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1 ereas its expression was concentrated in the paracortical and medullary regions of the LN at later st
2 nd SIV replication differed across cortical, paracortical, and medullary regions of the lymph node, b
3 t not rejectors, colocalize with APCs in the paracortical areas and express high levels of CCR7.
4 eal lymph nodes and localized to T cell-rich paracortical areas.
5  the cortical lymphatics or returning to the paracortical cords.
6      Interactions were also observed between paracortical DC of the recipient and OVA peptide-specifi
7 pecific T cells formed large clusters around paracortical DC that were pulsed in vitro with the OVA p
8 resentation is matched by a similarly biased paracortical distribution of CD4(+) T cells directed by
9 rm arrest occurred nearly exclusively in the paracortical HEVs.
10                    Lymph nodes showed marked paracortical hyperplasia.
11                                          The paracortical infiltrate was a result of both reduced apo
12                                  Many of the paracortical lymphocytes expressed markers associated wi
13 tive cellular debris within the cytoplasm of paracortical macrophages.
14 wo tumor types that also showed an activated paracortical phenotype.
15                                          The paracortical proliferation may be extensive enough to su
16 antigen-bearing DCs could be detected in the paracortical region of lymph nodes draining sensitized s
17 +) T cells are the major constituents of the paracortical region of lymphoid organs, the main site of
18               DC, the most potent APC in the paracortical region of lymphoid organs, were cocultured
19 lls are the major cellular components of the paracortical region of lymphoid tissue, the primary site
20 , by day 6 these cells were primarily in the paracortical regions and were able to proliferate and se
21 11.10 T cells accumulated in the T cell-rich paracortical regions of the draining lymph nodes, prolif
22  of Ag, the KJ1-26+ cells accumulated in the paracortical regions of the LN to a comparable degree, b
23 not exposed to the OVA peptide, homed to the paracortical regions of the lymph nodes but did not inte
24 sient accumulation of DO11.10 T cells in the paracortical regions, but these T cells never entered fo
25 ing therapy we found evidence of significant paracortical T cell zone damage associated with depositi
26 entially expressed on dendritic cells in the paracortical T cell zones of lymph nodes.
27 c cells in the germinal center and scattered paracortical T cells, but not by normal germinal-center
28 ely depleted, due in part to fibrosis of the paracortical T-cell zone (TZ) that impairs homeostatic m
29 itate with T cells in the parafollicular and paracortical zones and retain high level expression of C
30 in vivo fluorescence and MR imaging, that LN paracortical zones are profoundly acidic.