【Abstract】ObjectiveTo investigate the effect of RNA editing enzyme ADAR1 on the function of lymphocyte immune by transferring mouse lymphocytes with plasmid of sense siRNA and by suppressing the expression of ADAR1. MethodsThe cell strains of human hepatic cellular carcinoma （HCC） were frozen and thawed repeatedly to prepare for tumor soluble antigen. The isolated mouse lymphocytes, which were transferred with antisense siRNA plasmid of ADAR1 and were sensitized with soluble tumor antigen were used as the study group; those which were not transferred but were sensitized were used as the control group. The 3HTdR adulteration experiment was used to test the sensitivity of lymphocytes. The effect of ADAR1 on lymphocyte immunity was detected by lymphocytotoxicity tests. ResultsThe observation of the isolated lymphocytes implied that the growth cycle of lymphocyte was 10-14 days. The 3HTdR adulteration experiment showed the result was optimal. The number of HCCs decreased significantly for both of the groups compared with those in the blank holes, but the amplitude was much larger in the control group. The expression of ADAR1 in lymphocytes of the study group was significantly lower than that of the control group, which demonstrated that the RNA plasmid of ADAR1 suppressed the expression of ADAR1 in sensitized lymphocytes and the suppressing rate of the control group (87.47±4.62)% was significantly higher than that of study group （53.19±3.95）%. The function of lymphocytes killing targetcells in the study group was significantly inferior to that of control group (P＜0.05). ConclusionRNA editing enzyme ADAR1 may play an important role in mouse cellullar immunologic response and it is possible to attenuate the cellimmune response by depressing the expression of ADAR1.
SerumIgG,IgA,IgM,C3andC4weredeterminedbyneophelmetricimmunoassay,serumandbiliaryIL2,sIL2Rlevelsweremeasuredbyatwoantibodysandwichenzymelinkedimmunosorbentassayinpatientswithsimplegallbladdercarcinoma,withbothgallbladdercarcinomaandgallstone,withsimplegallstoneandhealthyindividuals.Theresultsshowedthat:①Comparedwithcontrols,thegallbladdercarcinomapatientshadobviouslyloweredserumandbiliarylevelsofIL2andCD+4cell;andtheypresentedamarkedincreasedserum,biliarylevelsofsIL2RandCD+8cell.②TherewascorrelationbetweenthelevelsofsIL2RandCD+8,IL2andCD+4inthepatientswithgallbladdercarcinomaandtheirclinicstage.③Comparedwiththepatientswithgallbladdercarcinoma,gallstonepatientspresentedamarkeddecreasedserumandbiliarylevelofsIl2RandCD+8cell,andamarkedincreasedserumandbiliarylevelofIL2andCD+4cell.Theresultssuggestthat:①Thepatientswithgallbladdercarcinomahaveimmunedepression;②Inthepatientswithgallbladdercarcinomaandgallstone,gallstoneasainjuryfactorbrokethebalancebetweenCD+4andCD+8,thebalancebetweenIL2anditsreceptor;③TcellsubpopulationandsIL2R,IL2levelsmaybeusedasmarkerstopredictthechangesinpatientswithgallbladdercarcinoma.
Objective Methylprednisolone (MP) is the only active drug for acute spinal cord injury (SCI), but the molecular mechanism is still further studied. To investigate the pathophysiology of SCI and the molecular mechanism of MP in treating SCI. Methods Nine rabbits were randomly divided into 3 groups, weighing (3 100 ± 140) g: sham operation group(group A, n=3), model group (group B, n=3), and drug treatment group (group C, n=3). After laminectomy was performed in3 groups, no treatment was given in group A, and the model of SCI was establ ished with modified Allen’s fall ing strike method in groups B and C at L4; then high-dose MP equivalent with human dose was adopted in group C at 2 hours after SCI and the normal sal ine in group B. All rabbits were sacrificed at 8 hours after SCI, and then the spinal cord tissues about 8 mm long which included the injuried site were obtained. Total RNA was isolated with Trizol one-step method to examine the gene expression profile by using Ogl io technologies with standard operating procedures and qual ity control as recently described respectively. GeneSpring11.0 analyzer software was used to filter potential candidate genes for statistical significance using Welch’s t test, and only genes with P lt; 0.05 and fold change (FC) ≥ 2 were retained for further analysis. Some differentially expressed genes were also verified by RT-PCR to ensure the rel iabil ity of microarray results. Results The SCI model was set up and the samples of spinal cord tissues were acquired successfully at 8 hours after SCI. The qual ify of total RNA from each group met the requirement for the microarray examination and data analysis. These differentially expressed genes involved inflammation, immunity, ion transportation, transcription factors, and so on. The results of genes IL-1α, IL-1β, and defensin 4 (NP-4) by RTPCR were consistent with that of gene-chips. The immuno-related genes included NP-3, NP-4, corticostatin 6, CAP-18, and antimicrobial peptide, which displayed obvious differential expression. Conclusion High-dose MP has protective effects on nervous function by the immunity mechanism, and the main effector may be neutrophil.
Wireless power transfer (WPT) is a new power transmission way, which can be widely used in electric vehicles and other fields. Its electromagnetic environment must be analyzed to ensure safe application. A low-power wireless power transfer system experimental platform was built, with 25 W receiving power and 47 kHz resonant frequency, which was used to carry out animal experiments. Treatment mice were exposed to environment of wireless power transfer system for 5 h a day and 6 days as one cycle. At the end of every cycle, learning memory behavior of mice were detected in T-shaped maze. The exposure experiment lasted for 12 weeks. Finally, immune parameters, sex hormones and part of organ physiological structure were detected. The results are as follows: as exposure time increased, memory behavior of mice did not change obviously with no statistical difference in sex hormone either (P > 0.05), the concentration of immune factors including tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and interleukin-1 beta (IL-1β) significantly increased (P < 0.05), and the structure of some organs showed some changes. The experimental results show that the environment of the wireless power transfer system has no effect on the memory behavior of mice, and has some effect on physiological properties of mice.
【Abstract】Objective To explore Toll-like receptor 4 (TLR4) expression and distribution in rat pancreas.Methods Reverse transcriptase-polymerase chain reaction (RTPCR) and immunohistochemistry (IHC) were applied to detect expression of TLR4-mRNA and TLR4 protein respectively. Results RT-PCR of RNA isolated from rat pancreatic tissue yielded the predicted amplicon for the TLR4. IHC/immunofluorescence revealed TLR4 protein mainly distributed in the epithelium of the pancreatic duct, vascular endothelium of the exocrine section, endocrine islet also had some signs of distribution. No TLR4 protein signal could be detected in the acinar cells. Conclusion TLR4 could be detected in rat pancreas. Its distribution is consistent with its roles in immune surveillance, mainly in tissues exposed to the external environment such as pancreatic duct as well as in immunologically important settings such as pancreatic vascular endothelium. Islet also has some signs of distribution. No TLR4 expression in acinar cells, suggesting TLR4 immunological involvement in the pathophysiology of pancreas.
Immune-mediated necrotizing myopathy (IMNM) is a type of autoimmune myopathy characterized by relatively severe proximal weakness with high serum muscle enzyme levels, myofiber necrosis with minimal inflammatory cell infiltrate on muscle biopsy, and infrequent extra-muscular involvement. The mechanism of necrotizing myopathy remains unclear. The new European Neuromuscular Centre criteria divides IMNM into three distinct subtypes according to different autoantibodies, which reminds us antibodies may be involved in the pathogenesis of IMNM and different subtypes may have different pathogenesis. This review summarizes the current understanding of the pathogenesis of IMNM.
To investigate the cause of septicemia in patients with obstructive jaundice,the correlationship between intra-biliary tract pressure(IBTP),portal veinous flow rate(PVFR)and interleukin-2(IL-2),soluble interleukin-2 receptor(sIL-2R),T lymphocyte subpopulation in patient with obstructive jaundice(Group A)has been studied.Group A was subdivided into A1,emergency operation group;A2,elective surgery group;A3,patient’s age over 60 years and A4,age under 60.Ninety patients with simple gallstone(Group B)were also tested as a contrast.The result showed that of all Group A,CD3+,CD4+,CD8+ before operation were much lower than those 10 days after operation(Plt;0.05 or Plt;0.01),while the postoperative sIL-2R was significantly higher than that of 10 days after operation(Plt;0.01),in Group A1,emergency surgery,the preoperative sIL-2R was much more higher than that in others of the jaundice group(Plt;0.01).Corralation analysis showed IBTP was negatively corralated to IL-2,CD3+,CD4+,CD8+,but it had positive correlation with sIL-2R(Plt;0.01).PVFR was positively correlated to IL-2(Plt;0.01).These indicate that obstructive jaundice with infection is closely related to the decreased host immunity.
ObjectiveTo learn further the local immunity changes of rectal cancer after neoadjuvant therapy and improve the cognition of this project. MethodsSixty cases of paraffin-embedded sections of the excised specimen from the two groups of middle and low rectal cancer patients, with (therapy group) or without (control group) neoadjuvant therapy, were studied respectively. Tumor infiltrating lymphocytes (TIL) in the two groups were counted under microscope, and also, dendritic cells (DC) were counted and morphology and distribution of the DCs were recorded through immunohistochemistry stain with monoclonal antibody, S-100. ResultsTILs and DCs in the two groups mainly assembled in the pericancerous tissues. The positive rate of TIL in therapy group was 75.00% (45/60) and 90.00% (54/60) in control group (χ2=10.58, P=0.014). S-100 positive DCs were (36.85±11.17)/HPF versus (26.50±7.68)/HPF in the therapy group and control group, respectively (P=0.001). ConclusionNeoadjuvant therapy for rectal cancer can influence the local tumor immunity enviroment by reducing TILs and increasing DCs.
Regulatory B cells (Bregs) are a subset of B cells with immunomodulatory effects. The study of Bregs began with a variety of animal models of immune diseases. Studies in patients with autoimmune diseases have further clarified that Bregs are a group of immune cells that secrete inhibitory cytokines such as interleukin-10. Abnormal functions and numbers of Bregs have been found in a variety of autoimmune diseases. The study of the negative immune regulatory network involving Bregs is expected to provide new therapeutic ideas for diseases such as immune diseases, cancer, infection and inflammation. Starting from the discovery and immune regulation mechanism of Bregs, this paper focuses on its regulatory mechanism and clinical research value in the occurrence and development of autoimmune diseases, tumors, infectious diseases and inflammation.
The pathogenesis of Vogt-Koyanagi Harada disease (VKH) has not yet been fully defined. Current studies mainly suggest that VKH is actually an autoimmune disease, especially related to the immune response mediated by various signal transduction pathways involved in the function of T cells. In recent years, the influence of the balance imbalance of various T cell subsets in cellular immunity on the pathogenesis of VKH has been a hot research direction. Currently, T helper cell 17/T regulatory cells, balance is the focus of clinical research, meanwhile, new discoveries and potential clinical treatment schemes have been made for related cellular pathways, particularly the Janus kinase/signal transducers and activators of transcription pathway and NF-kappa B pathway. The exploration of B cells in the pathogenesis of VKH has also achieved initial results through the successful application of various targeted drugs. In the future, further screening and localization of genes or proteins that are abnormally regulated or expressed in VKH, for which early comprehensive and in-depth exploration will be helpful, thus improve the efficacy of clinical treatment programs and develop new therapeutic targets.