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cell population. This phenomenon causes an imbalance of Th1/Th2, reduction of antiviral substance secreted by Th1, and attenuation of anti-HBV-specific T lymphocyte immune response, which cause chronic HBV infection. IL-35 is an immunosuppressive cytokine secreted by regulatoryT lymphocytes. In vitro experiments have shown that IL-35 can also inhibit the proliferation of HBV-specific CTLs, weaken the immune responses of anti-HBV cells, and play an important role in the formation of immune tolerance in HBV infection [ 21 ]. Therefore, IL-35 is considered to be
of extracellular and intracellular microbial infections and can defend against invasion of Brucella through cooperation with Th1 cells [ 12 ]. The antibody response to Brucella proteins, mediated by interleukin 17 (IL-17) secreted by Th17 cells, plays a key role in brucellosis vaccine [ 13 ]. RegulatoryTcells (Tregs) inhibit the immune function of effector Tcells, promoting Brucella invasion [ 14 ]. Therefore, the occurrence of brucellosis may be related to the imbalance in Treg/Th17 cells. Clapp et al. [ 15 ] have observed from nasal mucosa infection that
resulting data sets were explored, and influenza viruses containing titin peptide matches were manually identified and annotated.
In addition, reference proteomes of influenza A virus, H3N2 subtype (tax ID: 385580), influenza B virus (tax ID: 518987), and influenza C virus (tax ID: 11553) were used to investigate peptide matching at the 5-mer level.
Immunological potential of shared peptides was analyzed using the Immune Epitope Database (IEDB; www.iedb.org ) resource [ 38 ]. IEDB offers experimental data characterizing antibody and Tcell epitopes studied in human
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