过继转输胚胎抗原耐受T细胞诱导自然流产孕鼠母胎免疫耐受

探讨过继转输胚胎抗原耐受T细胞对小鼠自然流产模型妊娠预后及宿主孕鼠免疫细胞对父系抗原免疫耐受状态的影响。以CBA/J×BALB/c为正常妊娠模型 ,CBA/J×DBA/ 2为自然流产模型 ,将自然流产模型CBA/J孕鼠于孕 4d (着床期 )分别腹腔注射大鼠抗小鼠CD80和CD86mAb或大鼠同型IgG。于孕 9d ,应用免疫磁珠阴性分选三组孕鼠的脾脏T细胞 ,并将三组T细胞分别转输至孕 4d的CBA/J×DBA/ 2孕鼠。于宿主孕鼠孕第 9天 ,采用单向混合淋巴细胞反应分析宿主孕鼠脾脏免疫细胞对父系抗原的增殖能力 ,并用流式细胞术分析经父系抗原刺激的宿主孕鼠脾脏T细胞内IL 2表达水平。于孕 1 4d分别观察宿主孕鼠的胚胎吸收率。结果显示 ,过继转输胚胎抗原耐受T细胞和转输正常妊娠模型孕鼠的T细胞均可诱导宿主孕鼠脾脏免疫细胞对父系抗原的增殖能力及IL 2的表达显著下降 (P <0 0 5 ) ,孕 1 4d胚胎吸收率也显著下降 (P <0 0 5 )。这些结果表明 ,于孕早期过继转输胚胎抗原耐受T细胞和转输正常妊娠模型孕鼠的T细胞能诱导宿主孕鼠母 胎免疫耐受 ,防止母体对胚胎的免疫排斥 ,从而使自然流产模型的妊娠预后达到正常妊娠水平。     

过继转输胚胎抗原耐受T细胞对宿主母-胎界面细胞因子表达的影响

目的探讨过继转输胚胎抗原耐受性T、B细胞对宿主孕鼠妊娠预后及母胎界面TH1TH2型细胞因子表达的影响。方法♀CBAJ×♂DBA2为自然流产模型,于孕4d(着床期)分别腹腔注射大鼠抗小鼠CD80和CD86McAb或大鼠同型IgG。于孕9d,分选脾脏T细胞和B细胞,并过继转输至孕4d的自然流产模型♀CBAJ×♂DBA2孕鼠,孕第14天测定宿主母胎界面组织体外培养上清液中TH1TH2型细胞因子(IL4、IL10、TNFα、IFNγ)水平,并比较各组宿主孕鼠胚胎吸收率。结果转输胚胎抗原耐受T细胞和转输正常妊娠模型孕鼠的T细胞均使宿主孕鼠母胎界面IL4和IL10表达显著增加,而IFNγ和TNFα表达则显著下降,且胚胎吸收率也显著下降(P<0.05)。结论于孕早期过继转输胚胎抗原耐受T细胞和正常妊娠模型孕鼠的T细胞可通过调节宿主孕鼠母胎界面TH1TH2型细胞因子的平衡,从而诱导母胎免疫耐受。     

过继转输的胚胎抗原耐受T、B细胞在受体孕鼠体内的归巢和分析

目的 :观察过继转输的胚胎抗原耐受T、B细胞在受体孕鼠体内的归巢和分布 ,以探讨免疫耐受T细胞在诱导受体母 胎免疫耐受中的作用机制。方法 :于孕 4天 (着床期 )给小鼠自然流产模型CBA J×DBA 2孕鼠腹腔注射抗CD80和CD86mAb ,以诱导母 胎免疫耐受。孕 9天应用免疫磁珠分选孕鼠脾脏T、B细胞 ,并用CFSE体外荧光标记。将标记的T、B细胞分别转输至孕 4天的CBA J×DBA 2孕鼠 ,36小时后在双光子共聚焦显微镜下观察T、B细胞在受体体内脾脏、子宫引流淋巴结及母 胎界面组织中的分布。结果 :过继转输的T、B细胞分布在孕鼠体内脾脏和子宫引流淋巴结 ,但并不留驻在母 胎界面。结论 :过继转输的胚胎抗原耐受T细胞定居于外周免疫器官 ,从而介导受体孕鼠对相应父系抗原的免疫耐受。     

环孢素A诱导自然流产模型孕鼠脾脏CD4+CD25+Foxp3+的调节性T细胞扩增及外周母胎免疫耐受

目的探讨环孢素A(Cyclosporin A,CsA)对小鼠自然流产模型妊娠预后及外周母胎免疫耐受的影响.方法以正常妊娠模型CBA/J×BALB/c为对照组,自然流产模型CBA/J×DBA/2为研究组,CBA/J孕鼠于妊娠第4天分别腹腔注射5 mg/kg CsA.单向混合淋巴细胞反应分析孕鼠脾脏免疫细胞对父系抗原的增殖能力,ELISA分析上清液IL-2分泌水平,流式细胞术分析脾细胞CD4 CD25 Foxp3 调节性T细胞扩增,并观察两种模型各组胚胎吸收率.结果于妊娠第4天腹腔注射CsA显著降低自然流产模型孕鼠胚胎吸收率以及孕鼠外周免疫细胞对父系抗原的增殖能力与IL-2分泌(P＜0.01,P＜0.01,P＜0.01),促进脾脏CD4 CD25 Foxp3 调节性T细胞亚群扩增(P＜0.01).结论孕早期腹腔注射CsA可诱导自然流产模型孕鼠外周免疫细胞对父系抗原的特异性免疫耐受,从而使自然流产模型孕鼠的妊娠结局达到正常妊娠水平,提示CsA可能成为治疗妊娠失败的有效药物.     

过继转输TSA诱导的CD4^＋CD25^＋调节性T细胞对不明原因复发性流产的治疗作用

目的观察过继转输TSA诱导的CD4^＋CD25^＋调节性T细胞（CD4＋CD25＋Treg）对不明原因流产的作用机制及妊娠预后的影响。方法以雌性CBA/J×雄性BALB/c为正常妊娠模型,以雌性CBA/J×雄性DBA/2J为自然流产模型,使用免疫磁珠方法分选雌性CBA/J小鼠脾脏CD4^＋CD25^＋Treg细胞,并使用流式细胞术检测分选纯度。采用TSA对流产孕鼠外周CD4^＋/CD25^-T细胞Foxp3基因特定位点进行表观修饰,以实现Foxp3稳定、持久的表达,并将CD4^＋Treg分别转输至流产模型孕4d（着床期）的雌性CBA/J孕鼠,于孕14d分别观察宿主孕鼠的胚胎吸收率。结果与对照组比较,过继转输TSA诱导的CD4^＋CD25^＋Treg细胞的宿主孕鼠的胚胎吸收率（11.27%）显著下降。结论孕早期过继转输TSA诱导的CD4^＋CD25^＋Treg细胞疗法能诱导宿主母胎免疫耐受,有利于妊娠的维持。     

不同雄性淋巴细胞及其Exosomes过继转输改善妊娠丢失孕鼠胚胎发育的比较分析

目的:分析雄性T淋巴细胞及其Exosomes(Exo)过继转输对妊娠丢失孕鼠胚胎发育的保护作用。方法:分别将健康男性外周血单个核细胞(PBMC)、BALB/c及DBA/2雄鼠脾细胞体外诱导增殖,蔗糖密度梯度离心联合超滤制备Exo。CBA/J(♀)×BALB/c(♂)为正常妊娠对照,CBA/J(♀)×DBA/2(♂)为妊娠丢失URSA模型。将URSA孕鼠随机分组,经尾静脉或皮下注射,分别予以父方、非父方、无关雄鼠脾细胞或其Exo,以及男性PBMC来源Exo过继转输。观察胚胎发育,计算胎盘体积、胚胎吸收率及妊娠丢失率。结果:URSA组胎盘体积明显缩小,胚胎吸收率、妊娠丢失率显著升高(均P<0.000 5);尾静脉或皮下注射不同来源细胞及Exo后,孕鼠胎盘体积显著恢复,胚胎吸收率、妊娠丢失率显著下降(均P<0.000 5)。不同治疗组内两种注射途径产生的疗效无差异(均P>0.05);不同细胞来源Exo过继转输后,胚胎吸收率的下降幅度显著强于细胞治疗组(均P<0.05);男性Exo过继转输后,妊娠丢失率的下降幅度显著强于细胞治疗组及鼠源Exo治疗组(均P<0.05)。结论:过继转输不同来源雄性T淋巴细胞及其Exo均可明显改善胚胎发育。Exo作为非细胞成分生物学制剂,有望取代传统细胞过继免疫治疗。     

过继转输的胚胎抗原耐受T细胞在妊娠小鼠体内细胞因子及协同刺激分子的表达特征

目的 :分析过继转输的小鼠胚胎抗原耐受T细胞内细胞因子及细胞表面协同刺激分子的表达特征。方法 :以♀CBA/J×♂DBA/ 2为自然流产模型 ,将自然流产模型CBA/J孕鼠于孕 4天 (着床期 )分别腹腔注射大鼠抗小鼠CD80和CD86mAb或大鼠同型IgG。于孕 9天 ,应用免疫磁珠阴性分选两组孕鼠的脾脏T细胞 ,将T细胞进行碳氧氢化荧光素双乙酸盐琥珀酰亚胺酯 (CFSE)体外荧光标记 ,再分别过继转输至孕 4天的CBA/J×DBA/ 2孕鼠。在宿主孕鼠孕第 9天 ,处死小鼠取脾细胞 ,用流式细胞术分析在DBA/ 2父系抗原刺激下过继转输的T细胞细胞因子IL 2、IL 4、IL 10和IFN γ及协同刺激分子CD2 8和CTLA 4的表达。结果 :与过继转输的胚胎抗原非耐受T细胞相比 ,过继转输的胚胎抗原耐受T细胞IL 10的表达显著增加 ,IL 2和IFN γ的表达则显著下降 (P <0 0 5 ) ,IL 4的表达无明显改变 (P >0 0 5 ) ;细胞表面CD2 8的表达显著下降 ,而CTLA 4的表达却显著增加 (P <0 0 5 )。结论 :过继转输的小鼠胚胎抗原耐受T细胞内Th2型细胞因子和表面CTLA 4表达上调 ,而Th1型细胞因子和表面CD2 8的表达则下降。胚胎抗原耐受T细胞通过Th2型细胞因子表达优势和协同刺激信号降调节 ,在母 胎免疫耐受的维持中发挥着重要作用。     

环孢素A诱导妊娠失败模型孕鼠外周母-胎免疫耐受

目的探讨环孢素A(cyclosporin A,CsA)能否诱导妊娠失败模型CBA/J×DBA/2孕鼠外周母-胎免疫耐受。方法分别使用CBA/J×DBA/2及CBA/J×BALB/c作为妊娠失败模型和正常妊娠模型,CBA/J小鼠于妊娠第4天(着床期)腹腔注射不同剂量(0、5、10、15mg/kg)CsA,妊娠第9天和第14天时分别采用单向混合淋巴细胞反应分析孕鼠外周脾脏免疫细胞对父系抗原的增殖能力,并用RT-PCR分析细胞IL-2mRNA含量以研究脾脏细胞母-胎免疫耐受状态;妊娠第14天观察两组的胚胎吸收率。结果(1)于妊娠第4天腹腔注射5、10、15mg/kg CsA后,妊娠失败模型胚胎吸收率分别下降至2.86%、5.75%及11.24%,明显低于对照组(P<0.001,P<0.01,P<0.01);而对妊娠成功模型胚胎吸收率无显著性影响(P>0.05)。(2)混合淋巴细胞反应研究显示,于妊娠第4天腹腔注射CsA,可使妊娠第9、14天的妊娠失败模型孕鼠外周脾脏免疫细胞对父系抗原的增殖能力显著下降(P均<0.01);RT-PCR分析显示,孕鼠脾细胞受父系抗原刺激后IL-2转录显著下降(P均<0.01)。结论于孕早期腹腔注射CsA可诱导妊娠失败模型孕鼠外周免疫细胞对父系抗原的特异性免疫耐受,从而使自然流产模型孕鼠的妊娠结局达到正常妊娠水平,提示CsA可能成为治疗妊娠失败的有效药物。     

体外扩增的CD4~+CD25~+调节性T细胞过继转输对自然流产模型妊娠预后的影响

为了观察体外扩增的CD4~+CD25~+调节性T细胞(CD4~+CD25~+Treg)对不明原因复发性流产(RSA)妊娠预后的影响并探讨其作用机制。以雌性CBA/J×雄性BALB/c为正常妊娠模型,以雌性CBA/J×雄性DBA/2J为自然流产模型,磁珠分选雌性CBA/J小鼠脾脏CD4~+CD25~+Treg并流式细胞术(flow cytometry,FCM)分析细胞纯度。妊娠第14天的CBA/J雌鼠(与雄性DBA/2J交配)为流产组;妊娠第14天的CBA/J雌鼠(与雄性BALB/c交配)为正常妊娠组;处女型CBA/J雌鼠脾CD4~+CD25~+Treg过继转输到孕4 d(着床期)CBA/J雌鼠(与雄性DBA/2J交配)体内为对照组;经体外培养扩增4 d的脾CD4~+CD25~+Treg过继转输到孕4 d(着床期)CBA/J雌鼠(与雄性BALB/c交配)体内为治疗组。分别于孕14 d分别观察宿主孕鼠的胚胎吸收率并测定宿主血清细胞因子IFN-γ/IL-10/TGF-β1表达水平和脾细胞叉状头转录因子Foxp3 mRNA相对含量。结果与对照组比较,过继转输体外扩增的CD4~+CD25~+Treg的宿主孕鼠的胚胎吸收率(11.32%)显著下降;治疗组中血清IL-10/IFN-γ、TGF-β1/IFN-γ比例有显著升高,外周血细胞因子IFN-γ有显著升高,细胞因子IL-10、TGF-β1无显著差异;Foxp3 mRNA相对表达量显著升高。孕早期经体外扩增的CD4~+CD25~+Treg疗法能诱导妊娠免疫耐受,有利于向妊娠维持的Th2、Th3、Tr1细胞偏移,叉状头转录因子Foxp3在妊娠免疫耐受上起着重要作用。     

环孢霉素A对小鼠自然流产模型外周CD4~+CD25~+T细胞及妊娠结局的影响

为探讨着床期应用环孢霉素A(CsA)对小鼠自然流产模型外周CD4+CD25+T细胞及其妊娠结局的影响,以CBA/J♀×DBA/2♂为自然流产模型,在孕第4天给孕鼠单次口服不同剂量的CsA。孕第14天计数胚胎吸收率;并采用流式细胞术分析孕鼠脾脏CD4+CD25+T细胞比例。结果表明:与自然流产模型孕鼠比较,于着床期给予0.1 mg/kg、1 mg/kg、10mg/kg CSA,可显著降低自然流产模型胚胎吸收率(P<0.05)。在应用CsA后,自然流产模型孕鼠脾脏CD4+CD25+细胞占CD4+T细胞的比例显著增加(P<0.05)。表明CsA可通过上调外周CD4+CD25+T细胞,从而诱导母胎免疫耐受,改善妊娠预后。     

Role of L-selectin in the development of autoimmune diabetes in non-obese diabetic mice

Autoimmune diabetes is characterized by an early mononuclear infiltration of pancreatic islets and later selective autoimmune destruction of insulin-producing beta cells. Lymphocyte homing receptors have been considered candidate targets to prevent autoimmune diabetes. L-selectin (CD62L) is an adhesion molecule highly expressed in naive T and B cells. It has been reported that blocking L-selectin in vivo with a specific antibody (Mel-14) partially impairs insulitis and diabetes in autoimmune diabetes-prone non-obese diabetic (NOD) mice. In the present study we aimed to elucidate whether genetic blockade of leukocyte homing into peripheral lymph nodes would prevent the development of diabetes. We backcrossed L-selectin-deficient mice onto the NOD genetic background. Surprisingly NOD/L-selectin-deficient mice exhibited unaltered islet mononuclear infiltration, timing of diabetes onset and cumulative incidence of spontaneous diabetes when compared to L-selectin-sufficient animals. CD4, CD8 T cells and B cells were present in islet infiltrates from 9-week-old L-selectin-sufficient and -deficient littermates. Moreover, total splenocytes from wild-type, heterozygous or NOD/L-selectin-deficient donor mice showed similar capability to adoptively transfer diabetes into NOD/SCID recipients. On the other hand, homing of activated, cloned insulin-specific autoaggressive CD8 T cells (TGNFC8 clone) is not affected in NOD/L-selectin-deficient recipients. We conclude that L-selectin plays a small role in the homing of autoreactive lymphocytes to regional (pancreatic) lymph nodes in NOD mice.     

Auto-reactive B cells in transgenic mice

In order to understand how the natural occurrence of autoreactive B cells is controlled in normal individuals, and how self reactive B cells can escape this control during diverse clinical situations, many different transgenic mice have been generated expressing self reactive antibodies. In this review, we focus our attention on disease-associated self reactive transgenic models which show the variety of the tolerization mechanisms. The same transgenic lines are also used to analyse the effects of the autoimmune genetic background on the self reactive B cell fate, as well as to study the influence of infectious agents on the behaviour of the auto-reactive transgenic B cells.     

Immunological mechanisms of contact hypersensitivity in mice

Contact hypersensitivity (CHS) is an animal model in which the immunological mechanisms of allergic contact dermatitis (ACD) in humans can be studied but is also widely used in the study of many basic immunological mechanisms. In CHS, a pre-sensitized animal is re-exposed to an antigen, thereby eliciting an immunological reaction at the site of antigen exposure. CHS consists of two phases: sensitization and elicitation phase. In the sensitization phase, the first contact of the skin with a hapten leads to binding of the hapten to an endogenous protein in the skin where they form hapten-carrier complexes which are immunogenic. The hapten-carrier complex is taken up by Langerhans cells (LCs) and dermal dendritic cells (dDCs) which migrate from the epidermis to the draining lymph node. Here, they present the haptenated peptides to naive T cells which are subsequently activated. The newly activated T cells proliferate and migrate out of the lymph node and into circulation. In the elicitation phase, re-exposure of the skin to the hapten activates the specific T cells in the dermis and triggers the inflammatory process responsible for the cutaneous lesions. Originally CHS was regarded as being solely driven by T cells but recently other cell types such as B1 cells, natural killer (NK) T cells and NK cells have shown to mediate important functions during the response as well. Here, we have described the molecular and cellular pathways in the development of CHS and have focused on recent advances and novel knowledge in the understanding of the immunoregulatory mechanisms involved in CHS.     

口服生长抑素基因疫苗对小鼠免疫影响的初步研究

目的 研究口服生长抑素(SS)基因疫苗在体内表达HBsAg/SS融合蛋白情况.方法 用SS基因疫苗免疫小鼠,姬姆萨染色观察细菌在体内分布;观察小鼠质量增长情况;应用免疫组化法显示小肠乙肝表面抗原(HBsAg)和SS阳性细胞的分布及数量变化.结果 免疫后16 h空肠细菌数量达到高峰,免疫后4 d脾脏出现细菌;两试验组小鼠体质量较对照组均无显著变化;首次免疫后第3周两试验组小肠内出现HBsAg阳性细胞并维持至第7周;首次免疫后第5、7周两试验组小肠内SS阳性细胞数量比对照组极显著减少(P＜0.01).结论 口服型SS基因疫苗免疫小鼠后可在小肠表达HBsAg/SS融合蛋白,同时SS阳性细胞数量减少,推测该基因疫苗刺激机体表达蛋白后能产生SS抗体.     

Antigen-pulsed epidermal Langerhans cells protect susceptible mice from infection with the intracellular parasite Leishmania major

Efficient vaccination against the parasite Leishmania major, the causative agent of human cutaneous leishmaniasis, requires the development of a resistance-promoting CD4⁺ -mediated Th1 response. Epidermal Langerhans cells (LC) are critically involved in the induction of the primary immune response to Leishmania infection. They are able to ingest the parasites, to express MHC class II molecules with extraordinarily long half-life and to activate naive L. major -specific Th cells. Considering these unique properties, we studied the capacity of LC to mediate resistance to L. major in vivo. A single i.v. application of LC that had been pulsed with L. major antigen in vitro induced the protection in susceptible BALB/c mice against subsequent challenges with L. major parasites. Resistance could neither be induced by unpulsed LC, nor by L. major antigen alone or by L. major -pulsed macrophages. Development of resistance was paralleled by a reduced parasite burden and by a shift of the cytokine expression towards a Th1-like pattern. In contrast, control mice developed a Th2 response. In vitro exposure of LC to L. major antigen induced the expression of IL-12 (p40) mRNA. In conclusion, our data demonstrate that LC are able to serve as a natural adjuvant and to induce a protective immune response to L. major infection. This effect is based on the initiation of a Th1-like response that is likely to be mediated by IL-12.     

Voluntary exercise increases the new cell formation in the hippocampus of ovariectomized mice

Voluntary exercise, such as running, can induce dramatic increases in adult hippocampal neurogenesis and improve learning and memory function. A recent report showed that exercise also improved memory problems in postmenopausal women. In this study, we examined whether voluntary running exercise could increase new cell formation in the hippocampus under menopausal conditions, modeled with ovariectomized (OVX) mice. Voluntary running exercise for 1 week significantly increased the number of bromodeoxyuridine (BrdU)- and Ki-67-immunoreactive cells in the hippocampus of mice 2 weeks after ovariectomy. In addition, 1 week of voluntary running exercise after 2 weeks in OVX mice increased the numbers of doublecortin- and calretinin-immunoreactive cells in the hippocampus. These data demonstrate that exercise may increase the birth of new cells in the hippocampus under estrogen-deprived conditions, suggesting that exercise may be helpful in improving brain function in climacteric women.     

卵清白蛋白特异性T细胞免疫诱导BALB/c小鼠的调节性免疫应答

目的：研究T细胞免疫后正常小鼠的调节性免疫应答，方法：应用体外扩增的卵清白蛋白（OVA）特异的T细胞克隆免疫BALB／c小鼠，3H－TdR掺入法分析细胞增殖，3H－TdR标记靶细胞检测杀伤T细胞的杀伤效应，间接免疫荧光法分析血清中抗T细胞抗体水平。结果：T细胞免疫后能诱导BALB/c小鼠产生调节性T细胞的增殖反应，对靶细胞的杀伤效应以及针对于活化的T细胞的体液免疫应答，并进一步降低机体对OVA抗原的应答，结论：T细胞免疫能诱导正常机体的调节性免疫应答。     

水通道蛋白5基因对小鼠树突状细胞功能影响的研究

目的 探讨水通道蛋白5(AQP5)基因的表达对小鼠骨髓来源的树突状细胞(bonemarrow-derived dendritic cells,BMDC)分化成熟的影响.方法 分离培养AQP5基因敲除(AQP5-/-)的小鼠及野生型小鼠的BMDC,采用LPS诱导其成熟,采用FACS检测DC表型和内吞作用的变化,采用3H-TdR掺入法检测其对异种淋巴细胞的刺激能力.结果 与野生型小鼠相比,AQP5基因敲除后DC表面共刺激分子CD40、CD80、CD86的表达下降;其内吞能力下降;野生型小鼠来源的DC在与颗粒性蛋白质接触30 min后仍可继续上升,而AQP5-/- 来源的DC在相互作用30 min后内吞能力达到高峰;野生型小鼠来源的DC对异种淋巴细胞的刺激能力远大于AQP5-/-小鼠.结论 AQP5介导的跨膜水转运对于DC功能的正常发挥具有重要意义.其具体信号途径有待进一步研究.     

超重症联合免疫缺陷小鼠细胞免疫功能特征研究

超重症联合免疫缺陷小鼠(B.C.B-17scid-beige)是将自然杀伤细胞(NK)缺陷基因(bg 基因)导入重症联合免疫缺陷病小鼠(C.B-17scid)体内得到的一种新品系小鼠.为确定该鼠基本细胞免疫特征,我们测定了该鼠 T、NK 和淋巴因子激活的杀伤细胞(LAK)等的功能,以及聚肌胞(poly I-C)对该鼠 NK 细胞活性的影响。该小鼠脾淋巴细胞不能针对 T 细胞有丝分裂原刀豆蛋白(ConA)的刺激而产生增殖反应。同正常对照小鼠相差非常显著(P<0.01)。该鼠 NK 细胞活性(对 YAC-1细胞杀伤活性)明显低于亲代 scid 小鼠和正常小鼠(P<0.01),经聚肌胞(100μg/只)预先刺激后该鼠 NK 细胞活性未见增加.而亲代 scid 小鼠则有明显增加。该鼠脾脏细胞经白细胞介素—2刺激后,LAK 细胞活性(对 P815细胞杀伤活性)明显低于亲代 scid 小鼠和正常小鼠(P<0.01)。上述结果表明 B、C、B-17scid-beige 小鼠是一种 T、NK和 LAK 细胞联合免疫缺陷小鼠,该鼠 B 细胞功能也是缺陷的(详见它文)。上述缺陷是 scid 基因和 bg 基因共同作用的结果,该动物为建立人—免疫缺陷动物模型提供了一种更为理想的受体小鼠,并为基础免疫学研究提供了一种新的研究工具。