When dendritic cells were loaded with MEP-mel protein, weak cross presentation was induced.
Our results show that it is induced by the presentation of a syllable in an unlikely position that violates both word and rule learning.
Also, the mechanism by which cross‐presentation is induced for exogenous tumor Ag remains unknown.
So far, we have shown that cross-presentation can be induced when antigenic proteins are administered with a specific adjuvant, such as ISCOMs [ 5] or with TLR3 ligand poly(I C) [ 6].
Notably, with low dose of IFN- γ, the antigen presentation ability could be induced in MSCs.
We found that motion rivalry was rare and depended on continuous stimulus presentations, while form rivalry was induced whenever stimulus repetitions followed each other within 350 ms. These data show that motion-based rivalry has temporal characteristics different from form-based rivalry.
This is consistent with our data that show that genes involved with antigen presentation and pathogen associated receptor recognition are induced between D15 and D21, but not earlier.
Our previous data suggested that tolerance might be induced by functional presentation of donor immunogenic epitopes via self-sequences [20], [26].
However, presentation of the Trh4 peptide could be induced by overexpressing Trh4 in processing-proficient cells [ 25].
Since it is generally accepted that tumor tolerance and immunity are induced by cross-presentation of tumor antigens, even for class II MHC positive tumors, we have prepared B16 cells expressing Ep63K peptide as part of the influenza virus nucleoprotein (NP)(Fig. 1B) [34].
CD4+ T cell responses could be induced through cross-presentation, leading to secretion of inflammatory factors by dendritic cells, which can verify that Laminarin could act as Dectin-1 specific blocker in the animal models [ 4].
