Chronic exposure to house dust mite induces airway remodeling related to Th1 inflammation in mice

AIM: To investigate the inflammatory characteristics in the airway of mice with chronic exposure to dust mite. METHODS: The α-SMA-Cre/R26R transgenic reporter mice were intranasally exposed to dust mite extract for 60 d (DME group), and then subjected to the measurement of lung resistance. The performance of bronchoalveolar lavage, pathological changes of the lung tissues and splenocytes isolation 24 h after the last challenge were observed. The protein extracts from the lungs were subjected to the detection of α-smooth muscle actin (α-SMA) by Western blotting. The supernatants of the lung homogenate were collected for testing the levels of interleukin-4 (IL-4) and interferon-γ (IFN-γ) with enzyme-linked immunosorbent assay. CD4⁺ T-cell subsets of the splenocytes were analyzed by flow cytometry.RESULTS: The mice chronically exposed to dust mite extract demonstrated severe airway hyperresponsiveness. The pulmonary pathological sections with HE staining manifested strong evidence of airway remodeling in DME group, corresponding to an enhanced X-gal staining that is related to α-SMA activation in the subepithelial basement membrane of bronchia. Total cell and lymphocyte counts were increased in the lungs of DME group compared to control group. No difference was found in eosinophil count of mice between DME and control groups. There was an elevated level of IFN-γ in the lungs of DME challenged mice coordinated with an increased proportion of IFN-γ-producing CD4⁺ T cells in the splenocytes.CONCLUSION: Chronic exposure to dust mite in the mice induces Th1-dominant inflammation with an airway hyperresponsiveness and the development of airway remodeling.     

Expression of Th cytokines in peripheral blood before and after splenectomy in immune thrombocytopenia patients

AIM: To investigate the changes of Th cytokines before and after splenectomy in immune thrombocytopenia (ITP) patients. METHODS: The QuantiGene Plex method was used to measure the mRNA expression of Th1, Th2 (IL-4, IL-5, IL-6 and IL-10), Th3 (transforming growth factor β₁,TGF-β₁), and Th17 (IL-17) cytokines in peripheral blood of ITP patients before and after laparoscopic splenectomy and those in peripheral blood of healthy controls. RESULTS: The mRNA level of IL-2 was significantly decreased in ITP patients before operation compared with the healthy controls, whereas IL-17 was obviously over-expressed. No significant difference of the other cytokines between preoperative group and the normal controls was found. After splenectomy, the expression levels of both IL-2 and TGF-β₁ were significantly higher than those in preoperative group and the normal controls. IL-2 was also significantly increased after operation, but was still lower than that in the normal controls. No significant difference of other cytokines between postoperative group and healthy controls was observed. In addition, The Th1 cytokines (IL-2 and IFN-γ) were found to be positively correlated (r=0.647, P<0.01) in preoperative patients, while no correlation was found between the other cytokines. There was a positive correlation between IL-2 and IFN-γ (r=0.787, P<0.01) in postoperative patients. IL-17 also had positive correlations with IL-2 (r=0.554,P<0.01) and IFN-γ (r=0.461,P<0.05) in ITP patients after operation, respectively. CONCLUSION: There is an imbalance of Th cytokines in ITP patients. The mechanism of splenectomy for treating ITP may be associated with the balance regulation of Th cytokines.     

Cytokine production in mice with experimental cardiomyopathy treated with anti-L3T4 monoclonal antibody at different stages

AIM: To clarify the mechanism of treating autoimmune cardiomyopathy at different stages with anti-L3T4 monoclonal antibody. METHODS: Mice immunized with human mitochondria ADP/ATP peptides were used as the cardiomyopathy (DCM) group, and the sham-immunized mice were regarded as the controls. Mice receiving early treatment were immunized with the same peptides, followed by the injection of 400 μg of anti-L3T4 on day 0, 1 and 2 post-immunization. Mice in the late treatment group were immunized as of the early treatment group but anti-L3T4 was administered 3 months post-immunization. The cytokine expression was measured with three-color flow cytometry to quantitate the splenic Th1/Th2 cell subsets in the different groups of mice. In addition, serum and myocardial cytokines were measured by enzyme-linked immunosorbent assay and real-time PCR. RESULTS: Th1 and Th2 subsets in the early treatment group were similar to those in control group, but were drastically lower than those in DCM group. Mice in the late treatment group showed an increased level of Th1-related cytokines, while the Th2 level was between the DCM and early treatment group. IFN-γ and IL-6 levels in early treatment group were similar to those in control group. In the early treatment group, IL-4 level was higher than that in control and lower than that in DCM group, whereas IL-2 and TNF-α contents were lower than those in control and DCM group. In the late treatment group, IFN-γ and IL-2 levels were higher than those in DCM group and lower than those in the early treatment group, while IL-6 and IL-4 levels were lower than those in DCM group. CONCLUSION: These results suggest that the cytokine production in cardiomyopathic mice may be repressed by treatment with anti-L3T4 at different stages. Early treatment with anti-L3T4 has better inhibitory function than treatment in late stage of autoimmune cardiomyopathy.     

Immunomodulatory effect of Sema4D on Th1/Th2 in asthmatic rats induced by RSV and intervention of Kechuanning oral liquid

AIM To explore the effect of semaphorin 4D (Sema4D) on the immune regulation of Th1/Th2 in asthmatic rats induced by respiratory syncytial virus (RSV) and the effect of Kechuanning (KCN) intervention on the asthmatic rats. METHODS Healthy SPF female Wistar rats (n=100) were randomly divided into 10 groups: normal group, model group, Sema4D group, Sema4D antibody group, low, middle and high doses of KCN groups, and Sema4D+low, middle and high doses of KCN groups. Except the rats in normal group, the other rats were treated with RSV combined with ovalbumin (OVA) to induce asthmatic model. The pathological changes of the lung tissue were observed by HE staining, and the levels of interleukin-4 (IL-4), IL-6, IL-8, tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in bronchoalveolar lavage fluid (BALF) were measured by ELISA. RESULTS Inflammatory cell infiltration and inflammatory damage in lung tissues of the rats in model group, Sema4D group and Sema4D+low dose of KCN group were observed by HE staining, while these pathological changes were attenuated in Sema4D antibody group, low, middle and high doses of KCN groups, and Sema4D+middle and high doses of KCN groups. Compared with normal group, the levels of IL-4, IL-6, IL-8 and TNF-α in BALF of the rats in the other groups were significantly increased, and the level of IFN-γ was significantly lowered (P<0.05 or P<0.01). Compared with model group, the levels of IL-4, IL-6, IL-8 and TNF-α in Sema4D group were increased, and the content of IFN-γ was decreased (P<0.05 or P<0.01). Compared with model group, the levels of IL-4, IL-6, IL-8 and TNF-α in Sema4D antibody group, low, middle and high doses of KCN groups, and Sema4D+low, middel and high doses of KCN groups were significantly decreased (P<0.01), while the content of IFN-γ was significantly increased (P<0.05 or P<0.01). No significant difference among Sema4D antibody group, Sema4D+middle and high doses of KCN groups, and low, middle and high doses of KCN groups was observed (P>0.05). CONCLUSION Sema4D causes Th1/Th2 immune imbalance and aggravates asthma. Inhibition of Sema4D reduces the production of inflammatory factors and regulates the balance of Th1/Th2. KCN may attenuate RSV-induced immune inflammation of asthmatic rats by inhibiting Sema4D, so as to achieve the anti-asthma effect.     

Relationship between Th1/Th2 balance and CD28/CTLA-4 expression on peripheral blood T cells in patients with systemic lupus erythematosus

AIM: To investigate the pattern of Th1/Th2 balance in systemic lupus erythematosus(SLE) patients and the relationship between CD28/CTLA-4(cytotoxic T-lymphocyte antigen-4) molecule expression and Th1/Th2 balance.METHODS: Eighteen SLE patients met the ARA 1997 updated SLE criteria were selected in the study. According to Bombardier's SLEDAI criteria, all patients were classified into two groups: active group(12 cases) and static group(6 cases). Fourteen normal individuals, matched for age and sex of the patients, served as controls. The peripheral blood mononuclear cells(PBMCs) were isolated by density gradient centrifugation and cultured in RPMI-1640 culture medium. After treated with PMA(5 μg/L) and ionomycin(500 μg/L) for 72 h, the PBMCs were collected, the contents of IFN-γ and IL-10 in the supernatant of cultured PBMCs were detected using enzyme linked immunosorbent assay(ELISA). The expression of CD28 and CTLA-4 molecules on T cells were detected by flow cytometric technique with double staining by FITC or PE labeled monoclonal antibodies. RESULTS: The level of IL-10 was higher in the PBMCs of active and static SLE patients(351.29 ng/L±153.31 ng/L and 319.37 ng/L±153.39 ng/L) than that in controls(254.48 ng/L±120.69 ng/L), but the difference did not reach statistical significance(P>0.05). The level of IFN-γ was significantly lower in the PBMCs of active SLE patients(25.76 ng/L±16.09 ng/L) than that in controls(50.71 ng/L±27.92 ng/L, P＜0.05). The ratio of IL-10/IFN-γ was significantly higher in active SLE patients(18.74±13.77) than that in controls(6.66±4.95, P<0.05). Either before or after culture, the expression of CD28 molecule on CD3⁺and CD8⁺ T cells from all SLE patients was not remarkably different from that in the cells of controls. Before culture, the expression of CTLA-4 molecule on CD3⁺T cells of active SLE patients(0.79%+0.37%) was significantly lower than that in the cells of controls(1.31%+0.61%, P<0.05). After culture, the expression of CTLA-4 molecule on CD3⁺ T cells of SLE patients was still lower than that in the cells of normal controls without statistical significance(P＞0.05).The expression level of CD28 molecule on CD3⁺ or CD8⁺ T cells in active SLE patients and controls was not correlated with the levels of IFN-γ and IL-10 in the supernatants(P＞0.05). The level of CTLA-4 molecule expression on CD3⁺ T cells of active SLE patients was positively correlated with IFN-γ level(r=0.681, P<0.05), while was negatively correlated with IL-10 levels(r=-0.624,P＜0.05) and the ratio of IL-10/IFN-γ(r=-0.738, P<0.01). The level of CTLA-4 molecule expression on CD3⁺ or CD8⁺ T cells of controls showed no correlation with IFN-γ levels, while showed negative correlations with IL-10 level(r=-0.587, P<0.05; r=-0.563, P<0.05, respectively).CONCLUSION: There is a bias in the differentiation of Th0 cells towards Th2 in SLE patients. CTLA-4 probably plays an important role in this mechanism through suppressing the signal transmitted by CD28.     

IgE-FcεRI crosslink accelerates atherosclerosis development in allergic asthmatic mice

AIM:To investigate whether allergic asthma accelerates the development of atherosclerosis in mice related to Th2 cells and interleukin-4 (IL-4), and the roles of activation of macrophages by immunoglobulin E (IgE)-Fc ε receptor I (FcεRI) crosslink during the process. METHODS:Six-week-old ApoE^-/- mice were sensitized and challenged by ovalbumin to establish the allergic asthma model, and then assigned to 3 groups:control group, asthmatic placebo group and asthmatic IL-4 monoclonal antibody (mAb) intervention group (intervention for 8 weeks). The lesion area was measured by oil red O staining. The percentages of Th2 cells in the splenocytes of the mice were analyzed by flow cytometry. The mRNA expression of IL-4 and the macrophage-related inflammatory factors, monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α) and IL-6, in the spleen was detected by real-time PCR. Local IgE and FcεRIα expression in the plaque was evaluated by immunofluorescence/immunohistochemical staining, and the circulating IL-4 and IgE were measured by ELISA. RESULTS:Accompanied by aggravated atherogenesis in asthmatic ApoE^-/- mice, the proportion of Th2 cells and IL-4 mRNA in the spleen, IgE and FcεRIα expression in the aortic root, and the mRNA expression of MCP-1, MIP-1α and IL-6 were markedly increased. After 8-week treatment with IL-4 mAb, the lesion area in the aortic root of asthmatic ApoE^-/- mice was markedly decreased, the elevated IgE and FcεRIα expression was significantly decreased, and the mRNA expression of macrophage-related inflammatory factors was also decreased. CONCLUSION:Allergic asthma accelerates the atherosclerosis in ApoE^-/- mice, which is associated with the increased Th2 cells and IL-4, and the activation of macrophages by IgE-FcεRI crosslink.     

Protective effects and mechanism of astragalus injection on asthmatic rats

AIM: To explore the protective effects and mechanism of astragalus injection on asthmatic rats.METHODS: OVA was injected intraperitoneally and inhaled to produce the asthmatic model.Forty rats were randomly divided into five groups: control group,asthma group and astragalus groups of high,medium and low dose.The concentrations of IL-4,IFN-γ in BALF,the expression of IL-4 mRNA,IFN-γ mRNA and phospho-p38 MAPK in lung tissues were respectively measured by ELISA,RT-PCR and Western blotting.The number of inflammatory cells in BALF and histropathology changes were observed.RESULTS: In asthmatic group,the number of inflammatory cells and the concentrations of IL-4 in BALF and the expression of IL-4 mRNA,phospho-p38 MAPK in lung tissue were higher,but IFN-γ and IFN-γ mRNA were lower than those in normal control rats (P<0.01).In astragalus group,the number of inflammatory cells,the concentrations of IL-4 in BALF and the expression of IL-4 mRNA,phospho-p38 MAPK in lung tissue were lower,but IFN-γ and IFN-γ mRNA were higher than those in normal control rats (P<0.01),and histropathology damage was alleviated significantly.The efficacies in the astragalus groups of high,medium and low dose were similar,which no significant difference was observed among them.There were positive correlations between the expression of 〖JP3〗phospho-p38 MAPK and the number of eosinophil,the concentration of IL-4,IL-4 mRNA (r=0.63,r=0.69,r=0.71,〖JP〗 P<0.01),and negative correlations between the expression of phospho-p38 MAPK and IFN-γ and IFN-γ mRNA (r=-0.65,r=-0.68,P<0.01).CONCLUSION: p38 MAPK may play a role in pathological process of asthma.Astragalus effectively treats asthma by inhibiting the expression of phospho-p38 MAPK,correcting the inbalance of IFN-γ/ IL-4 and decreasing the number of inflammatory cells.     

Abnormal T-cell receptor signal pathway in murine autoimmue cardiom yophy induced with adenine nucleotide translocase

AIM: To explore the molecular mechanism in the pathogenesis of dilated cardiomyopathy (DCM) by analyzing the expression of T cell signaling molecules in mice with autoimmune DCM. METHODS: Mouse DCM model was induced by immunizing the animals with adenine nucleotide translocase (ANT) synthetic peptides. P56lck in T cells was detected with real-time fluorescent quantitative PCR in both DCM-group and the sham-immunized controls. At the same time, flow cytometry was used for quantity of Th cell intracellular cytokine IFN-γ and IL-4, ELISA for examining the level of serum anti-ANT antibody, immune histochemistry for investigating the expression of CD45 in Th cells. RESULTS: The mRNA expression of P56lck (1 369.51±874.05 vs 47.93±10.21, P<0.01), the percentage of IFN-γ and IL-4 (especially IL-4) (8.27±1.29 vs 5.58±0.59, P<0.01; 9.93±1.53 vs 2.05±0.21, P<0.01), the level of anti-ANT autoantibody (0.105±0.015 vs 0.006±0.002, P<0.01) and expression of CD45 (0.154±0.021 vs 0.026±0.008, P<0.01) were all elevated significantly in DCM-group compared with the controls. CONCLUSION: Impairment of T cell receptor (TCR) signal transduction pathway plays an important role in the development of DCM induced with ANT synthetic peptides in mice.     

Influence of GPIF on the expression of costimulatory molecules lineaged T cells in mice with immunodeficiency in vivo

AIM:To investigate the effects of goat placenta immunoregulating factor (GPIF) on the expression of costimulatory molecules lineaged T cells in BALB/c mice. METHODS:Animal model for immunodeficiency made from BALB/c mice with whole-body irradiation by 5 Gy 60Coγ-ray was applied for research. The immunosuppressive mice were injected with GPIF for seven days continuously. FACS was applied to analyze the rate of CD28+, CD152+, CD4+CD28+, CD8+CD28+, CD4+CD152+ and CD8+CD152+ cells in splenic lymphocytes and ELISA method was employed to measure the amount of IL-2 and IFN-γ in serum of mice. RESULTS:GPIF increased the percentage of CD28+, CD4+CD28+ and CD8+CD28+ cells (P<0.05, P<0.01), and decreased the percentage of CD152+ (P<0.05, P<0.01), CD4+CD152+ cells (P<0.05, P<0.01) in splenic lymphocytes of immunosuppressive mice significantly. GPIF increased the content of IL-2 and IFN-γ in serum of mice simultaneously (P<0.01). CONCLUSION:Immuno-enhancing effect of GPIF facilitates the costimulation of CD28 pathway, which can activate T cells and accelerate the course of renewing T cell activity. The function of GPIF may have close relationship with an immune network formed by the secretion of IL-2 and IFN-γ and the expression of CD28 and CD152.     

Mechanism responsible for pulmonary fibrosis induced by concomitant chronic smoke exposure and pentoxifylline administration

AIM: To investigate the impact of long-term administration of pentoxifylline (PTX) on morphology and inflammation of the lung in mouse models with chronic exposure of cigarette smoke. METHODS: Male BALB/c mice were randomized into the following four study groups: smoke-exposure only, shamed smoke-exposure, smoke-exposure and PTX administration, shamed smoke-exposure and PTX administration. Animals assigned to smoke-exposure were put inside a chamber twice a day for cigarette smoke exposure. The oral dose of PTX allocated to each mouse was about 20 mg·kg-1·d-1. Animals were sacrificed anaesthetically at day 120. Slices of lung were stained with H&E for pathological analysis. Modified ashcroft pulmonary fibrosis score (mAPFS) was estimated, and IFN-γ (a Th1 cytokine), IL-4 (a Th2 cytokine) in broncho-alveolar lavage fluid (BALF) and hydroxyproline in mouse lung tissue were measured by commercial kits of ELISA assay. RESULTS: Lungs in smoke-exposure only group exhibited emphysema-like morphology, low mAPFS (median 1.50, 95%CI 1.25-3.75), lowest hydroxyproline (2.43±0.11) mg/L and lowest ratio of IL-4 to IFN-γ (20.3±25.5), whereas lungs in smoke-exposure and PTX interference group exhibited interstitial fibrosis-like morphology, highest mAPFS (4.75, 4.09-5.71), highest hydroxyproline (5.57±0.55) mg/L and highest ratio of IL-4 to IFN-γ (70.7±59.9) among the four study groups (P<0.01). CONCLUSION: Interference of pulmonary inflammation induced by chronic smoke-exposure with PTX leads to the development of pulmonary fibrosis, which may relate to the turnover of Th1 polarized inflammation into Th2 polarized inflammation of the lungs.     

Effects of inactivated HIV-1 particles on human CD4+T cell activation and Th1/Th2 cytokine secretion in whole blood

AIM: To investigate the effects of AT-2-inactivated HIV-1 particles on human CD4+T cell activation and cytokine secretion in whole blood (WB) in vitro. METHODS: HIV-1ⅢB particles were inactivated by AT-2 chemical and the concentration of p24 antigen was determined by p24 ELISA. AT-2-inactivated HIV-1ⅢB particles were added to human WB culture system in serial concentrations to stimulate the cells. PHA was used as positive control. After 24 h, all the cultural supernatants were harvested and the concentrations of Th1 (IL-2, IFN-γ and TNF-α) and Th2 (IL-4, IL-6 and IL-10) cytokines released to the supernatants were detected by cytometric bead array (CBA). The percentage of CD69 expression on CD4+T cells from WB was detected by immuno-fluorescence staining plus flow cytometry. RESULTS: The concentration of p24 antigen in the AT-2-inactivated specimen was 85.5 μg/L. 24 h later, the percentage of CD69 expression on CD4+T cells from control group was (1.62±0.63) %, whereas it was (38.82±6.00)%, (3.83±1.07)%, (5.94±0.85)% and (9.30±1.22)% in PHA group, HIV-1 (1/500) group, HIV-1 (1/50) group and HIV-1 (1/5) group, respectively. Cytokines secreted by WB in control group were mainly TNF-α and IL-6. However, all the six cytokines tested were strikingly increased in PHA group, as well as in HIV-1ⅢB groups. CONCLUSION: AT-2-inactivated HIV-1ⅢB particles activate CD4+T cells from WB, and up-regulate both Th1 and Th2 cytokine secretion in WB. Besides the effects of viral proteins, other mechanisms may be proposed that HIV-1 particles act as antigen presenting cell (APC) because many host-derived immune molecules are incorporated into HIV-1 envelop when it is released from infected cells by budding, and exert immune modulation.     

中国园艺学会2012年学术年会暨庆祝《园艺学报》创刊50周年—园艺学进展论坛征文通知

"中国园艺学会2012年学术年会暨庆祝《园艺学报》创刊50周年—园艺学进展论坛"将于2012年10月在西安举行,即日起征集:①研究论文摘要,②有关园艺学进展的综述文章。经审查合格的摘要和综述将分别收入"中国园艺学会2012年学术年会论文摘要集"和"庆祝《园艺学报》创刊50周年—园艺学进展论坛专辑",并于会前以     

Specific antitumor immune response induced by pcDNA3.1+/MAGE-3 DNA vaccine in mice

AIM: To construct pcDNA3.1+/MAGE-3 DNA vaccine and investigate the antigen-specific antitumor immune responses induced by pcDNA3.1+/MAGE-3 DNA vaccine in vivo. METHODS: C57BL/6 mice challenged with B16/MAGE-3 cells were immunized by intramuscular injection of pcDNA3.1+/MAGE-3 DNA vaccine every 10 days. pcDNA3.1+ plasmid and PBS were used as controls. After three cycles of immunization, murine splenic lymphocytes, serum, and tumor were obtained for cytotoxity assay, detections of cytokines (IL-2 and IFN-γ), measurement of MAGE-3 antibody, and tumor inhibitory rates, respectively. RESULTS: The pcDNA3.1+/MAGE-3 DNA vaccine immunized murine lymphocytes induced specific cytotoxicity against B16/MAGE-3 cells. Significantly increased secretions of IL-2 and IFN-γ were detected. The titres of antibody against MAGE-3 were 1∶1 and 1∶20, while controls were negative. The tumor inhibitory rate in pcDNA3.1+/MAGE-3 group was significantly different from that in controls. CONCLUSION: The pcDNA3.1+/MAGE-3 DNA vaccine was constructed successfully. pcDNA3.1+/MAGE-3 DNA vaccine activates both cellular and humoral immune responses, and induces antigen-specific antitumor immune responses in vivo.     

Effect of glucocorticoid-treated dendritic cells on asthmatic Th2 response

AIM: To investigate the effect of dexamethasone-treated dendritic cells (DCs) on Th2 cytokine production from autologous T cells in asthmatic patients and explore the mechanisms by studying the effect of dexamethasone on differentiation, maturation and function of DCs from patients with asthma. METHODS: Human peripheral blood monocyte-derived DCs generated from asthmatic patients and healthy subjects were cultured in the absence or presence of dexamethasone. The phenotypic characterization of DCs was analyzed by flow cytometry. The mature DCs were harvested, washed, and then cocultured in vitro with autologous T cells purified by a nylon cotton column. The DC-T coculture supernatants were collected after 72 h incubation and analyzed for levels of IL-5 and IFN-γ by ELISA. RESULTS: The concentrations of IL-5 in the culture supernatants of DC-T coculture were significantly up-regulated in patients with asthma compared with that in healthy controls ［(145.13±89.76) ng/L vs (50.28±22.37) ng/L, P<0.01］. The level of IFN-γ in the DC-T coculture supernatants tended to be decreased in asthmatic patients than that in healthy controls, although this difference did not achieve statistical significance ［(197.58±76.32) ng/L vs (220.46±65.34) ng/L, P>0.05)］. There were significantly decreased levels of IL-5 by autologous T cells primed by dexamethasone-treated mature DCs from asthmatic patients ［(45.39±19.61) ng/L vs (145.13±89.76) ng/L, P<0.01］, alterations not observed from healthy controls (P>0.05). IFN-γ production was decreased by autologous T cells primed by dexamethasone-treated mature DCs from both asthmatic patients and healthy controls ［asthma group: (40.21±22.89) ng/L vs (197.58±76.32) ng/L, P<0.01; healthy controls: (56.78±20.37) ng/L vs (220.46±65.34) ng/L, P<0.01］. Dexamethasone-treated DCs exhibited decreased expression of CD83 (P<0.01) and increased expression of CD14 (P<0.01) in both asthmatic patients and healthy controls. CONCLUSION: DCs of asthmatic patients induce a Th2-skewed cytokine production from autologous T cells. Dexamethasone-treated DCs inhibit the Th2 reactions, and this effect is probably mediated through the pathway that dexamethasone inhibits DCs maturation and skews the macrophage/DC balance towards the macrophage side and thus directs the development more towards the macrophage lineage.