CD8 + T cells are promising targets for vaccination against influenza A virus (IAV) infection. Their induction via peptide vaccination is not trivial, because peptides are weakly immunogenic. One strategy to overcome this is by vaccination with chemically enhanced altered peptide ligands (CPLs), which have improved MHC-binding and immunogenicity.
View Article and Find Full Text PDFH2N2 influenza virus, the causative agent of the 1957 "Asian flu" pandemic, has disappeared from circulation. However, H2-influenza viruses are still circulating in avian reservoirs. Combined with the waning of H2N2-specific immunity in the human population, there is a risk of reintroduction of H2N2 influenza virus.
View Article and Find Full Text PDFPneumococcal conjugate vaccines reduce pneumococcal colonization via serotype-specific immunoglobulin G (IgG) at mucosal surfaces. The infant immunization schedule with the ten-valent pneumococcal conjugate vaccine (PCV10) changed from a 3 + 1 schedule (2-3-4-11 months) to a 2 + 1 schedule (2-4-11 months) in The Netherlands in 2013. We compared anti-pneumococcal IgG concentrations in saliva between the schedules.
View Article and Find Full Text PDFTraditional influenza vaccines primarily induce a narrow antibody response that offers no protection against heterosubtypic infections. Murine studies have shown that T cells can protect against a broad range of influenza strains. However, ferrets are a more potent model for studying immune correlates of protection in influenza infection.
View Article and Find Full Text PDFUntil universal influenza vaccines become available, pandemic preparedness should include developing classical vaccines against potential pandemic influenza subtypes. We here show that addition of SWE adjuvant, a squalene-in-water emulsion, to H7N9 split influenza vaccine clearly enhanced functional antibody responses in ferrets. These were cross-reactive against H7N9 strains from different lineages and newly emerged H7N9 variants.
View Article and Find Full Text PDFAcquired thrombotic thrombocytopenic purpura (TTP) is a life-threatening disorder resulting from the development of autoantibodies against ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13). HLA-DRB1*11 provides a risk factor for developing acquired TTP. Pulsing of antigen-presenting cells from HLA-DRB1*11- and HLA-DRB1*03-positive individuals with ADAMTS13 resulted in presentation of peptides derived from the CUB2 domain of ADAMTS13 with core sequences FINVAPHAR or ASYILIRD.
View Article and Find Full Text PDFBiochem Biophys Res Commun
December 2014
Macrophages determine the outcome of atherosclerosis by propagating inflammatory responses, foam cell formation and eventually necrotic core development. Yet, the pathways that regulate their atherogenic functions remain ill-defined. It is now apparent that chromatin remodeling chromatin modifying enzymes (CME) governs immune responses but it remains unclear to what extent they control atherogenic macrophage functions.
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