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1 LA surface and exhibited a greater degree of crossreactivity.
2 amined for antigen specificity, isotype, and crossreactivity.
3 o distinguish true double sensitization from crossreactivity.
4 es it encounters is based on T cell receptor crossreactivity.
5 more, we conclude that MOR1(C)-ir represents crossreactivity.
6 eneous Tregs is not due to alloreactivity or crossreactivity.
7 of genotypes 2a, 3a, 4a, 5a, and 6a to study crossreactivity.
8 emonstrated their specificity and absence of crossreactivity.
9 y insensitive to ligand structure, to enable crossreactivity.
10 a "rigid adaptation" mechanism governs such crossreactivity.
11 al vaccine trials was shown to elicit M-type crossreactivity.
12 munogen carrying the 3D pattern would elicit crossreactivity against other M types carrying the 3D pa
14 d with distinct ligands revealed significant crossreactivity among MAIT TCRs both ex vivo and upon in
16 a cooperative fashion such that specificity, crossreactivity and MHC restriction are inextricably lin
18 alysis of TCR antigen specificity, affinity, crossreactivity, and CD8 coreceptor dependence was perfo
20 t work from our laboratory identified T cell crossreactivity between epitopes of OspA and lymphocyte
21 olecular-mimicry theory proposes that immune crossreactivity between microbial and self-antigen is th
23 ow how binding by a self-reactive TCR favors crossreactivity between self and microbial antigens.
24 mechanisms, indicating that receptor-ligand crossreactivity can occur in the absence of molecular mi
30 ot retained on heparin agarose showed strong crossreactivity in immunoblot assays with anti-rat liver
35 terminally adjacent to the LBD increased the crossreactivity of monobodies to the apo-ER alpha-LBD, s
37 report results of experiments examining the crossreactivity of TCRs recognizing the myelin basic pro
38 of these proteins which participate in their crossreactivity or in their direct interaction, represen
39 gnition either through T cell receptor (TCR) crossreactivity or independently from TCR recognition.
42 functionally relevant indication of MAIT TCR crossreactivity, suggesting a potentially broader role o
44 determined and used to identify and exclude crossreactivity to noncognate peptides derived from the
45 e analyzed T-cell activation in the GALT and crossreactivity to the same antigen in the liver as well
46 s both sequence similarity and immunological crossreactivity to yeast Rrn3 and is capable of rescuing
47 gatively selected TCRs exhibited promiscuous crossreactivity toward multiple other major histocompati
50 eterologous CIDR1; however, a broad range of crossreactivity was detected in mice that were immunized
51 GlyRbeta (mAb-GlyRbeta) and does not exhibit crossreactivity with any of the GlyRalpha1-4 subunits.
53 me selectivity of the TCR and its remarkable crossreactivity with different MHC-peptide complexes.
55 es that in vitro demonstrate strong cellular crossreactivity with DR molecules expressed by the previ
56 s process through an unprecedented degree of crossreactivity with myelin-associated inhibitory ligand
57 6D2 bound tumor melanin and demonstrated no crossreactivity with normal melanized tissues in black m
60 re we report the structural mechanism of TCR crossreactivity with two distinct peptides from human pa