心肺复苏后犬炎症因子和氧自由基变化及意义的探讨

目的了解心肺复苏后犬炎症因子和氧自由基的变化及意义。方法12只犬随机分为2组：心肺复苏组（CPK组）和空白对照组，每组6只，抽血检测血清肿瘤坏死因子-α（TNF-α）、白介素-6（IL-6）水平，复苏后6h取肺组织行MDA、SOD和NO测定以及行肺形态学检查。结果血清TNF-α、IL-6浓度在复苏后随时间的延长而增高，并高于本组电击前及同时间的空白对照组（P〈0．05），CPK组肺组织的MDA、NO的含量高于空白组（P〈0．01），而CPK组肺组织的SOD的含量低于空白组（P〈0．05）。CPK组肺组织的病理损害大于空白对照组。结论炎症因子TNF-α、IL-6和氧自由基参与了心肺复苏后再灌注损伤的发生发展过程。     

IL-18对慢性乙型肝炎患者Th1/Th2细胞分化的影响

目的：观察IL—18对慢性乙肝患者Thl／Th2细胞分化的影响。方法：分离40例慢性乙型肝炎患者外周血单个核细胞(peripheral blood monoclear cells，PBMC)，分别与植物血凝素(PHA，100mg/L)、HBcAg(1mg／L)、HBeAg(1mg/L)单独或联合IL—18(10μg／L)体外培养48h，ELISA法检测培养液中IL—2、IFN—γ、IL-4、IL—10水平。20例健康人群作对照。结果：IL—18对健康人群PBMC产生的Thl／Th2类细胞因子无明显影响，但对慢性乙肝患者在IL—18和HBcAg或IL—18和HBeAg联合诱导下则显著增强PBMC产生的Thl类细胞因子IL—2和IFN—γ，但对Th2类细胞因子IL-4和IL—10无明显影响。结论：IL—18增强慢性乙肝患者Thl类细胞因子的优势表达，从而促进Thl细胞的优势分化，而对Th2类细胞因子的表达无影响。     

Selective Depletion of the Allo-Antigen Specific T Cells by Fas/FasL Pathway by Cytokine IFN-γ and IL-2

Severegraft versus hostdisease (GVHD)isthemajorcauseoffailureofallogeneichematopoieticstemcelltransplantation (allo HSCT) .Thedonormatu rateTlymphocytesareactivatedwhentheyrecognizeallo histocompatibilityantigenofrecipients ,anddi rectlyswitchongraft versus hostreactionandcausetargettissueinjury[1] .DepletionofTcellsingraftorinhibitionoftheirfunctioncoulddeceleratetheoccur renceanddevelopmentofGVHD[2 ] .However ,Tcellsareabletoresistinfection ,killtumorcellsandsecretecytokinessuchasIL 3…     

A type 2 (Th2-like) pattern of immune response predominates in the pulmonary interstitium of patients with cryptogenic fibrosing alveolitis (CFA).

CFA is an inflammatory condition of the lungs resulting in scarring, pulmonary failure and death. The etiology of the disease is unknown, but the pathogenesis is believed to involve a persistent immunological reaction to unidentified antigen in the lung resulting in tissue damage. Recent advances in our understanding of the immune system have shown that different patterns of stimulatory cytokines are produced at sites of inflammation by a range of cell types. Patterns of cytokine reproduction by inflammatory cells are recognized to be associated with different patterns of immunological response, and these have been described as type 1 (or Th1-like) and type 2 (or Th2-like) on this basis. We have studied cytokine expression in the intestinal inflammatory cell infiltrate in lung tissue from patients with CFA using mRNA in situ hybridization and immunohistochemistry. Our results show that while there is evidence for both a type 1 (characterized by interferon-gamma (IFN-gamma) and type 2 (characterized by IL-4 and IL-5) response present in CFA, the type 2 (or Th2) pattern of cytokines appears to predominate. This would be consistent with a possible role for the humoral immune response in the pathogenesis of this condition. In addition, recent evidence suggests that IL-4 and IFN-gamma may be important regulatory factors for pulmonary fibroblasts. The relative paucity of IFN-gamma may contribute to the excessive fibroblast activation, deposition of collagen and scar formation that occurs in CFA.     

Cytokine treatment of mast-cell-mediated skin diseases

Abstract Cytokines released by mast cells as well as their effects on mast cell functions appear to be of major importance in the pathogenesis of mast cell mediated skin diseases. In addition, the identification of some key mediators which were found to play a crucial in vivo rôle in certain disease states may allow the development of new therapeutie strategies using cytokines or cytokine antagonists for the treatment of inflammatory skin diseases. So far, encouraging results have been obtained when diseases with mast cell involvement such as atopic eczema or mastocytosis have been treated with different IFNs. Future trials using IFNs and other newly detected cytokines or their antagonists are required to establish effective therapy regimens.     

Investigation of functional gene polymorphisms: IL-1B, IL-6 and TNFA in benign migratory glossitis in Brazilian individuals

BACKGROUND: Benign migratory glossitis (BMG) is a very common immunological oral disease of unknown aetiology. METHODS AND SUBJECTS: Fifty-three consecutive subjects affected by BMG and 53 age- and sex-matched control subjects were genotyped for IL-1B, IL-6 and TNFA polymorphisms. Binary logistic regression models were fitted and values of P < 0.05 were considered significant. RESULTS: A significant difference in the distribution of IL-1B genotypes was observed in the group with BMG in univariate analyses (P = 0.01). The multivariate analyses showed that the CT genotype of the IL1-B gene was significantly associated with a high risk to develop BMG (P = 0.02, OR 2.76). The combined presence of IL-1beta high and intermediate producers genotypes was also associated with BMG in multivariate analyses (P = 0.01, OR 3.05). IL-6 and TNFA polymorphisms were not associated with BMG in the univariate and multivariate analyses. CONCLUSION: Our findings demonstrate that the polymorphism +3954 IL-1B is associated with an increased risk of BMG development and suggest a genetic basis for disease development.