慢性乙型肝炎病毒感染者辅助性T淋巴细胞亚群的变化

目的 了解慢性乙型肝炎病毒（HBV）感染者体内辅助性T淋巴细胞（Th细胞）亚群的变化,探讨HBV感染慢性化与Th细胞亚群变化的关系。方法 通过细胞内染色技术,采用流式细胞术检测HBV感染者外周血中Th1细胞和Th2细胞的水平。结果 慢性HBV感染者中,乙型肝炎病毒e抗原（HBeAg）阳性感染组和HBV-DNA复制组Th1数量明显低于健康对照组（9．46±2．06,9．52±2．41与11．18±3．12相比,P〈0．05）;HBeAg阳性组、丙氨酸氨基转移酶（ALT）升高组、HBV-DNA复制组Th2细胞数量明显高于健康对照组（3．05±1．12,3．12±1．12,2．97±1．12与2．38±0．96相比,P〈0．05）;HBeAg阳性感染组、ALT升高组和HBV-DNA复制组Th1／Th2比值都明显低于健康对照组差异有统计学意义（P〈0．05）。结论 慢性HBV感染者Th1／Th2比例失衡,表现为Th1／Th2比值下降,Th2细胞数量优势,Th1／Th2比例失衡可能与肝脏损伤程度和病毒复制水平有关,Th1／Th2比值可以作为监测HBV慢性感染者免疫状态的重要指标。     

Abnormality of helper/suppressor T cell ratio in patients with hemophilia

Lymphocyte subpopulations in patients with hemophilia were analyzed. The results were compared with those in age- and sex-matched controls. The patients had been receiving blood and blood products including Factor VIII or Factor IX for a number of years as required at the time of the onset of the disease. Heparinized peripheral blood was used in direct tests for cell marker analysis with OKT4, OKT8 and OKT11 monoclonal antibodies. There were less OKT4+ cells in the hemophiliac blood as compared with the controls, while both the groups had the same number of OKT8+ cells. As a result, the OKT4/OKT8 ratio was markedly depressed in the hemophiliac group and the conversion of the OKT4/OKT8 ratio was observed in the group of patients receiving long-term therapy with anti-hemophiliac products. Alteration of lymphocyte subpopulations in patients with hemophilia in relation to antihemophiliac therapy was discussed.     

类风湿关节炎患者Th亚群在其发病机制中的作用

目的在单细胞水平上研究类风湿关节炎 (RA)患者滑液及外周血中 Th1/Th2细胞因子模式,探讨 Th亚群在 RA发病机制中的作用和意义. 方法15例 RA患者的滑液单个核细胞 (SFMC)和外周血单个核细胞 (PBMC) 及 10例正常人的 PBMC用 PMA离子霉素和莫能菌素刺激培养 6 h,细胞内细胞因子免疫荧光双标染色后,用流式细胞仪检测 Th亚群. 结果与 PBMC[Th1, Th2, Th0分别为( 8.1± 2.1)%,( 2.8± 1.0)%,( 1.8± 0.5)% ]相比, RA患者 SFMC中 Th1和 Th0的比例明显增高 [Th1( 29.2± 3.9)%, Th0( 4.0± 1.4)% ],而 Th2则明显降低 [(1.2± 0.6)% ]; RA患者和正常人 PBMC中, Th1,Th2,Th0差异均无显著性意义 [正常人 Th1, Th2, Th0分别为( 7.3± 2.2)%,( 3.4± 1.1)%,( 2.1± 0.8)% ]. 结论RA患者关节内存在 Th亚群的不平衡, Th1和 Th0占明显优势, Th2则明显减少,恢复 Th1/Th2平衡对 RA的疾病进程和治疗将有重要意义.     

An integrated view of suppressor T cell subsets in immunoregulation

The immune system evolved to protect organisms from a virtually infinite variety of disease-causing agents but to avoid harmful responses to self. Because immune protective mechanisms include the elaboration of potent inflammatory molecules, antibodies, and killer cell activation--which together can not only destroy invading microorganisms, pathogenic autoreactive cells, and tumors, but also mortally injure normal cells--the immune system is inherently a "double-edged sword" and must be tightly regulated. Immune response regulation includes homeostatic mechanisms intrinsic to the activation and differentiation of antigen-triggered immunocompetent cells and extrinsic mechanisms mediated by suppressor cells. This review series will focus on recent advances indicating that distinct subsets of regulatory CD4+ and CD8+ T cells as well as NK T cells control the outgrowth of potentially pathogenic antigen-reactive T cells and will highlight the evidence that these suppressor T cells may play potentially important clinical roles in preventing and treating immune-mediated disease. Here we provide a historical overview of suppressor cells and the experimental basis for the existence of functionally and phenotypically distinct suppressor subsets. Finally, we will speculate on how the distinct suppressor cell subsets may function in concert to regulate immune responses.     

T辅助淋巴细胞亚群平衡变化与支气管哮喘发病的关系研究

目的研究大鼠哮喘模型以及哮喘患者静脉血中T辅助淋巴细胞(T     

雷公藤氯内酯醇对急性肺损伤患者T辅助淋巴细胞功能的调节作用体外研究

目的观察急性肺损伤(ALI)患者T辅助淋巴细胞(Th)亚群平衡变化及雷公藤氯内酯醇(T4)的调节作用。方法实验分健康对照组、ALI组、雷公藤T4组、地塞米松(DX)组。采用酶联免疫斑点法(Elispot)测定ALI患者外周血单个核细胞(PBMC)中Th亚群,酶联免疫吸附法(ELISA)测单个核细胞培养上清中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-10含量。结果与对照组比较,ALI组、雷公藤T4组、DX组Th2/Th1比值明显升高(P<0.01);与ALI组比较,雷公藤T4组、DX组Th2/Th1比值下降(分别P<0.01,P<0.05)。Th1亚群与TNF-α含量呈正相关(γ=0.78,P<0.01)。Th2亚群与IL-10含量呈显著正相关(γ=0.66,P<0.01)。结论ALI时Th亚群比例失调,提示促炎/抗炎反应失衡。雷公藤T4能够调控Th亚群失衡状态,防止ALI炎症瀑布反应的放大。     

Schistosoma japonicum egg antigen-specific T cell lines in man. Induction of helper and suppressor T cell lines and clones in vitro in a patient with chronic schistosomiasis japonica.

T cell lines (TCLs) specific for Schistosoma japonicum egg antigen were established from a patient with chronic schistosomiasis japonica to investigate the regulatory mechanism of S.japonicum egg antigen-driven T cell responses in man. All five TCLs tested were CD2+, CD4+, CD8-, and were strongly proliferative only to S. japonicum egg antigen in the absence of exogenous IL-2. All but one TCL produced IL-2-like lymphokines in vitro, indicating their helper T cell functions. One TCL, SjE-3, failed to produce IL-2-like lymphokines. Moreover, this TCL suppressed the specific proliferation of autologous peripheral blood lymphocytes to S. japonicum egg antigen. This TCL produced a soluble suppressor factor(s). These functional diversities among established TCLs were also confirmed by cloned T cells. Our observations might suggest that the regulatory system through helper and suppressor T-T interactions somehow involved in T cell responses to the egg antigen in human chronic schistosomiasis japonica.     

T suppressor cell growth factor and anti-CD3 antibodies stimulate reciprocal subsets of T lymphocytes

Because of the central role of IL-2 in clonal expansion of T cells, we have postulated that lymphocyte subpopulations with opposing regulatory functions might be independently regulated by differential requirements for expression of cell-surface IL-2-R. Purified CD4+ and CD8+ cells proliferated in an IL-2-dependent manner to crosslinked anti-T cell receptor antibodies (anti-CD3-Seph). Similarly, both CD4+ and CD8+ cells became IL-2 responsive after incubation in T suppressor cell growth factor (TsGF), a newly described approximately 8,000 Mr product of activated CD4+ cells. In support of our hypothesis, however, we observed that subpopulations of CD4+ and CD8+ cells, possessing distinct cell-surface antigens, showed differential responses to these stimuli. Those cells of suppressor-inducer or suppressor-effector phenotype failed to proliferate when cultured in anti-CD3-Seph plus IL-2, but did proliferate in an IL-2-dependent manner to TsGF. Furthermore, the suppressor-effector population was unresponsive to TsGF plus IL-2 when cocultured in anti-CD3-Seph, suggesting that functionally induced Ts may be refractory to growth stimuli. Conversely, cells with helper-inducer or cytolytic phenotype proliferated when incubated in anti-CD3-Seph and IL-2, while remaining essentially unresponsive to TsGF and IL-2. The results could not be explained by differences in the level of CD3 expression by the T cell subsets. Thus, cells within the helper and suppressor lineages appear to have distinct and reciprocal patterns for the induction of IL-2 responsiveness.     

Clinical approach to urethritis, mucocutaneous lesions, and inguinal lymphadenopathy in homosexual men

The spectrum of sexually transmitted diseases observed among homosexual men is diverse, but in general includes the same infections observed among heterosexuals. A systematic approach to the diagnosis of these diseases, incorporating sexual history, predominant symptoms, findings from physical examination, and office laboratory evaluation will frequently yield a specific diagnosis. Prompt diagnosis and treatment of patients, and when appropriate, of contacts are of critical importance to the prevention of unnecessary morbidity and further transmission of disease.     

Two subsets of naive T helper cells with distinct T cell receptor excision circle content in human adult peripheral blood

During ageing thymic function declines and is unable to meet the demand for peripheral T helper (Th) cell replenishment. Therefore, population maintenance of naive Th cells must be at least partly peripherally based. Such peripheral postthymic expansion of recent thymic emigrants (RTEs) during ageing consequently should lead to loss or dilution of T cell receptor excision circles (TRECs) from a subset of naive T cells. We have identified two subsets of naive Th cells in human adult peripheral blood characterized by a striking unequal content of TRECs, indicating different peripheral proliferative histories. TRECs are highly enriched in peripheral naive CD45RA(+) Th cells coexpressing CD31 compared with peripheral naive CD45RA(+) Th cells lacking CD31 expression, in which TRECs can hardly be detected. Furthermore we show that CD31(-)CD45RA(+) Th cells account for increasing percentages of the naive peripheral Th cell pool during ageing but retain phenotypic and functional features of naive Th cells. As CD31 is lost upon T cell receptor (TCR) engagement in vitro, we hypothesize that TCR triggering is a prerequisite for homeostatically driven peripheral postthymic expansion of human naive RTEs. We describe here the identification of peripherally expanded naive Th cells in human adult blood characterized by the loss of CD31 expression and a highly reduced TREC content.     

Immunoregulatory T cell circuits in man. Alloantigen-primed inducer T cells activate alloantigen-specific suppressor T cells in the absence of the initial antigenic stimulus

Although alloantigen-specific suppressor T cells are generated in MLR, the cellular signals that lead to activation of suppressor T cells as opposed to cytotoxic T cells are unknown. The current study was undertaken to characterize interactions among T cell subsets involved in the generation of suppressor T cells in MLR. Human peripheral blood Leu-2+ (suppressor/cytotoxic) and Leu-3+ (helper/inducer) T cell subsets were activated with allogeneic non-T cells and then examined for their inductive effects on fresh autologous T cells. Fresh Leu-2+ cells proliferated in response to alloantigen-primed Leu-3+ cells and subsequently suppressed the response of fresh autologous Leu-3+ cells to the original, but not third party, allogeneic stimulator non-T cells. Moreover, only Leu-2+ cells that lacked the 9.3 marker, an antigen present on the majority of T cells including precursors of cytotoxic T cells, differentiated into suppressor cells. The alloantigen-specific suppressive effect of Leu-2+,9.3-cells was not mediated by cytolysis of allogeneic stimulator cells, nor could it be explained by alteration of MLR kinetics. Suppression was observed only when activated Leu-2+ cells were added to fresh MLRs within 24 h of initiation of cultures, suggesting that these cells block an early phase of the activation of Leu-3+ cells in MLR. These results indicate that alloantigen-primed inducer T cells can activate alloantigen- specific suppressor T cells in the absence of allogeneic stimulator cells.     

肿瘤病人T细胞核仁嗜银蛋白和辅助性T细胞亚群变化

目的:探讨肿瘤病人外周血单个核细胞(PBMC)中T细胞核仁嗜银蛋白(AgNORs)变化和辅助性T(Th)细胞亚群变化的关系及其临床意义。方法PBMC经多克隆T细胞活化剂刺激,以图像分析法检测AgNORs区面积与细胞核仁面积的百分比(1.S％):PBMC被离子霉素和佛波醇酯活化5h后,以酶联免疫斑点法(ELISPOT)检测IFNY、和IL-4产生细胞的频度(％):以离子霉素加佛波醇酯刺激24h,用ELISA试刑盒检测培养上清液中的IFNY、和IL-4水平。结果 肿瘤病人(n=86)和正常人(n=44),PBMC中活化T细胞的AgNORs表达分别为4.9±1.21.S％和.7.82±1.28 1.S％,肿瘤组非常显著下降,P<0.05:肿瘤组PBMC中1112细胞额度显著上升,Th1／Th2比值显著下降:同时,肿瘤组PBMC产生IFN和IL-4水平发生相应变化,变化方式与Th亚群变化相似:在肺癌组中,转移的与未转移的,复发的与未复发的相比,Th1细胞数、Th1／Th2之比和IFNY、产生水平非常显著下降:在肿瘤组AgNORs表达与Th1细胞频度、Th1／Th2比值、IFNY产生和肿瘤病人生活状态的Kamofsky评分正相关。结论 现有病例观察结果表明,肿瘤病人PBMC小T细胞表达AgNORs下降,与患者Th1细胞功能下降正相关。     

重型再生障碍性贫血患者骨髓中辅助性T细胞亚群数量及功能的变化

目的　研究重型再生障碍性贫血 (SAA)患者在免疫抑制治疗 (IST)恢复前后骨髓中辅助性T细胞 (Th细胞 )亚群改变情况及与造血功能的关系。方法　以流式细胞仪测定 2 4例发病期、15例恢复期SAA患者及 16名正常对照者骨髓中Th细胞亚群及CD3 CD8 细胞改变情况 ;以放射免疫法测定 2 0例发病期SAA患者、12例IST后恢复期患者及 16名正常对照者血清中TNF α、IL 4水平 ;评价Th1与CD3 CD8 细胞、TNF α的相关关系 ;评价Th1、CD3 CD8 细胞、TNF α、IL 4及Th1/Th2平衡与网织红细胞、中性粒细胞绝对值的相关关系。结果　正常对照组骨髓中Th1细胞、Th2细胞百分率及Th1/Th2比值分别为 (0 .4 2± 0 .30 ) %、(0 .2 4± 0 .17) %、1.5 7± 0 .93;发病期SAA分别为 (4 .87± 2 .6 4 ) %、(0 .4 1±0 .2 6 ) %、2 1.2 2± 5 .0 7,均显著多于正常对照 (P <0 .0 1,P <0 .0 5 ,P <0 .0 1) ,恢复期分别为 (0 .5 3± 0 .2 2 ) %、(0 .4 4± 0 .15 ) %、1.38± 0 .4 5 ,与正常对照组相当 (P均 >0 .0 5 ) ;CD3 CD8 细胞亦由发病期的(32 .32± 18.6 9) %显著下降为 (13.76± 2 .96 ) % (P <0 .0 1) ;SAA发病期血清中TNF α、IL 4为 (4 .2 9± 3.15 ) μg/L、(1.2 4± 0 .73) μg/L ,高于正常对照组的 (1.2 1± 1.16 ) μg/L     

肿瘤病人T细胞核仁嗜银蛋白和辅助性T细胞亚群变化

目的　探讨肿瘤病人外周血单个核细胞 (PBMC)中T细胞核仁嗜银蛋白 (AgNORs)变化和辅助性T(Th)细胞亚群变化的关系及其临床意义。方法　PBMC经多克隆T细胞活化剂刺激 ,以图像分析法检测AgNORs区面积与细胞核仁面积的百分比 (I.S % ) ;PBMC被离子霉素和佛波醇酯活化 5h后 ,以酶联免疫斑点法 (ELISPOT)检测γ干扰素 (IFNγ)和白细胞介素 4(IL 4)产生细胞的频度( % ) ;以离子霉素加佛波醇酯刺激 2 4h ,用ELISA试剂盒检测培养上清液中的IFNγ 和IL 4水平。结果86例肿瘤病人和 44名正常人 ,PBMC中活化T细胞AgNORs表达分别为 ( 4 90± 1 2 0 )I S %和 ( 7 82±1 2 8)I S % ,肿瘤组下降非常显著 (P <0 0 5 ) ;肿瘤组PBMC中Th2细胞频度显著上升 ,Th/Th2比值显著下降 ;同时 ,肿瘤组PBMC产生IFNγ 和IL 4水平发生相应变化 ,变化方式与Th亚群变化相似 ;肺癌转移组与未转移组、复发组与未复发组相比 ,Th1细胞数、Th1/Th2之比和IFNγ 的产生下降非常显著 ;在肿瘤组AgNORs表达与Th1细胞频度、Th1/Th2比值、IFNγ 产生和肿瘤病人生活质量评分呈正相关。结论　肿瘤病人PBMC中T细胞表达AgNORs下降 ,与患者Th1细胞功能下降呈正相关。     

T cell regulation of B cell activation. I-A-restricted T suppressor cells inhibit the major histocompatibility complex-restricted interactions of T helper cells with B cells and accessory cells

The present studies were carried out to characterize the cellular interactions involved in the activation and function of the antigen-specific and antigen-nonspecific T suppressor (Ts) cells that regulate the IgG responses of Lyb-5-B cells. The in vitro activation of both Lyt-1+2- antigen-nonspecific Ts cells and Lyt-1-2+ antigen-specific Ts cells was shown to require the interaction of accessory cells and antigen-primed T cells. It was further demonstrated that this interaction was major histocompatibility complex (MHC)-restricted in that T cell recognition of I-A-encoded determinants on accessory cells was required for Ts cell activation. The activation of antigen-primed (A X B)F1 T cells with antigen in the presence of parentA or parentB accessory cells resulted, respectively, in the generation of parentA-restricted or parentB-restricted Ts cells. ParentA-restricted F1 Ts cells suppressed the responses generated by (A X B)F1 T helper (Th) cells cooperating with parentA (B + accessory) cells but did not suppress responses by the same (A X B)F1 Th cell population cooperating with parentB (B + accessory) cells. Neither parentA-restricted Ts cells alone nor parentB-restricted Ts cells alone suppressed the responses of (A X B)F1 (B + accessory) cells, whereas a mixture of these two Ts cell populations was able to significantly suppress the responses of F1 (B + accessory) cells. In contrast, responses of (A X B)F1 leads to parentA Th cells (restricted to recognizing parentA but not parentB MHC determinants on F1 cells) and (A X B)F1 (B + accessory) cells was suppressed by parentA-restricted Ts cells but not by parentB-restricted Ts cells. Collectively these findings suggest that the Ts cell populations characterized here do not function by directly inhibiting the activity of Th cells, B cells or accessory cells of a given MHC genotype, but rather that they appear to function through a unique mechanism involving highly specific inhibition of the interaction between MHC-restricted Th cells and the (B + accessory) cells required for these responses.     

实验性自身免疫性脑脊髓炎小鼠模型视神经炎发病机制：与辅助性T细胞亚群的关系

背景：视神经炎的病因多为自身免疫引起的炎性脱髓鞘,很多的视神经炎为多发性硬化的早期表现。在外周CD4+T细胞中,有5%-10%为调节性T细胞,其免疫抑制能力很强。自身免疫性脑脊髓炎所引起的视神经炎发病机制是否与辅助性T细胞亚群的有关呢？目的：分析实验性自身免疫性脑脊髓炎小鼠模型视神经炎发病机制与辅助性T细胞亚群的关系。方法：将小鼠腹腔注射百日咳菌液建立实验性自身免疫性脑脊髓炎模型,分别免疫11,15,19 d,并设腹腔注射生理盐水的佐剂组小鼠作对照。
　　结果与结论：酶联免疫吸附检测显示,与佐剂组相比,免疫后19 d组视神经白细胞介素4蛋白含量降低(P<0.05);免疫后11,15 d组视神经白细胞介素17蛋白含量升高(P<0.05);免疫后15,19 d组视神经干扰素γ蛋白含量升高(P <0.05);免疫后11,15,19 d组视神经Foxp3蛋白含量显著降低(P <0.05)。实时PCR检测显示,与佐剂组相比,免疫后11,15,19 d组视神经中干扰素γ、Foxp3 mRNA表达降低(P<0.05), RORt mRNA表达升高;免疫后15,19 d组视神经中白细胞介素4,白细胞介素17,T-beat mRNA表达升高(P<0.05)。免疫后19 d组GATA3 mRNA表达降低(P<0.05)。结果证实,实验性自身免疫性脑脊髓炎小鼠模型视神经炎的发生发展可能受到Foxp3和调节性T细胞表达减少的影响,免疫后早期白细胞介素17可能介导对炎症损伤,发病高峰期干扰素γ可能使炎症损伤程度加重。     

The relationship between 2-5A synthetase levels and persistent lymphadenopathy in homosexual men with antibodies to HTLV-III

This study compared clinical and laboratory parameters in 37 individuals with serologic evidence of exposure to human T-cell lymphotropic virus type 3 (HTLV-III) and generalized lymphadenopathy. Basal levels of the interferon-induced enzyme, 2-5A synthetase were also measured and compared with the clinical parameters. A significant linear relationship (p less than .05) was demonstrated between the logarithm of the basal synthetase level and both the number and size of palpable nodes in the posterior cervical triangles of the men studied. No other lymph node chains demonstrated such a relationship. In addition, men with more than 3 palpable nodes (the median number) in the posterior triangles had lower mean levels of lymphocytes, reduced mean mitogen responses to PWM, PHA, and ConA, elevated mean levels of IgG, IgA, and IgM, and were more frequently anergic on skin testing. These findings suggest the need for further longitudinal study of the possibility that extent of lymphadenopathy and level of 2-5A synthetase might serve as useful parameters to monitor disease activity.     

Effect of oral colchicine on T cell subsets, monocytes and concanavalin A-induced suppressor cell function in asthmatic patients

Asthmatic patients have a deficiency of concanavalin A-(Con A) induced suppressor cell function. We tested whether oral colchicine 0.5 mg twice daily for 7 days could correct this immunoregulatory abnormality. Peripheral blood mononuclear cells were incubated with Con A and then suppression of proliferation was measured by coculture of these cells with healthy volunteers' mononuclear cells and phytohaemagglutinin. Sixteen asthmatic patients had significantly (P less than 0.002) decreased Con A-induced suppressor cell function (17.0 +/- 17.2%, mean +/- s.d.) as compared to 13 healthy volunteers (37.9 +/- 14.9%). Oral colchicine significantly (P less than 0.05) increased, though only partially corrected, these 16 asthmatic patients' Con A-induced suppressor cell function (28.1 +/- 14.3%). Asthmatic patients had an increased number of monocytes (691 +/- 289 vs 388 +/- 271/mm3 for normals, P less than 0.01) and a normal number of lymphocytes, Leu 4+ total T cells, Leu 3+ helper/inducer T cells, and Leu 2+ suppressor/cytotoxic T cells as well as a normal Leu 3/Leu 2 ratio. Oral colchicine significantly (P less than 0.005) decreased the number of monocytes (451 +/- 255/mm3) without significantly affecting the number of lymphocytes, Leu 4+, Leu 3+, or Leu 2+ T cells, or the Leu 3/Leu 2 ratio. These results are consistent with the hypothesis that the deficiency of Con A-induced suppressor cell function in asthmatic patients may be due, in part, to an increased number and/or abnormal activity of monocytes. If so, then oral colchicine may have partially corrected the deficiency of Con A-induced suppressor cell function by decreasing the number and/or modulating the activity of monocytes.     

慢性乙型肝炎患者T细胞亚群及NK细胞检测的临床意义

目的 探讨T细胞亚群及NK细胞在慢性乙型肝炎诊断中的临床价值。方法 应用流式细胞术检测58例慢性乙型肝炎患者和38例正常志愿者外周血T细胞亚群及NK细胞 ,用Coulter-JT型血细胞计数仪作血细胞计数。结果 慢性乙型肝炎患者外周血CD、CDCDT细胞及CDCD细胞比例增高 ,CDCD/CDCD比值降低 ,与正常组比较(p<0.01,p<0.01,p<0.05,p<0.05) ,CDCDT细胞比例无差异。NK细胞比例也明显低于正常对照组(p<0.001)。慢性乙型肝炎患者外周血淋巴细胞数、CDCDT细胞及NK细胞数与对照组比较均明显降低(p<0.05、p<0.05、p<0.001) ,CD、CDCDT细胞数与对照组相比虽有增高趋势 ,但无统计学意义 ,CDCD细胞数与对照组比较无差异。结论 慢性乙型肝炎患者机体的免疫功能下降及比例失衡 ,对指导乙肝的临床治疗、判断预后有一定的意义。