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1                                              X-SCID, the most common form of human SCID, is due to mu
2 rr virus-transformed cell line (LCL) from an X-SCID patient with a gamma-c null mutation.
3  arising as secondary, adverse effects in an X-SCID gene therapy trial.
4 opriate IL-2R function can be restored in an X-SCID LCL by transduction of a wild-type gamma-c gene.
5 cells, confirming correction of the cellular X-SCID phenotype.
6  X-linked severe combined immune deficiency (X-SCID) in gene-therapy trials using haematopoietic stem
7 d severe combined immunodeficiency diseases (X-SCID).
8 d severe combined immunodeficiency disorder (X-SCID) suggests that we might now be at the point where
9                      Gene-therapy trials for X-SCID, which have been based on the assumption that IL2
10 iral vector insertions in T-cell tumors from X-SCID patients in gene therapy trials.
11 unological defects that are similar to human X-SCID.
12 , X-linked severe combined immunodeficiency (X-SCID) and DOCK8 deficiency, were followed longitudinal
13 h X-linked severe combined immunodeficiency (X-SCID) are deficient in gammac and provide a useful mod
14 r X-linked severe combined immunodeficiency (X-SCID) has prompted safety concerns.
15 r X-linked severe combined immunodeficiency (X-SCID) have led to a re-evaluation of risks following g
16   X-linked severe combined immunodeficiency (X-SCID) is an immune disorder caused by mutations in the
17 e X-linked severe combined immunodeficiency (X-SCID).
18 e downstream signalling through the IL-2R in X-SCID cell lines, suggesting that gene therapy may be a
19  phosphorylation and DNA binding activity in X-SCID B cells with a wide range of gammac mutations.
20 rentiation at the T cell progenitor stage in X-SCID cells.
21                         Here I argue that in X-SCID it is the parents and children whom we should lis
22                                     To model X-SCID in vitro, we generated a mouse embryonic stem cel
23 ypothesis that the molecular pathogenesis of X-SCID is due primarily to gamma(c)-mediated defects in
24 re proposed to cause the severe phenotype of X-SCID patients.
25   We found that although IL-4 stimulation of X-SCID B cells did not result in Janus tyrosine kinase-3
26      Using a mouse model for gene therapy of X-SCID, we find that the corrective therapeutic gene IL2
27                                          The X-SCID background in transplanted cells was required for
28             However, reconstitution of these X-SCID B cells with gammac enhanced IL-4-mediated respon
29                                   Transduced X-SCID LCL expressed the G1gamma-cSvNa transcript.
30 can also occur in T-cell receptor-transgenic X SCID mice lacking HSV-specific T cells.
31 on of diarrhea post-HSCT in the patient with X-SCID was consistent with norovirus infection but not w
32 ctor integration in one of the patients with X-SCID.