黄芪皂甙Ⅳ对小鼠T、B淋巴细胞增殖和腹腔巨噬细胞功能的影响(英文)

目的:探讨黄芪皂苷Ⅳ(ASI)对小鼠T、B淋巴细胞增殖和腹腔巨噬细胞分泌的细胞因子的影响.方法:采用MTT法检测T、B淋巴细胞的增殖;采用分光光度计测定法检测抗体活性;IL-1活性用胸腺细胞增殖法测定;TNF-α活性用L929细胞杀伤法测定.结果:1)ASI50-200mg/kg ig 7天能够促进T淋巴细胞增殖和抗体生成,而ASI 50-100mg/kg能够促进B淋巴细胞增殖,但是220mg/kg对B淋巴细胞增殖无影响;2)ASI体外仅在100nmol/L对T、B淋巴细胞有促进作用;3)ASI 1 nmol/L可以促进腹腔巨噬细胞分泌IL-1,而100-1000nmol/L则抑制腹腔巨噬细胞分泌IL-1;4)ASI体外可以抑制LPS刺激或无LPS刺激下的腹腔巨噬细胞分泌TNF-α.结论:ASI能够促进小鼠T、B淋巴细胞的增殖和抗体生成,同时可以抑制腹腔巨噬细胞体外分泌IL-1和TNF-α.     

rhIL-10对银屑病动物模型的治疗作用及免疫功能的影响

目的　研究重组人白细胞介素 10 (rhIL 10 )对银屑病动物模型的治疗作用以及免疫功能的影响。方法　用小鼠雌激素期阴道上皮模型、鼠尾鳞片表皮模型观察重组人白细胞介素 10的抗银屑病作用 ,并检测ConA诱导T淋巴细胞增殖、LPS诱导B淋巴细胞增殖、NK细胞活性及细胞因子(IFN γ、IL 2、IL 1、TNF α)水平。结果　rhIL 10 (5 ,2 0 ,80μg·kg-1·d-1,sc)对小鼠阴道上皮细胞有丝分裂有抑制作用 ,促进小鼠尾鳞片颗粒层的形成。对ConA诱导T淋巴细胞增殖反应及IL 2、IFN γ产生有抑制作用 ;对LPS诱导小鼠腹腔巨噬细胞产生IL 1、TNF α具有抑制作用 ;对NK细胞活性有抑制作用 ;对LPS诱导B淋巴细胞增殖有促进作用。结论　rhIL 10可能是通过抑制表皮细胞增殖与促进其分化 ,并参与抗炎与免疫调节过程而发挥治疗银屑病动物的作用     

江苏地产白首乌C21甾体苷对荷瘤小鼠的免疫保护作用

目的：探讨白首乌C21甾体苷对肝癌实体型（Heps）小鼠的抗肿瘤作用和免疫保护机制。方法：建立小鼠Heps移植模型，进行抑瘤率计算，对肿瘤病理组织进行观察；计算小鼠的胸腺、脾脏指数；用腹腔巨噬细胞吞噬中性红及分泌NO反映整体免疫功能；MTT法检测T、B淋巴细胞增殖；双抗体夹心ABC-ELISA法检测脾淋巴细胞诱生IL-2及腹腔巨噬细胞诱生TNF—α. 结果：C21甾体苷三个剂量组的抑瘤率分别为34．79％、47．08％和50．23％，病理检查可见肿瘤组织中有片状坏死；各剂量组均可降低荷瘤后异常增高的脾指数，升高胸腺指数；增强巨噬细胞吞噬能力；明显增强T、B淋巴细胞增殖反应；使脾细胞分泌IL-2及腹腔巨噬细胞分泌．TNF-α量显著提高：结论：白首乌C21甾体苷可提高荷瘤小鼠特异性和非特异性细胞免疫功能，促进抗肿瘤细胞因子的分泌．     

雷帕霉素对小鼠脾淋巴细胞走后门殖及产生细胞因子的影响

目的：研究雷帕霉素（RAPA）对ConA、PHA、LPS诱导的小鼠脾细胞增殖反应,混合淋巴细胞反应,脾T淋巴细胞亚型及细胞因子IL-2、IFN-γ、TNF-α含量的影响。方法：MTT法测定淋巴细胞增殖实验、混合淋巴细胞反应,流式细胞法测定脾T淋巴细胞亚型,结晶紫染色法测定TNF-α,E-LASI法测定IL-2,IFN-γ。结果：RAPA可显著抑制ConA、PHA和LPS诱导的小鼠脾细胞增殖和混合淋巴细胞反应（MLR）,对小鼠脾T淋巴细胞亚型无明显影响。RAPA还可明显抑制小鼠脾淋巴细胞分泌IL-2,IFN-γ,但对小鼠腹腔巨噬细胞分泌TNF-α无效。结论：RAPA抑制小鼠免疫功能的作用机制与CsA不同。     

决明子蒽醌苷对小鼠免疫功能的调节作用

目的研究决明子蒽醌苷（SCAG）体外给药对小鼠细胞免疫功能的影响。方法将小鼠淋巴细胞或巨噬细胞与不同浓度的SCAG共培养，用二甲氧唑黄（XTT）法测定T及B淋巴细胞的增殖能力、对混合淋巴细胞反应（MLR）的影响、对丝裂霉素C所致淋巴细胞增殖抑制的拮抗作用，用中性红染色法观察SCAG对巨噬细胞吞噬功能、自然杀伤（NK）细胞活性、小鼠脾细胞分泌肿瘤坏死因子（TNF）活性的影响。结果SCAG体外给药可明显促进小鼠T及B淋巴细胞的增殖，增强巨噬细胞吞噬中性红的能力，提高NK细胞活性及分泌TNF活性，并可促进MLR，拮抗丝裂霉素C对淋巴细胞增殖的抑制作用。结论SCAG体外给药可显著增强小鼠细胞免疫功能。     

玉郎伞多糖对体外BALB/C小鼠淋巴细胞和巨噬细胞分泌细胞因子的影响

目的:探讨玉郎伞多糖（YLSPS）体外对BALB/C小鼠淋巴细胞、巨噬细胞分泌肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、γ-干扰素（IFN-γ）及白细胞介素-2（IL-2）的影响及作用机制。方法:分离BALB/C小鼠腹腔巨噬细胞和脾淋巴细胞,分为空白对照组、LPS或ConA对照组和各浓度YLSPS组(50,100,200 mg·L^-1),MTT法检测脾淋巴细胞增殖,ELISA法检测细胞培养液中TNF-α、IL-6、IFN-γ、IL-2的浓度,RT-PCR法检测TNF-α、IL-6、IFN-γ、IL-2 mRNA的表达。结果:各浓度YLSPS组能剂量依赖性地促进BALB/C小鼠脾淋巴细胞增殖和TNF-α、IL-6、IFN-γ、IL-2的分泌,显著增强这些细胞因子的mRNA的表达（P<0.01或P<0.05）。结论:YLSPS体外能促进BALB/C小鼠脾淋巴细胞和腹腔巨噬细胞分泌IFN-γ、IL-2、TNF-α和IL-6,其作用机制可能与上调上述细胞因子mRNA表达有关。     

银杏内酯B对脂多糖刺激的小鼠腹腔巨噬细胞TNFα生成及大鼠胸腔多形核白细胞NF-кB活化的影响

目的研究银杏内酯B对脂多糖刺激的小鼠腹腔巨噬细胞TNFα生成及大鼠胸腔多形核白细胞NF-κB活化的影响.方法用L929细胞结晶紫染色法检测TNFα的含量,用电泳迁移率改变检测法检测NF-κB的结合活性.结果1和10 μmol·L-1银杏内酯R能够显著抑制LPS刺激的小鼠腹腔巨噬细胞TNFα的生成,其IC50为0.26μmol·L-1:1 mg·L-1LPS和1 nmol·L-1PAF均可活化大鼠胸腔多形核白细胞NF-κB;银杏内酯B能够抑制LPS或PAF刺激的NF-κR活化.结论银杏内酯B能够抑制LPS刺激的小鼠腹腔巨噬细胞TNFα生成及大鼠胸腔多形核白细胞NF-κB的活化.PAF参与LPS激活NF-κB的过程.     

丹皮总苷体外对三类免疫细胞功能的影响

目的研究丹皮总苷（ＴＧＭ）体外对３类免疫细胞功能的影响。方法采用［３Ｈ］－ＴｄＲ参入法,检测Ｔ淋巴细胞增殖反应和分泌白介素２（ＩＬ－２）活性,Ｂ淋巴细胞增殖反应以及巨噬细胞产生ＩＬ－１。结果ＴＧＭ２～５０ｍｇ·Ｌ－１可明显促进刀豆蛋白Ａ诱导小鼠Ｔ淋巴细胞增殖反应和大鼠Ｔ淋巴细胞产生ＩＬ－２,ＴＧＭ还可促进脂多糖诱导Ｂ淋巴细胞增殖反应以及大鼠腹腔巨噬细胞产生ＩＬ－１,它们的浓度－效应曲线呈钟罩形。结论ＴＧＭ具有浓度依赖性双向免疫调节作用。     

木瓜苷对大鼠佐剂性关节炎的治疗作用

目的　研究木瓜苷对佐剂性关节炎 (AA)大鼠的治疗作用及部分机制。方法　大鼠足跖皮内注射弗氏完全佐剂诱发大鼠AA模型 ;足容积法测量继发侧足肿胀度 ,进行疼痛评分和多发性关节炎评分 ,MTT法检测胸腺T淋巴细胞和脾脏B淋巴细胞的增殖反应以及腹腔巨噬细胞产生IL 1水平 ,放射性免疫法测定腹腔巨噬细胞产生TNFα 和PGE2含量。结果　大鼠免疫后d 17开始分别灌胃木瓜苷 30、6 0、12 0mg·kg-1和阿克他利 6 0mg·kg-1对照药 ,连续给药 8d。木瓜苷 6 0、12 0mg·kg-1于d 2 1、d 2 4降低AA大鼠继发侧关节肿胀度、关节疼痛评分、多发性关节炎指数 ;木瓜苷 12 0mg·kg-1恢复AA大鼠胸腺T淋巴细胞增殖能力 ;木瓜苷各剂量还可不同程度抑制AA大鼠腹腔巨噬细胞产生IL 1、TNFα 和PGE2 。结论　木瓜苷可减轻AA大鼠关节肿胀、疼痛和多发性关节炎程度 ;该作用可能与调节T淋巴细胞的功能 ,抑制腹腔巨噬细胞过度分泌炎性细胞因子有关     

毛蚶多肽提取物的体外免疫活性

目的考察毛蚶多肽提取物(PEAS)的体外免疫活性。方法 MTT法测定PEAS对小鼠脾淋巴细胞增殖的影响及对小鼠NK细胞杀伤活性的影响;中性红吞噬法测定PEAS对小鼠腹腔巨噬细胞吞噬功能的影响;流式细胞术测定PEAS所致小鼠脾淋巴细胞周期的变化;双抗体夹心ELISA法测定PEAS对主要细胞因子IFN-γ和IL-4分泌水平的影响。结果 PEAS能够显著促进小鼠脾淋巴细胞增殖(P<0.05或0.01),能够增强小鼠腹腔巨噬细胞吞噬中性红活性和小鼠NK细胞杀伤活性(P<0.05或0.01);PEAS能够促进脾淋巴细胞G0/G1期向DNA合成期(S期)转化;PEAS协同Con A作用,能够增加IFN-γ的分泌(P<0.05或0.01),并且能够抑制IL-4的分泌(P<0.05或0.01)。结论 PEAS体外可促进小鼠脾淋巴细胞、腹腔巨噬细与NK细胞的免疫功能,其机制可能与促进脾淋巴细胞DNA合成,增加IFN-γ的分泌量有关。     

Effects and mechanisms of glucosides of chaenomeles speciosa on collagen-induced arthritis in rats

Effects of glucosides of chaenomeles speciosa (GCS)-a Chinese traditional herbal medicine (CTM) on inflammatory and immune responses and its mechanisms in collagen-induced arthritis (CIA) rat were studied. Hind paw volumes of rats were measured by volume meter; lymphocyte proliferation, interleukin-1, interleukin-2, TNF-alpha level was determined by 3-(4,5-2 dimethylthiazal-2yl)2,5-diphenyltetrazoliumbromide (MTT) assay; cAMP level in synoviocytes was analyzed by competitive protein binding assay (CPBA). mRNA expression of G(i,), G(s), and TNF-alpha of synoviocytes in CIA rats was measured by RT-PCR and antibodies to collagen type II (CII) were determined by enzyme-linked immunosorbent assay (ELISA), respectively. There was a marked secondary inflammatory response in CIA model, which accompanied with the decrease of body weight and the weight of immune organs simultaneously. The administration of GCS (30, 60, 120 mg x kg(-1), ig x 7 days) inhibited the inflammatory response and restored body weight and the weight of immune organs of CIA rats. Lymphocyte proliferation and IL-2 production of CIA rats increases, together with IL-1 and TNF-alpha in peritoneal macrophages and synoviocytes. The administration of GCS (30, 60, 120 mg x kg(-1), ig x 7 days) reduced above changes significantly. GCS at the concentration of 0.5, 2.5, 12.5, 62.5, 125 mg x l(-1) increased cAMP level of synoviocytes, which decreased in CIA rats in vitro. At the same time, GCS inhibited mRNA expression of G(i,) and TNF-alpha of synoviocytes and increased mRNA expression of G(s) of synoviocytes in CIA rats. GCS had no effect on the concentration of antibodies to CII. GCS possesses anti-inflammatory and immunoregulatory actions and has a therapeutic effect on CIA rats due to G protein-AC-cAMP transmembrane signal transduction of synoviocytes, which play a crucial role in pathogenesis of this disease.     

Immune alterations in mice exposed to the herbicide simazine

Simazine, a triazine herbicide, was investigated for its in vivo immunomodulatory properties. Male C57Bl/6 mice were treated with vehicle or 300 or 600 mg/kg body weight (bw) simazine daily orally for 4 wk. The immune system was evaluated by the antibody response to sheep red blood cells (SRBC; plaque assay and serum immunoglobulin G), natural killer (NK) and macro-phage activities, lymphocyte subpopulations in the spleen and thymus, and concanavalin A (Con A)- and lipopolysaccharide (LPS)-stimulated lymphocyte proliferation using splenocytes. Body weight and spleen and thymus weight decreased generally in simazine-treated mice, while the weight of adrenal glands was higher than in the control. Simazine treatment (600 mg/kg) induced an increase in the percentage of CD4(+) cells in spleen and CD8 + in thymus. Simazine inhibited the IgM plaque-forming cell numbers and lowered the level of IgG and the proliferation of mitogen-stimulated B cells and T cells. In addition, splenic NK and peritoneal macrophage activities in exposed mice were significantly decreased. Exposure to simazine also decreased cytokine production by macrophages, such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-alpha). Taken together, data indicate that the immune system was suppressed by oral simazine exposure.     

Total glucosides of paeony suppresses adjuvant arthritis in rats and intervenes cytokine-signaling between different types of synoviocytes

Total glucosides of paeony (TGP) are active compounds extracted from the roots of Paeonia lactiflora Pall. In this study, we investigated the mechanisms of total glucosides of paeony (TGP) in the treatment of adjuvant arthritis (AA). AA in rats was established. Synoviocytes proliferation and activity of IL-1 were determined by 3-(4, 5-2dimethylthiazal-2yl) 2, 5-diphenyltetrazoliumbromide (MTT) assay. Tumor necrosis factor alpha (TNF-alpha) and prostaglandin E2 (PGE2) were measured by radioimmunoassay. Ultrastructure of synovioctes was observed under transmission electron microscope. Phosphorylation of c-Jun N-terminal kinase (JNK), extracellular regulating kinase (ERK) and p38 kinase and expression of matrix metalloproteinases (MMPs) were detected by Western blot analysis. TGP (25, 50 and 100 mg kg(-1), ig, days 14-21) inhibited secondary inflammatory reaction, bone destruction and ultrastructure change of synoviocytes in AA rats. The administration of TGP (50 and 100 mg/kg, ig, days 14-21) in AA rats significantly decreased the production of IL-1, PGE2 and TNF-alpha by macrophage-like synoviocytes (MLS). TGP (25 mg/kg) also decreased the production of PGE(2) by MLS in AA rats. Furthermore, the increased phosphorylation of MAPKs, cell proliferation, and MMPs expression in fibroblast-like synoviocytes (FLS) stimulated by supernatants of MLS in AA rats could also be inhibited by TGP (50 and 100 mg/kg, ig, days 14-21). The results suggest that TGP possesses anti-inflammatory effects by modulating the pro-inflammatory mediators production from MLS and phosphorylation of MAPKs from FLS.     

Immunomodulatory effect of caffeic acid phenethyl ester in Balb/c mice

Caffeic acid phenethyl ester (CAPE), an the active component of propolis, is known to have anticarcinogenic, antiviral and various biological activities; however, the effect of CAPE on the immunomodulatory activity in vivo remains unknown. We have investigated the effect of CAPE on the immune system in female Balb/c mice. CAPE (0, 5, 10, 20 mg/kg) was given to mice orally for 14 days. Immunomodulatory activity was evaluated by assessment of body and organ weight, lymphocyte blastogenesis, plaque-forming cell (PFC) assay, lymphocyte subpopulation by flow cytometry and cytokine production. Even though the change of body weight was not observed in CAPE-administered group, thymus weight and/or cellularity of thymus and spleen are decreased at the all dose groups of CAPE (5, 10, 20 mg/kg). On the other hand, CAPE had no effect on B lymphocyte proliferation induced by lipopolysaccharide (LPS) but increased T lymphocyte blastogenesis induced by concanavalin A (Con A) at the dose of 20 mg/kg. In the case of lymphocyte subpopulation, the population of T and B cells was not changed but CD4(+) T cell subsets are significantly increased in exposure to CAPE. The antibody responses to T lymphocyte dependent antigen, sheep red blood cell and keyhole limpet hemocyanin (KLH) were increased more than 10 mg/kg in CAPE-treated group. Likewise, the cytokine, IL-2, IL-4 and IFN-gamma were significantly increased at the dose of 20 mg/kg CAPE group. These results suggest that CAPE could have immunomodulatory effects in vivo.     

Astragaloside II triggers T cell activation through regulation of CD45 protein tyrosine phosphatase activity

Aim:

To investigate the immunomodulating activity of astragalosides, the active compounds from a traditional tonic herb Astragalus membranaceus Bge, and to explore the molecular mechanisms underlying the actions, focusing on CD45 protein tyrosine phosphatase (CD45 PTPase), which plays a critical role in T lymphocyte activation.

Methods:

Primary splenocytes and T cells were prepared from mice. CD45 PTPase activity was assessed using a colorimetric assay. Cell proliferation was measured using a [³H]-thymidine incorporation assay. Cytokine proteins and mRNAs were examined with ELISA and RT-PCR, respectively. Activation markers, including CD25 and CD69, were analyzed using flow cytometry. Activation of LCK (Tyr505) was detected using Western blot analysis. Mice were injected with the immunosuppressant cyclophosphamide (CTX, 80 mg/kg), and administered astragaloside II (50 mg/kg).

Results:

Astragaloside I, II, III, and IV concentration-dependently increased the CD45-mediated of pNPP/OMFP hydrolysis with the EC₅₀ values ranged from 3.33 to 10.42 μg/mL. Astragaloside II (10 and 30 nmol/L) significantly enhanced the proliferation of primary splenocytes induced by ConA, alloantigen or anti-CD3. Astragaloside II (30 nmol/L) significantly increased IL-2 and IFN-γ secretion, upregulated the mRNA levels of IFN-γ and T-bet in primary splenocytes, and promoted CD25 and CD69 expression on primary CD4⁺ T cells upon TCR stimulation. Furthermore, astragaloside II (100 nmol/L) promoted CD45-mediated dephosphorylation of LCK (Tyr505) in primary T cells, which could be blocked by a specific CD45 PTPase inhibitor. In CTX-induced immunosuppressed mice, oral administration of astragaloside II restored the proliferation of splenic T cells and the production of IFN-γ and IL-2. However, astragaloside II had no apparent effects on B cell proliferation.

Conclusion:

Astragaloside II enhances T cell activation by regulating the activity of CD45 PTPase, which may explain why Astragalus membranaceus Bge is used as a tonic herb in treating immunosuppressive diseases.     

Oxidative stress and pro-inflammatory responses induced by silica nanoparticles in vivo and in vitro

Oxidative stress and inflammatory responses induced by silica nanoparticles were evaluated both in mice and in RAW264.7 cell line. Single treatment of silica nanoparticles (50 mg/kg, i.p.) led to the activation of peritoneal macrophages, the increased blood level of IL-1β and TNF-α, and the increased level of nitric oxide released from the peritoneal macrophages. mRNA expressions of inflammation-related genes such as IL-1, IL-6, TNF-α, iNOS, and COX-2 were also elevated in the cultured peritoneal macrophages harvested from the treated mice. When the viability of splenocytes from the mice treated with silica nanoparticles (50 mg/kg, 100 mg/kg, and 250 mg/kg, i.p.) was measured, the viability of splenocytes was significantly decreased in the higher dose-treated groups (100 mg/kg, 200 mg/kg i.p.). However, cell proliferation without cytotoxicity was shown in group treated with relatively low dose of 50 mg/kg i.p. When leukocyte subtypes of mouse spleen were evaluated using flow cytometry analysis, it was found that the distributions of NK cells and T cells were increased to 184.8% and 115.1% of control, respectively, while that of B cells was decreased to 87.7%. To elucidate the pro-inflammatory mechanism of silica nanoparticles in vivo, in vitro study using RAW 264.7 cell line which is derived from mouse peritoneal macrophage was done. Treatment of silica nanoparticles to the cultured RAW264.7 cells led to the reactive oxygen species (ROS) generation with a decreased intracellular GSH. In accordance with ROS generation, silica nanoparticles increased the level of nitric oxide released from the cultured macrophage cell line. These results suggested that silica nanoparticles generate ROS and the generated ROS may trigger the pro-inflammatory responses both in vivo and in vitro.     

低剂量白藜芦醇增强小鼠免疫反应

目的:研究低剂量白藜芦醇的免疫调节作用.方法:用ConA和Sac分别刺激T淋巴细胞和抗原细胞并诱导细胞因子产生;[~3H]-胸腺嘧啶核苷掺入法检测淋巴细胞增殖;ELISA法检测IL-2,IL-12,IL-10和IFN-γ;用DNFB诱导小鼠迟发型超敏反应(DTH),小鼠耳肿胀作为DTH反应指标;流式细胞仪检测小鼠脾淋巴细胞亚群的变化.结果:白藜芦醇(0.75-6μmol/L)剂量依赖性地促进小鼠T淋巴细胞的增殖和IL-2的产生;白藜芦醇还剂量依赖性地促进脾脏淋巴细胞IFN-γ和IL-12的生成,同时抑制IL-10的产生;白藜芦醇(4 mg/kg)灌胃给药能对抗乙醇(16％,w/v)对小鼠DTH反应的抑制作用;白藜芦醇对脾脏淋巴细胞亚群无明显改变,但能逆转乙醇对脾淋巴细胞中巨噬细胞数量和 MHC-II分子表达的下调作用.结论:低剂量白藜芦醇能促进小鼠细胞介导的免疫反应,促进Th1细胞因子产生及影响巨噬细胞功能是其可能的机制.     

Ginsenoside compound K suppresses the abnormal activation of T lymphocytes in mice with collageninduced arthritis

Aim： To investigate the anti-arthritis and immunomodulatory activities of ginsenoside compound K （C-K） in mice with collagen-induced arthritis （ClA）. Methods： DBA/1 mice with ClA were treated with C-K （28, 56 or 112 mg.kg-l.d-1, ig） or the positive control methotrexate （2 mg/kg, ig, every 3 d） for 34 d. Splenic T and B lymphocytes were positively isolated using anti-CD3-coated magnetic beads or a pan B cell isolation kit. T lymphocyte subsets, and CD28, T cell receptor （TCR）, cytotoxic T lymphocyte-associated antigen-4 （CTLA-4） and programmed death-1 （PD-1） expression in purified splenic T lymphocytes were analyzed using flow cytometry, Western blotting and laser confocal microscopy. Results： C-K treatment significantly ameliorated the pathologic manifestations of ClA mice, remarkably inhibited T lymphocyte proliferation, and marginally inhibited the proliferation of B lymphocytes. C-K treatment significantly suppressed TNF-α and anti- Cll antibody levels, and increased IFN-y level in the joints of CIA mice, but did not alter IL-4 production. Treatment of CIA mice with C-K significantly decreased the percentages of activated T cells, co-stimulatory molecule-expressing T cells and effector memory T cells, and increased the frequencies of naive T cells and regulatory T cells. Furthermore, C-K treatment significantly decreased the expression of CD28 and TCR, whereas it increased the expression of CTLA-4 and PD-1 on T lymphocytes of ClA mice. Methotrexate treatment exerted comparable effects in all these experiments. Conclusion： C-K suppresses the progression of ClA through regulating TCR, CD28, CTLA-4 and PD-1 expression, thus inhibiting the abnormal activation and differentiation of T lymphocytes.