Our data suggest that the structural background for T-cell activation could also be due to a shift in the expression of splice forms.
Additionally, there was a shift in the latency of the P1 (t (17) = 7.06, p<0.001), with earlier peaks for highly complex objects.
A shift in the latency of N350 was also found (F (2, 16) = 6.06, p<0.05), driven by shorter latencies for coloured pictures as opposed to both line drawings (t (17) = 3.59, p<0.01) and textured drawings (t (17) = 2.21, p<0.05).
It is generally agreed that a shift in T-cell and cytokine profile toward a type 2 phenotype and the emergence of regulatory T cells 39– 41 are responsible for disease protection in EAE and EAU 5, 42.
Another in vitro study found that insulin induces a shift in T-cell differentiation toward T helper type 2 cells.
Current literature contains many reports describing a shift in T cell subsets from naïve to memory in aged humans (for review see [ 3]).
During the pregnancy, there is a shift in immune cells response, T helper 1 (to1) To T helper 2 (Th2), for favorable implantation, thus inducing maternal tolerance and suppression [ 6].
The histogram for the carbohydrate metabolism category reflected a shift in their distribution towards positive t-values.
In contrast, the shift in the Gli2ΔN2 T cells was negligible.
T cells specific for proteolipoprotein (PLP) 131-159 and selected under Th2-favoring conditions show a shift in peptide-TCR primary contact residues compared with Th1 clones [ 16].
