IFN-γ induces IFN-α and IFN-β expressions in cultured rat intestinal mucosa microvascular endothelial cells

Although researchers have recently begun to pay more attention to the immunological characteristics of microvascular endothelial cells (MVECs), there are no reports on whether activation of MVECs by interferon-γ (IFN-γ) exerts any influence on the expressions of IFN-α/β. In the present study, we examined the influence of IFN-γ on the expressions of IFN-α/β in rat intestinal mucous MVECs (RIMMVECs). Different concentrations of IFN-γ were used to stimulate cultured RIMMVECs in vitro, and the cells and cell supernatants were collected at different time intervals. The influence of IFN-γ on the expressions of IFN-α/β in the RIMMVECs was examined at the mRNA and protein levels by real-time quantitative PCR and enzyme-linked immunosorbent assay (ELISA), respectively. The results indicated that IFN-γ was able to activate RIMMVECs, thereby leading to upregulated expressions of IFN-α/β. The real-time quantitative PCR analyses indicated that the IFN-α/β mRNA expression levels in RIMMVECs achieved their peak values after stimulation with IFN-γ at 20?ng/mL for 6?h and were increased by 14.88- and 3.82-fold, respectively, when compared with the levels in negative control cells. The ELISA analyses revealed that the IFN-α/β protein expression levels achieved their peak values after stimulation with IFN-γ at 40?ng/mL. The expression of IFN-α protein achieved its peak value at 12?h, while the expression of IFN-β protein achieved its peak value after 6?h. The present results suggest that the expression and secretion of IFNs may participate in the immunologic barrier function of MVECs.     

Evolution of the cellular response in P2-induced experimental allergic neuritis.

We examined the development of the inflammatory cellular response and demyelination in P2 protein-induced experimental allergic neuritis (EAN). Collections of inflammatory cells were first identified in nerve roots 14 days after immunization. Ia+ cells predominated in the evolving lesions and T-helper cells were the dominant T-cell type with T-suppressor/cytotoxic cells appearing later in the course of the disease. Vesiculation, the earliest change seen in the myelin sheath, appeared before the wave of cellular infiltration. These results indicate that myelin injury precedes inflammation in P2 protein-induced EAN, and provide further evidence that this disorder is indistinguishable from EAN induced with whole peripheral nerve myelin.     

Pioglitazone, PPARγ Agonist, Attenuates Experimental Autoimmune Neuritis

Recent advances demonstrate peroxisome proliferator-activated receptors gamma (PPARγ) agonist, pioglitazone, as an anti-inflammatory drug. We investigated the effect of pioglitazone on experimental autoimmune neuritis (EAN) rats. Pioglitazone was given once daily (10 mg/kg) by oral gavage feeding from day 1-24 (suppressive group) and day 11-24 (therapeutic group). Pioglitazone ameliorated the clinical score of EAN, decreased expression of TNF-α, IFN-γ, and the activation of NF-κB, while increasing the expression of PPARγ and IL-4. Furthermore, we observed higher expression of PPARγ and IL-4 and lower expression of TNF-α, IFN-γ and reduced activation of NF-κB in suppressive group than those in the therapeutic group, which corresponds to lower clinical score and earlier disease recovery. Our data effectively demonstrate the anti-inflammatory properties of pioglitazone in EAN by inhibition of NF-κB signaling pathway.     

Treatment for experimental autoimmune neuritis with clodronate (Bonefos)

Experimental autoimmune neuritis (EAN) serves as an animal model for human Gullain–Barre syndrome (GBS), an autoimmune disease causing demyelination and inflammation of peripheral nerves. Macrophages, which play a major role in this autoimmune inflammatory process, can be selectively targeted by high doses of bisphophonates. The goal of this study was to examine the effect of the bisphosphonate, clodronate, on the severity of the EAN model. EAN was induced in female adult rats by immunization with bovine peripheral myelin. A number of treatment protocols with clodronate were used based on the common dosage regimen of 20 mg/kg in humans starting with the appearance of clinical signs on day 10 post-immunization. The clinical parameters measured included a clinical score, a motor performance test performed on a Rotarod and body weight. The expression of the matrix metaloprotease (MMP-9) in the sciatic nerves was measured as a marker of inflammatory macrophages. Treatment with clodronate, 20 mg/kg daily and 40 mg/kg every 2 days, significantly reduced the disease severity (a 75 % decrease in severity, p < 0.01 by ANOVA) as measured by the clinical score compared to controls. Performance on the Rotarod test and body weight confirmed the clinical score findings. MMP-9 expression levels were significantly lower in the sciatic nerves of clodronate-treated rats. The present findings support the efficiency of clodronate in inflammatory diseases of the peripheral nervous system. The mechanism of action includes inhibition of inflammatory macrophages. The results suggest the use of bisphosphonates be considered in humans with GBS.     

Effect of Stilbene-Type Anion Channel Blockers on the Immune Response During Experimental Allergic Neuritis (EAN)

Abstract

We have studied the role of anion channel gating for the autoimmune response in experimental allergic neuritis (EAN) induced by bovine peripheral myelin (BPM). The influence of the stilbene-type anion channel blockers SITS and DIDS on T cell function was assessed by measurement of proliferation and by counting of interferon-gamma (IFN-γ) secreting cells (IFN-γ-sc) in response to BPM and phytohemagglutinin (PHA). SITS caused a dose-dependent increase of spontaneous proliferative activity as well as of proliferation in response to the antigenic stimulus BPM. In contrast, the drug caused a decrease of proliferation of cells stimulated with PHA. The number of cells induced to IFN-γ secretion was reduced by SITS. The suppressive effect was dependent on the degree of activity of cells without drugs. Cultures showing high numbers of BPM reactive T cells were more easily suppressed than cultures with low numbers of BPM reactive T cells. Our results suggest that anion channel gating is involved in the triggering of T cells to IFN-γ secretion. The anion channel signal pathway in lymphocytes could be a target for pharmacological intervention in inflammatory disorders. In the presently used autoimmune model, EAN, the net effect of in vivo treatment with SITS resulted in worsening of clinical signs and increased inflammatory cell infiltration in sciatic nerve, whereas the in vitro conductivity of sciatic nerve was not significantly affected by the drug. Thus anion channel gating seems to regulate activities of immune cells, and drugs with anion channel blocking properties may have effects that enhance autoimmune disease.     

人血单核细胞和U937细胞产生IFN-α的比较

一般认为人体单核-巨噬细胞(Mo-Mφ)系在体外诱生IFN-α较为困难,本文试图找到适合的培养条件,使Mo-M(?)系能在体外诱生IFN-α.结果显示:经M-CSF长期预处理和IFN-γ的短期预处理或单用IFN-γ短期预处理后,NDV刺激均能使人外周血Mo-M(?)产生较高水平的IFN-α;U937细胞只能产生低水平的IFN-α.     

Lipooligosaccharide of Campylobacter jejuni prevents myelin-specific enteral tolerance to autoimmune neuritis--a potential mechanism in Guillain-Barre syndrome?

Campylobacter jejuni-induced enteritis is the most common infection preceding Guillain-Barre syndrome (GBS), an immune-mediated polyradiculoneuritis. The acute autoimmune attack is thought to be based on C. jejuni antigens which may mimick antigens of the peripheral nervous system. Additional pathomechanisms, like disturbance of natural T cell immunoregulation by C. jejuni, have not been evaluated so far. In experimental autoimmune neuritis (EAN), a T lymphocyte-mediated animal model of human GBS, tolerance to myelin-derived autoantigens can be induced by oral feeding of the respective antigen. Here we investigated whether the lipooligosaccharide (LOS) fraction of C. jejuni may directly alter immunologic tolerance through gastrointestinal pathways. While EAN, actively induced by immunization with bovine peripheral nerve myelin could be ameliorated by precedent feeding of myelin, feeding of C. jejuni LOS along with the myelin antigen not only prevented the tolerizing effects of oral myelin but even accelerated the onset of overt EAN and augmented the myelin-specific B cell response. These findings provide evidence that LOS of C. jejuni, as produced in the gut during C. jejuni-induced enteritis, can disturb natural tolerance to definite proteins which may be or may mimic peripheral nerve antigens. In human patients this may be one of the potential mechanisms to explain why C. jejuni enteritis is a common trigger of GBS.     

Evidence for Cytokine Dysregulation in Multiple Sclerosis: Peripheral Blood Mononuclear Cell Production of Pro-inflammatory and Anti-inflammatory Cytokines During Relapse and Remission

We investigated circulating anti-inflammatory and pro-inflammatory cytokines, and their ex vivo PBMC production in the absence or presence of the neuroantigens myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG) and T cell mitogen (PHA) in MS patients in relapse and remission, patients with other neurological disorders (OND) and normal healthy controls. MS patients in relapse exhibited significantly increased PBMC production of TNF-α spontaneously compared with MS remission and healthy controls and with MBP compared with MS remission. Patients in relapse had significantly increased spontaneous, PHA- and MBP-induced PBMC IL-1β production compared with remission MS, and was increased compared (PHA only) with OND and healthy controls. In relapse there was also significantly increased PBMC IFN-γ production (PHA only) compared with remission and a significantly lower production of biologically active TGF-β1 (PHA only) compared with remission MS and OND. In contrast, MS patients in remission produced significantly less spontaneous and MBP-induced TNF-α, spontaneous, PHA- and MBP-induced IL-1β and PHA-induced IFN-γ together with increased production of biologically active TGF-β1. MOG non-specifically increased PBMC TNF-α and IL-1β production in all groups. Pro-inflammatory cytokines in corresponding plasma samples were undetectable whilst the concentration of biologically active TGF-β1 was the reverse of ex vivo PBMC findings. The increase in biologically active TGF-β1 production ex vivo in OND patients, despite active disease, compared with the low level in the MS relapse may indicate a regulatory defect in MS. We conclude that the balance between biologically active TGF-β1 and the pro-inflammatory TNF-α, IL-1β and IFN-γ is dysregulated during MS relapse-remission and that normal counter-regulatory mechanisms during the relapse phase are defective.     

Thalidomide Prolongs Experimental Autoimmune Neuritis in Lewis Rats

Thalidomide is reported to have immunomodulatory and anti-inflammatory effects, which have led to its use in the treatment of a number of immune-mediated disorders, including leprosy, discoid lupus and Behcet's disease, and to prevent immunological rejection phenomena following skin and bone marrow grafts. Experimental autoimmune neuritis (EAN) is a CD4⁺ T-cell-mediated demyelinating autoimmune disease, which represents an animal model for the study of the immunopathogenesis and immunotherapy of Guillain–Barré syndrome (GBS) in humans. We examined the effect of thalidomide in Lewis rats with EAN, which was induced by immunization with bovine peripheral nerve myelin (BPM) and complete Freund's adjuvant (CFA). Thalidomide prolonged clinical EAN when given at a dose of 200 mg/kg/day by gavage. This clinical effect was associated with increased numbers of inflammatory cells in sciatic nerve sections and elevated numbers of interferon-γ (IFN-γ) mRNA-expressing cells among lymph node mononuclear cells from thalidomide-treated EAN rats on day 17 postimmunization, i.e. at the peak of clinical EAN. The finding that thalidomide prolongs clinical EAN is in agreement with the clinical polyneuropathy reported in patients receiving treatment with thalidomide and limits its clinical usefulness.     

Proinflammatory Cytokines Regulate the Gene Expression of Hyaluronic Acid Synthetase in Cultured Rabbit Synovial Membrane Cells

To elucidate the mechanism of accumulation and fragmentation of hyaluronic acid (HA) under inflammatory conditions, we investigated the effect of proinflammatory cytokines on hyaluronic acid synthetase (HAS) mRNA expression using cultured rabbit synovial membrane cells. HASs mRNA levels were determined by real-time PCR. HAS2 mRNA expression was maximally enhanced 3.3- and 2.8-fold after 3-hour stimulation with IL-1β (1 ng/ml) and after 1-hour stimulation with TNF-α (10 ng/ml). HAS3 mRNA expression was increased by a maximum of 4.3 times after 3-hour stimulation with IL-1 β (10 ng/ml), whereas 1-hour stimulation with TNF-α (10 ng/ml) and IFN-γ (10 ng/ml) induced around a 2.5-fold increase in HAS3 mRNA. Although IFN-γ (1–100 ng/ml) alone showed little effect on HAS2 mRNA expression, the effect was synergized by combined with both IL-lβ and TNF-α, substantially increasing HAS2 mRNA expression.

These results suggest that proinflammatory cytokines regulate the HAS expression, and consequently may contribute to the accumulation and fragmentation of HA.     

两种HLA-B分子对外周血单个核细胞分泌细胞因子的影响

为了解HLA B2 7和B39分子对外周血单个核细胞 (PBMC )分泌IFN γ和TNF α的影响。我们将外源HLA B 2 70 4和B 390 5 2基因分别表达在HLAI类分子缺陷的K5 6 2细胞表面 ,与PBMC作用 12h后 ,用ELISA法检测IFN γ和TNF α的含量。结果显示 :HLA B2 7分子能显著抑制PBMC分泌IFN γ ,而对TNF α分泌的影响不显著 ;而HLA B39表达于K5 6 2细胞后 ,均不能影响IFN γ、TNF α分泌。提示HLA B2 7分子与HLA B39分子影响PBMC分泌细胞因子的能力不同     

Nasal tolerance in experimental autoimmune myasthenia gravis (EAMG): induction of protective tolerance in primed animals

Nasal administration of μg doses of acetylcholine receptor (AChR) is effective in preventing the development of B cell-mediated EAMG in the Lewis rat, a model for human MG. In order to investigate whether nasal administration of AChR modulates ongoing EAMG, Lewis rats were treated nasally with AChR 2 weeks after immunization with AChR and Freund's complete adjuvant. Ten-fold higher amounts of AChR given nasally (600 μg/rat) were required to ameliorate the manifestations of EAMG compared with the amounts necessary for prevention of EAMG. In lymph node cells from rats receiving 600 μg/rat of AChR, AChR-induced proliferation and interferon-gamma (IFN-γ) secretion were reduced compared with control EAMG rats receiving PBS only. The anti-AChR antibodies in rats treated nasally with 600 μg/rat of AChR had lower affinity, reduced proportion of IgG2b and reduced capacity to induce AChR degradation. Numbers of AChR-reactive IFN-γ and tumour necrosis factor-alpha (TNF-α) mRNA-expressing lymph node cells from rats treated nasally with 600 μg/rat of AChR were suppressed, while IL-4, IL-10 and transforming growth factor-beta (TGF-β) mRNA-expressing cells were not affected. Collectively, these data indicate that nasal administration of AChR in ongoing EAMG induced selective suppression of Th1 functions, i.e. IFN-γ and IgG2b production, but no influence on Th2 cell functions. The impaired Th1 functions may result in the production of less myasthenic anti-AChR antibodies and contribute to the amelioration of EAMG severity in rats treated with AChR 600 μg/rat by the nasal route.     

Increasing proliferation of murine adipose tissue-derived mesenchymal stem cells by TNF-α plus IFN-γ

The objective of the current study was to assess the effects of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) along with their simultaneous application on proliferation and pluripotency genes of murine adipose tissue-derived mesenchymal stem cells (AT-MSCs). The proliferation, doubling time (DT), colony-forming unit–fibroblast (CFU-F), pluripotency genes expression, and proliferation-related immunomodulatory markers of MSCs were analyzed upon activation with TNF-α (10?ng/ml), IFN-γ (10?ng/ml) and both TNF-α and IFN-γ (5?ng/ml?+?5?ng/ml). Pluripotency genes including Oct-4, Sox-2, and Nanog as well as proliferation-associated immunomodulatory cytokines such as insulin-like growth factor 1 (IGF-1) and transforming growth factor-β (TGF-β) expression were evaluated using real-time PCR. Surface expression of Qa2 (HLA-G) was analyzed by flow cytometry. Pretreatment of MSCs with TNF-α plus IFN-γ led to significantly increased proliferation, DT and CFU-F as well as expression of pluripotency genes in AT-MSCs (p < 0.01). MSCs expressed more IGF-1, TGF-β, and Qa2 upon activation with TNF-α plus IFN-γ and IFN-γ. MSCs expressed significantly decreased amounts of TGF-β and Qa2 in presence of TNF-α. TNF-α combined with IFN-γ may be improved the proliferation of AT-MSCs. Conversely, expanded MSCs pointed out low levels of the immunomodulatory marker, s especially Qa2 in the presence of TNF-α. In conclusion, we showed that TNF-α together with IFN-γ increased the proliferation of MSCs and slightly enhanced the expression of pluripotency genes.     

Augmented expression of daintain/allograft inflammatory factor-1 is associated with clinical disease: dynamics of daintain/allograft inflammatory factor-1 expression in spleen, peripheral nerves and sera during experimental autoimmune neuritis

Experimental autoimmune neuritis (EAN) is an animal model of Guillain-Barré syndrome, characterized by inflammation and demyelination of the peripheral nervous system (PNS). Daintain/allograft inflammatory factor-1 (daintain/AIF-1) is a novel interferon-gamma-inducible protein expressed by macrophages during organ specific autoimmune diseases. To study the involvement of daintain/AIF-1 in EAN we induced EAN in Lewis rats by immunizing with bovine PNS myelin (BPM) and complete Freund's adjuvant (CFA). The expression of daintain/AIF-1 was examined in the spleen, peripheral nerves and sera during the course of EAN by immunohistochemistry and radioimunoassay (RIA). The expression of daintain/AIF-1 in the spleen and in the sciatic nerves peaked at the preclinical stage (day 7 post immunization (p.i.)) and at the height (day 15 p.i.) of clinical EAN, consistent with a disease promoting role for daintain/AIF-1. Daintain/AIF-1 expressing cells represented a subset of ED1+ or CD11b/c+ mononuclear cells. A significant increase of daintain/AIF-1-like immunoreactivity in sera occurred at the preclinical stage of EAN. Taken together, these data indicate that daintain/AIF-1 may play a proinflammatory role in the pathogenesis of EAN.     

The critical role of IL-12p40 in initiating,enhancing, and perpetuating pathogenic events in murine experimental autoimmune neuritis

Interleukin 12 (IL-12) is a proinflammatory cytokine with important immunoregulatory activities and is critical in determining the differentiation and generation of Th1 cells. For the present study, we investigated the role of endogenous IL-12 in the pathogenesis of experimental autoimmune neuritis (EAN), which is a CD4+ T-cell mediated autoimmune inflammatory disease of the peripheral nervous system. EAN is used as an animal model for Guillain-Barré syndrome of humans. Here, EAN was established in IL-12 p40 deficient mutant (IL-12-/-) C57BL/6 mice by immunization with P0 peptide 180-199, a purified component of peripheral nerve myelin, and Freund's complete adjuvant. In these IL-12-/- mice the onset of clinical disease was delayed, and the incidence and severity of EAN were significantly reduced compared to that in wild-type mice.The former group's clinical manifestations were associated with less P0-peptide 180-199 induced secretion of interferon-gamma (IFN-gamma) by splenocytes in vitro and low production of anti-P0-peptide 180-199 IgG2b antibodies in serum. Fewer IFN-gamma and TNF-alpha producing cells, but more cells secreting IL-4, were found in sciatic nerve sections from IL-12-/- mice, consistent with impaired Th1 functions and response. However, the IL-12 deficiency appeared not to affect P0 peptide 180-199-specific T-cell proliferation. These results indicate that IL-12 has a major role in the initiation, enhancement and perpetuation of pathogenic events in EAN by promoting a Th1 cell-mediated immune response and suppressing the Th2 response. This information augments consideration of IL-12 as a therapeutic target in Guillain-Barré syndrome and other T-cell-mediated autoimmune diseases.     

Simultaneous measurement of antigen-stimulated interleukin-1 beta and gamma interferon production enhances test sensitivity for the detection of Mycobacterium bovis infection in cattle

In order to identify cytokines that may be useful as candidates for inclusion in diagnostic tests for Mycobacterium bovis infection in cattle, we compared the levels of gamma interferon (IFN-γ), interleukin 1β (IL-1β), IL-4, IL-10, IL-12, macrophage inflammatory protein 1β (MIP-1β), and tumor necrosis factor alpha (TNF-α) in whole-blood cultures from tuberculosis (TB) reactor animals or TB-free controls following stimulation with M. bovis-specific antigens (purified protein derivative from M. bovis [PPD-B] or ESAT-6/CFP-10). In addition to IFN-γ responses, the production of IL-1β and TNF-α was also statistically significantly elevated in TB reactor cattle over that in uninfected controls following stimulation with PPD-B or ESAT-6/CFP-10 peptides. Thus, we evaluated whether the use of these two additional readouts could disclose further animals not detected by measuring IFN-γ alone. To this end, receiver operating characteristic (ROC) analyses were performed to define diagnostic cutoffs for positivity for TNF-α and IL-1β. These results revealed that for ESAT-6/CFP-10-induced responses, the use of all three readouts (IFN-γ, TNF-α, and IL-1β) in parallel increased the sensitivity of detection of M. bovis-infected animals by 11% but also resulted in a specificity decrease of 14%. However, applying only IFN-γ and IL-1β in parallel resulted in a 5% increase in sensitivity without the corresponding loss of specificity. The results for PPD-B-induced responses were similar, although the loss of specificity was more pronounced, even when only IFN-γ and IL-1β were used as readout systems. In conclusion, we have demonstrated that the use of an additional readout system, such as IL-1β, can potentially complement IFN-γ by increasing overall test sensitivity for the detection of M. bovis infection in cattle.     

Regulation of transforming growth factor-β production by interleukin-12

The induction of peripheral tolerance following oral antigen administration in several autoimmune disease and conventional animal models correlates with the production of transforming growth factor-β (TGF-β) and T helper type 2 (Th2) cytokines. The factors regulating TGF-β production and its relation to the Th2 response, however, have not been defined. We demonstrate that the systemic administration of antibodies to interleukin (IL)-12 to ovalbumin (OVA)-T cell receptor (TCR) transgenic mice fed high doses of OVA, followed by systemic OVA challenge, substantially enhances TGF-β, but not IL-4 production by peripheral T cells. Furthermore, we demonstrate in an in vitro T cell differentiation model that naive (CD4⁺/Mel-14^hi) OVA-TCR-T cells stimulated with OVA-pulsed dendritic cells (DC) produce four-to fivefold higher amounts of TGF-β when cultured with anti-IL-12 or anti-interferon-γ (IFN-γ). In this in vitro system, IL-4 was not required for TGF-β production by T cells; however, it appeared to enhance levels of TGF-β by promoting the growth of TGF-β-producing cells. Our findings demonstrate that IL-12 and IFN-γ are important negative regulators of TGF-β production both in vivo and in vitro, and that their modulation may be of benefit for the treatment of autoimmune disorders.     

口服S抗原对抗原诱导性葡萄膜视网膜炎影响的实验研究

目的:观察口服牛视网膜S抗原对Wistar大鼠抗原诱导性葡萄膜视网膜炎(ATU)的影响。方法:用纯化牛视网膜S抗原和福氏完全佐剂的混合乳剂致敏大鼠,14d后接种S抗原于致敏鼠眼玻璃体腔复制AIU模型。观察致敏前后口服S抗原或牛血清白蛋白(BSA)对AIU眼部表现,组织学改变、血清抗体效价、迟发型超敏反应(DTH)、淋巴细胞增殖反应的影响。结果:致敏前后口服BSA对AIU的炎性反应和免疫反应无影响。与口服BSA组比较,预口服S抗原组在AIU第1、3、5d的临床分级参数显著降低,炎症持续时间显著缩短,组织炎性细胞浸润显著减轻,血清特异性抗体滴度降低,DTH显著降低,受S抗原刺激的脾淋巴细胞增殖反应显著降低,加入IL-2共孵育后S抗原刺激的淋巴细胞增殖反应增高。致敏后口服S抗原组在AIU第5d的临床分级参数、炎症持续时间和DTH显著降低,血清特异性抗体滴度降低。结论:口服S抗原可以抑制AIU的炎性反应、细胞免疫反应和体液免疫反应。     

核因子-κB诱骗剂处理的DC对胶原诱导性关节炎大鼠外周血IFN-γ、IL-1O、抗Ⅱ型胶原抗体水平的影响

目的 探讨核因子-κB诱骗剂(NF-κB ODN Decoy)处理的DC对Ⅱ型胶原诱导性关节炎(CIA)大鼠血清IFN-γ、IL-10、抗Ⅱ型胶原抗体水平的影响及作用机制.方法 建立Ⅱ型胶原诱导性大鼠关节炎模型,NF-κB诱骗剂处理并负载牛Ⅱ型胶原(BⅡC)的大鼠脾脏来源的DC,在初次免疫第5天经尾静脉注射到CIA大鼠体内,并设空白对照组、CIA模型组和BⅡC-decoy-DC实验组.42 d后观察各组关节炎指数和病理变化,采用酶联免疫吸附法(ELISA)检测各组大鼠血清中IFN-γ、IL-10、抗Ⅱ型胶原抗体的含量.结果 与空白对照组相比,CIA模型组大鼠血清中IFN-γ、抗Ⅱ型胶原抗体含量升高,而IL-10含量降低(P＜0.05),而BⅡC-decoy-DC实验组经NF-κB诱骗剂处理并负载BⅡC获得的DC注射后,与CIA模型组相比,血清中IFN-γ、抗Ⅱ型胶原抗体含量降低,而IL-10含量升高,差异有统计学意义(P＜0.05).结论 NF-κB诱骗剂处理并负载BⅡC的DC具有明显抑制CIA大鼠外周血IFN-γ和抗BⅡC抗体产生,促进IL-10水平的增加,对类风湿关节炎有较好的治疗作用.