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1 function to maintain hepatic homeostasis and tolerogenicity.
2 ing to I-A(k) molecules, immunogenicity, and tolerogenicity.
3 enhance their in vivo survival and potential tolerogenicity.
4 and may potentiate their previously reported tolerogenicity.
5 al donor DCs, may account for inherent liver tolerogenicity.
6 on of the fusion protein is not required for tolerogenicity.
7 allografts governs their immunogenicity and tolerogenicity.
8 ory responses and may promote inherent liver tolerogenicity.
9 nt results in DCs with in vitro hallmarks of tolerogenicity.
10 at LPS-stimulated HSCs might promote hepatic tolerogenicity by influencing naturally occurring immuno
11 eptidase (gGT), have been reported to induce tolerogenicity by reprogramming dendritic cells (DCs).
12 es to the enhancement of dendritic cell (DC) tolerogenicity for the promotion of cell or organ allogr
14 of the details of the molecular basis of DC tolerogenicity have yet to be elucidated, emerging infor
17 to compare the relative immunogenicities and tolerogenicities of HBV structural (envelope [ENV]) and
20 pproaches that have been used to promote the tolerogenicity of donor-derived DC in experimental model
25 rted that, in B10.A mice, immunogenicity and tolerogenicity of the self-MHC class I peptide, Ld 61-80
26 ere, we have examined the immunogenicity and tolerogenicity of various self-peptides derived from reg
28 CD4+ Th cells into TRAMP mice abrogated TADC tolerogenicity, which was associated with reduced Foxo3
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