natural antibodies to trigger natural defense mechanisms, and prevent the spread of malaria. McClemens et al . [ 44 ] observed that the use of Lactobacillus bulgaricus (JB-1) strains can mediate IL-10 signaling pathways during intestinal parasite infection to promote the elimination of parasites.
Human microecology has been extensively investigated. The microecological system has been regarded as an organ with physiological functions in the human body. The normal flora plays an important role in human immunity, metabolism, development, nutrition
of CHB patients is diminished [ 13 ]. HBcAg can activate Toll-like receptor 2 on Kupffer cells, causing Kupffer cells to secrete additional IL-10 and inhibit the immune function of HBV-specific CD8 + T lymphocytes [ 14 ]. This process mediates the depletion of anti-HBV CD8 + T lymphocytes and induces liver immune tolerance to HBV. Programmed death molecule 1 (PD-1)/B7 homolog 1 (B7-H1) signaling pathway can negatively regulate the immune response of T and B lymphocytes, is closely related to the functional depletion of HBV-specific CD8 + T lymphocytes, and
traditional PCR, nested PCR, real-time quantitative PCR, nucleic acid sequence-based amplification (NASBA), loop-mediated isothermal amplification (LAMP) technology, and RNA simultaneous amplification and testing (SAT). On the basis of the basic principles of these experimental methods, domestic and foreign scholars have developed a composite technology that can simultaneously detect multiple pathogens. The target genes frequently amplified in the experiment include P1 protein coding gene, 16S rRNA, card gene, ATPase gene, etc. The types of clinical specimens available are
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factor (vWF) multimers into smaller forms thereby controlling vWF-mediated platelet thrombus formation [ 8 ]. However, the molecular basis and the mechanism(s) that lead to the loss of immunotolerance toward ADAMTS13 and permit the production of anti-ADAMTS13 AAbs are still unknown [ 9 ].
Therefore, it assumes a scientific relevance the clinical observation by Kosugi et al. [ 10 ], that influenza infection triggers TTP by producing anti-ADAMTS13 IgGs. The observation is crucial in light of the fact that the association between influenza infection and TTP is
region includes a helix domain, a turn-helix region, and a protease-like domain. The formation of a groove of approximately 1 nm in the protein-like structure is the main site of interaction between TfR1 and Tf. The binding of Tf and iron ions changes their spatial structures accordingly. This process results in the incorporation of iron ions into the protein to form Tf-Fe 2+ . TfR binds to Tf-Fe 2+ at physiological pH, and the Tf–TfR complex is internalized by clathrin-mediated endocytosis by pits. The intracellular Tf–TfR complex is transported to endosomal
effectively eliminate the phosphodiester bond of the target RNA and degrade target genes [ 16 ]. Given the high specificity and selectivity of siRNA, the siRNA-mediated RNAi process is widely used to prevent and control various viral infections.
Study of siRNA in anti-influenza viral infection
In 2003, Ge et al . [ 17 ] first applied the siRNA-mediated RNAi process to investigate the influenza viral infection. This study opened up a new approach for the treatment of influenza viral infection.
Study of siRNA in anti-influenza viral infection
, Hoehlig K, Roch T, et al . TLR-activated B cells suppress T cell-mediated autoimmunity. J Immun, 2008, 180(7):4763-73.
14 Evans JG, Chavez-Rueda KA, Eddaoudi A, et al . Novel suppressive function of transitional 2Bcells in experimental arthritis. J Immun, 2007, 178(2):7868-78.
15 Cross AH, Trotter JL, Lyons J. B cells and antibodies in CNS demyelinating disease. J Neuroimmunol, 2001, 112(1-2):1-14.
16 Bouaziz JD, Calbo S, Maho-Vaillant M, et al . IL-10produced by activated human B cells regulates CD4+ T-cell activation in vitro. Eur J Immun, 2010
pathways [ 13 ]. Under stimulation of vascular pathology stimulating factors, growth factors, inflammatory mediators, ultrasmall particles, calcium ions and drugs, organisms produce highly expressed and highly active protein NOX and excessive ROS formation of oxidative stress [ 14 ]. High levels of ROS can lead to a number of pathological changes, such as protein and DNA damage, cell senescence and apoptosis, and induce cardiovascular disease, inflammation, diabetes, kidney disease and activation of oncogene [ 15 ]. ROS produced by NOX1 can also promote the growth and
Yan-hui Chen, Heng-hui Zhang, Yan Wang, Xing-wang Xie, Ran Fei, Xue-yan Wang, Lai Wei and Hong-song Chen
Objective The forkhead transcription factor FOXP3 is a key molecular which can mediate regulatory T cells immune-related inhibitory functions. Increased levels of FOXP3-positive Tregs in peripheral blood have been proved to be associated with a less favorable prognosis in various inflammatory diseases. It is of great interest to investigate the correlation between single nucleotide polymorphism (SNP) of FOXP3 gene and the susceptibility of chronic hepatitis B (CHB).
Methods Two SNPs rs2280883 and rs3761549 of FOXP3 gene in 285 patients with CHB and 295 matched controls were analyzed by Matrix-Assisted Laser Desorption/Ionization Time of Flight Mass Spectrometry (MALDI-TOF).
Results At rs2280883, there were no significant differences in the distribution of C and T alleles between CHB donors and healthy donors, but at rs3761549, C allele was associated with CHB (P = 0.001). Compared with healthy controls, patients with CHB had high frequencies of TT genotype (73.7%) at rs2280883 or CC genotype (73.6%) at rs3761549 of FOXP3 gene. Patients who carried rs2280883 CC genotype [OR 1.744 (95% CI 1.068 - 2.848), P = 0.011] or rs3761549 CC genotype [OR 1.633 (95% CI 1.146 - 2.327), P = 0.0001] had higher risk of suffering from CHB. Stratified analysis showed that rs3761549 CC genotype was significantly associated with high incidence of HBeAg (P = 0.019).
Conclusions These results suggested that FOXP3 gene polymorphism at rs2280883 and rs3761549 might be associated with the increased susceptibility to CHB.