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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
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
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
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the transcription of CXCR5 after combining with these regulatory elements [ 7 ]. E2A activates the transcription of CXCR5, whereas Blimp1 causes its inhibition. In addition to directly regulating the expression of CXCR5, transcription factors Blimp1 and E2A may also form transcription pathways with inhibitor of differentiation 2 (Id2) and Id3 profiling of B cell lymphoma-6 (Bcl6), T-cell factor 1 (TCF-1), and E2A, thereby controlling expression of CXCR5 and formation of TFCs. Expressions of inhibitory molecules such as Tcell immunoglobulin domain and mucin domain
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