鼠机体免疫力有关。     

菟丝子对小鼠免疫功能影响的实验研究

目的 探讨菟丝子对小鼠免疫功能的影响。方法 将昆明种小鼠50只分为阴性对照组、阳性对照组、低剂母组、中剂量组、高剂量组。给药8d后测定各组动物脏器系数、腹腔巨噬细胞吞噬功能、脾淋巴细胞增殖反应、白介素活性。结果 菟丝子可促进小鼠免疫器官脾脏、胸腺增长（P〈0．05），并提高巨噬细胞吞噬功能（P〈0.05）；促进淋巴细胞增殖反应（P〈0.05）；诱导白介素产生。结论 菟丝子具有增强小鼠机体免疫功能和免疫调节作用。     

骨髓间充质干细胞对致敏小鼠淋巴细胞增殖的影响及其作用方式

本研究探讨骨髓间充质干细胞(mesenchymal stem cells,MSC)在体外对致微小鼠淋巴细胞增殖的影响及其作用方式,以便进一步了解MSC对致敏小鼠影响的可能机制.建立致敏模型后,将应用贴壁培养法体外培养的正常小鼠骨髓MSC或其培养上清液作为免疫细胞或免疫因子,致敏小鼠的淋巴细胞作为效应细胞,用植物血凝素( phytohemagglutinin,PHA)刺激淋巴细胞增殖,在体外应用MTT法检测两者的混合淋巴细胞增殖反应.结果表明,正常小鼠骨髓MSC在体外能很好地抑制致敏小鼠脾淋巴细胞增殖,同时在MSC培养上清液也能观察到类似现象,而且随着两者细胞比例或浓度比的增大,抑制作用有所加大,当两者比例为1∶1时抑制作用最大(有明显的统计学意义).结论:MSC能在体外明显抑制致敏小鼠脾淋巴细胞增殖,该作用可以通过细胞与细胞(MSC和淋巴细胞)直接接触抑制,也可通过细胞与细胞的间接作用(如MSC的培养上清液与淋巴细胞)方式发挥作用.     

模拟微重力环境下虫草多糖促进淋巴细胞增殖和CD分子表达的实验研究

本研究旨在探索旋转式细胞培养系统(RCCS)模拟微重力环境下虫草多糖促进淋巴细胞增殖和表面CD分子表达的作用。体外分离培养小鼠脾淋巴细胞,在RCCS模拟微重力环境中分别添加6.25、12.5、25和50μg/ml的虫草多糖溶液培养,在24、48和72 h检测虫草多糖对淋巴细胞增殖及表面CD分子表达的作用。结果表明,模拟微重力环境抑制了淋巴细胞的增殖能力,25和50μg/ml虫草多糖对淋巴细胞的增殖和CD4、CD8的表达均具有促进作用,但50μg/ml虫草多糖促进淋巴细胞增殖的作用随时间延长变为抑制作用。结论:适宜浓度范围内的虫草多糖具有对抗模拟微重力环境下淋巴细胞增殖能力下降和表面CD分子表达减少的作用,为筛选对抗失重效应、促进免疫力的药物提供理论依据和实验基础。     

SBHL对小鼠免疫功能影响的实验研究

目的探讨澳洲茄胺盐酸盐（SBHL）对环磷酰胺（CTX）处理小鼠免疫功能的影响。方法 Balb/c小鼠用环磷酰胺造成免疫抑制模型,同时尾静脉注射SBHL7d,观察小鼠免疫器官重量,脾细胞特异性抗体的产生、血清凝集素滴度、溶血素CH50值、ConA刺激的小鼠脾淋巴细胞增殖和小鼠腹腔巨噬细胞吞噬功能及血清中肿瘤坏死因子α含量的变化。结果 SBHL（40 mg/kg）尾静脉注射7 d,小鼠胸腺、脾脏重量增加。ConA刺激的小鼠脾淋巴细胞增殖明显。小鼠腹腔巨噬细胞吞噬功能显著增强。给药组小鼠血凝素滴度、溶血素CH50值、TNF-α也高于对照组。结论 SBHL能明显的改善环磷酰胺抑制的小鼠免疫功能,这可能是澳洲茄胺盐酸盐抗肿瘤的另一作用机理。     

Suppression of footpad reaction in mice by anthralin

In the preceding papers, we showed that the treatment of BALB/c mice with 12-O-tetradecanoylphorbol 13-acetate (TPA), a typical tumor promoter, suppressed footpad reaction (FPR) against sheep red blood cells (SRBC) temporarily but that this effect became lasting when TPA was administered to mice which had been treated with 7,12-dimethyl[a]-anthracene (DMBA), a typical tumor initiator, and that the effect of DMBA and TPA was caused by the induction of antigen-nonspecific T suppressor cells. In this work, we studied the effect of anthralin, a tumor promoter which has not the structure of phorbol ester, on FPR of BALB/c mice against SRBC. Painting of anthralin (80 nmol) suppressed FPR continuously (more than 7 days) unlike that of TPA. However, when anthralin was administered for 7 days following the treatment with 400 nmol of DMBA, the suppressive effect could be transferred with Thy-1 and Lyt-2 positive spleen cells whereas the suppressive effect by the painting of anthralin only for 7 days could not be transferred with the spleen cells.     

Immunosuppression during Trypanosoma musculi infection in inbred strains of mice

Inbred strains of mice inoculated with T. musculi behaved as either sensitive (A/J, CBA/J and C3H/He/J) or relatively resistant (BALB/c, DBA/2, and C57B1/6) with respect to the magnitude of parasitaemia but not to the length of infection. Spleen cells from T. musculi infected C57B1/6 (resistant) and C3H/HeJ (sensitive) mice inhibited the response of normal spleen cells to PHA and ConA; this suppressive activity was concentrated in T-cells and was higher in the resistant mice. However, infection in T-cell-deprived C57B1/6 and C3H/HeJ mice, although more severe and of much longer duration than in the respective control mice, revealed that T-cells were not responsible for the natural resistance to T. musculi.     

Impaired T-dependent immune response in L-dopa treated BALB/c mice

Various neurotransmitters and neuropharmacological agents can affect lymphocyte responses. The purpose of the present study was to investigate the potential immunological effects of L-dihydroxyphenylalanine (L-dopa), the direct precursor of dopamine, by examining the influence of the in vivo administration of the drug on different functional and phenotypic parameters in BALB/c mice. L-dopa at the dose of 100 mg/kg/day altered T-dependent immune responses. The antibody response to sheep red blood cells (SRBC) was abolished by the drug. The delayed-type hypersensitivity reaction to SRBC was also depressed. Lymphocyte proliferation and generation of cytotoxic T cells in response to allogeneic stimulator cells in vitro were decreased by L-dopa treatment. These suppressive effects were correlated with a decrease in spleen T cells number. However, the proliferative response of spleen cells to concanavalin A was greatly enhanced by the L-dopa treatment. Conversely, there was no evidence for alteration of T-independent immune responses by L-dopa. Hence, the antibody response to TNP-Ficoll, and the proliferation of B spleen cells induced by E. coli lipopolysaccharide were unchanged. Altogether, these results showed that L-dopa which is converted to dopamine in the organism, could selectively affect T-dependent immune responses. The integration of these findings in the immune-neuroendocrine interactions, and the possible sites and mechanisms of action are discussed.     

Cell therapy with preimmunized effector cells mismatched for minor histocompatible antigens in the treatment of a murine mammary carcinoma

Cell therapy with allogeneic donor cells mismatched for minor histocompatible (MiHC) antigens was applied to a murine mammary carcinoma (4T1) model to test the feasibility of graft versus tumor (GVT) effect against metastatic epithelial tumor cells. BALB/c mice bearing a 4T1 tumor of BALB/c origin were given syngeneic or MiHC-mismatched splenocytes. GVT effects were determined in secondary recipients of adoptively transferred lung cells derived from primary hosts who had previously been inoculated intravenously with 4T1 cells, and injected with one of the following: 1) naive BALB/c splenocytes, 2) naive DBA/2 splenocytes, 3) 4T1-immune DBA/2 splenocytes, or 4) DBA/2 splenocytes immunized with host-derived BABL/c spleen cells. Naive DBA/2 splenocytes inhibited tumor growth only slightly and only slightly prolonged the survival of secondary recipients, in comparison with fully matched tumor/host BALB/c spleen cells. An efficient GVT reaction was demonstrated in vitro and in vivo with MiHC-mismatched DBA/2 splenocytes from mice presensitized by multiple injections of irradiated tumor or BALB/c-derived spleen cells. All 30 mice adoptively inoculated with lung cells from primary hosts that had previously been treated with these presensitized effector cells were tumor free for >250 days. Secondary recipients inoculated with lung cells from mice given naive BALB/c or DBA/2 spleen cells died of metastatic tumors within 33 to 46 days. These results suggest that preimmunized donor cells represent an effective tool against metastatic disease; hence, the next goal should be to control graft-versus-host disease while exploiting the GVT potential.     

新型免疫抑制剂J2对角膜移植小鼠淋巴细胞中白细胞介素10及干扰素γ分泌的影响

背景：小分子化合物J2是以CD4为靶点的新型免疫抑制剂,课题组以往的实验已经验证了J2对正常小鼠及角膜移植后小鼠脾细胞的影响。目的：探讨小分子化合物J2对异基因角膜小鼠的淋巴细胞中白细胞介素10及干扰素γ分泌的影响。方法：BalB/c（H2d）小鼠随机数字表法分为4个组,安慰剂组、环孢素A组和J2组接受C57BL/6-BALB/c同种异体角膜移植后给予相应药物干预,空白对照组不接受角膜移植,观察各组角膜移植片存活时间。取各组大鼠脾细胞给予刀豆蛋白Ⅵ型刺激细胞增生,采用ELISA法测定细胞上清中白细胞介素10及干扰素γ水平,比较各组细胞增生指数及细胞因子含量。结果与结论：J2可能通过抑制CD4＋T淋巴细胞而抑制角膜排斥反应的发生,延长角膜植片存活时间;J2能够明显抑制ConA刺激角膜移植后小鼠脾细胞的增生及Th1细胞因子的产生。这些效应与环孢素A的效果相似。     

BIOLOGICAL EXPRESSIONS OF LYMPHOCYTE ACTIVATION : I. EFFECTS OF PHYTOMITOGENS ON ANTIBODY SYNTHESIS IN VITRO

The effects of nonspecific phytomitogens on primary plaque-forming cell (PFC) responses of mouse spleen cells to heterologous erythrocytes in vitro were studied. Spleen cell cultures treated with concanavalin A or phytohemagglutinin in vitro or established with spleen cells derived from mice injected with concanavalin A 24 h previously were similarly affected. In both cases, submitogenic doses resulted in substantial enhancement of PFC responses, whereas 10-fold larger doses were profoundly inhibitory. In contrast to the suppressive effects of mitogenic doses of phytomitogens added at culture initiation, addition of these same doses to cultures 48 h later resulted in increased PFC responses. This enhancement could be observed within 1 h after treatment and consequently could not be ascribed only to mitotic expansion of the antibody-synthesizing clone. Activation of spleen cells with specific antigen before mitogen treatment was not required for expression of the enhancing or suppressing effects on PFC responses. IgM and IgG PFC responses were similarly affected. Studies of cell interactions revealed that as few as 10⁵ spleen cells obtained from mice treated with concanavalin A in vivo synergistically enhanced the PFC responses of 10⁷ normal spleen cells. This enhancement was mediated by mitogen-activated T lymphocytes which were resistant to 2000 R irradiation 24 h after activation. The relevance of these observations to emerging concepts of helper and suppressor T cell activity is discussed.     

IN VITRO STIMULATION OF ANTIBODY FORMATION BY PERITONEAL CELLS : II. CELL INTERACTIONS AND EFFECTS OF IMMUNOCHEMICAL OR METABOLIC INHIBITORS

Peritoneal cells (PC) from normal, unimmunized mice were placed in ultra-thin monolayer cultures containing carboxymethylcellulose (CMC), sheep red blood cells (SRBC), and complement, and tested for the appearance of plaques of lysis. The behavior of PC from young male mice and from female mice that had given birth to several litters (retired breeder mice) was studied. It was found that cells from spleen, mesenteric lymph node, thymus, bone marrow, thoracic duct lymph, or Peyer's patches could not form plaques in the CMC microcultures. Also, various combinations of these cells did not lead to plaque formation. When cells from any of these sources were mixed with PC, there was either no effect or an actual inhibition of plaque formation, the plaque counts being lower than would have been expected from the number of PC present in the mixture. Optimal plaque formation by peritoneal cells was found to be dependent on an optimal cell concentration, this optimum being around 5 x 10⁶/ml for young male mice and 0.5 x 10⁶/ml for retired breeders. Inhibition of plaque formation was found with either supra- or suboptimal cell concentrations. The inhibition by excess cell concentration may have been a simple nutritional or nonspecific overcrowding effect, as it could also be induced by an addition of an excess of spleen or lymph node cells. The failure of more dilute PC preparations to give adequate numbers of plaques appeared to be more specific, as plaque numbers could not be restored to normal by addition of spleen cells. The suggestion was that some cell to cell interaction between PC was involved. This dependence on cell concentration was not seen with immunized spleen PFC. Plaque appearance could be specifically and reversibly suppressed by placing PC in a medium containing rabbit anti-mouse IgM serum. Anti-IgG serum had no such effect. These experiments strengthened our view, expressed in the accompanying paper, that plaque formation was due to the formation of IgM, hemolytic antibody to SRBC by the PC. Metabolic inhibitors were incorporated into monolayer cultures and had different effects with the different types of PFC used. In the case of spleen cells from mice actively immunized against SRBC 4 days before killing, actinomycin D had no effect on plaque counts and puromycin reduced plaque numbers by a factor of 2. In the case of PC from young male mice, actinomycin D in concentrations above 0.01 µg/ml caused reductions down to < 2% of control values in plaque counts, and puromycin (10 µg/ml) had a similar effect. The PC from retired breeder mice occupied an intermediate position between the two cases just discussed. A compartment of cells, equal to about one-fifth of the total normal PFC compartment, was identified as resistant to high concentrations of either actinomycin D or puromycin, being similar in these respects to PFC from spleens of intentionally preimmunized mice. The mitotic poison, Colcemid, did not affect plaque counts in any situation tested. The theoretical implications of these results are briefly discussed.     

EVIDENCE OF SUPPRESSOR CELL ACTIVITY IN SPLEENS OF MICE BEARING PRIMARY TUMORS INDUCED BY MOLONEY SARCOMA VIRUS

Spleens from Moloney sarcoma virus (MSV) tumor-bearing C57BL/6N mice contained four times the normal number of mononuclear cells and displayed a markedly elevated "spontaneous" (mitogen-independent) DNA synthesis on a per cell basis. The number of macrophages were increased three-fold while there was a slight reduction in the percentage of T lymphocytes. The phytohemagglutinin (PHA) response on a per cell basis of spleens from tumor-bearing mice was decreased about 90% when compared with normal control mice. The primary in vitro immune response to sheep red blood cells was also suppressed to levels of less than 10% of normals. The PHA response could be restored by purification of MSV spleen cells by rayon adherence columns and by removal of phagocytic cells by an iron/magnet technique. The activity of suppressor cells in MSV spleens was demonstrated in mixtures with syngeneic normal spleen cells where a marked impairment of the PHA response was observed. Spleen cells from tumor-free nude mice and normal spleen cells treated by anti-θ serum plus guinea pig complement (C'), both totally unreactive to PHA, had no such effect. The inhibitor cell in MSV spleens was shown to be insensitive to inactivation by anti-θ plus C', but could be removed by the adherence columns and the iron/magnet technique. These data suggest that this suppressor cell is a cell of the monocyte/macrophage series. Suggestive evidence was also presented that the suppressor cells belong to a proliferating population in MSV spleens. Similar suppressor cells have been previously demonstrated in spleens of mice during a variety of immune responses. Our data show, that a tumor, although stimulating the immune system, nevertheless may be suppressive on certain immune functions through the activation of suppressor cells.     

Suppression of hapten-specific delayed-type hypersensitivity responses in mice by idiotype-specific suppressor T cells after administration of anti-idiotypic antibodies

Delayed-type hypersensitivity (DTH) responses specific for the phosphorylcholine (PC) hapten were induced in BALB/c mice by immunization with syngeneic peritoneal exudate cells (PEC) coupled with diazotized phenyl-phosphoryl-choline. PC-specific DTH responses were elicited in such immunized mice after footpad challenge with PC-derivatized syngeneic spleen cells. Moreover, PC-immune lymph node cells could passively transfer PC-specific DTH responses to naive BALB/c mice and it was possible to demonstrate that the cells responsible for such passively transferred responses were T lymphocytes. Because the T-15 idiotypic determinant displayed on the TEPC-15 PC-binding myeloma protein is known to be a dominant idiotype associated with anti-PC antibody responses in BALB/c mice, an analysis was made of the effects of anti-T-15 idiotypic antibodies on the induction and expression of murine PC-specific DTH responses. Repeated injections of anti-T-15 idiotypic antiserum, raised in A/J mice by immunization with TEPC-15 myeloma protein, into recipient BALB/c mice both immediately before and after sensitization with PC-PEC virtually abolished the development of PC-specific DTH responses. Although administration of anti-T-15 antiserum effectively inhibited the induction phase of PC-specific DTH responses, these anti-idiotypic antibodies had no suppressive activity at the effector phase of these responses. The inhibition observed with anti-T-15 antibodies was highly specific for the PC hapten, and for PC-specific DTH responses of BALB/c but not A/J mice. Studies were conducted to address the possibility that anti-Id treatment induced suppressor T lymphocytes capable of specifically inhibiting the activity of PC-specific T cells participating in DTH responses. The results demonstrate that idiotype-specific suppressor T cells are, indeed, induced by treatment with anti-Id; moreover, such suppressor T cells, once induced, are highly effective in abrogating both the induction and the effector phases of PC-specific T cell-mediated DTH responses in BALB/c mice.     

异基因骨髓移植并发移植物抗宿主病小鼠体内IL-22的细胞来源

本研究探讨小鼠经异基因骨髓移植后发生移植物抗宿主病（GVHD）时体内IL-22的细胞来源。分别以C57BL／6和BALB／c小鼠为供受鼠,受鼠经致死剂量全身照射后输注供鼠骨髓和脾淋巴细胞悬液,建立GVHD模型。实验分为正常组（normal）、单纯照射组（TBI）、骨髓移植组（BMT）和骨髓联合脾细胞诱导GVHD组（BS）。ELISA法检测小鼠血浆中IL-22的水平;流式细胞术检测IL-22的细胞来源及所属亚群情况。结果表明,Bs组小鼠血浆中IL-22水平最高,与正常小鼠相比差异有统计学意义（P〈0．01）;BS组小鼠脾、淋巴结和外周血中淋巴细胞均可产生IL-22,且IL-22＋CD4＋T细胞百分率高于IL-22＋CD8＋T细胞;除Th22细胞外,Th1细胞和Th17细胞也是GVHD小鼠体内IL-22的细胞来源,但以Th22细胞分泌IL-22为主。结论：GVHD小鼠体内可产生高水平的IL-22,其主要来源于IFN-γ-IL-17-IL-22＋的Th22细胞。