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1 capsules of SCID mice (ie, mice with severe combined immunodeficiency).
2 mbined immunodeficiency, Omenn syndrome, and combined immunodeficiency.
3 tenuated MM tumor growth in mice with severe combined immunodeficiency.
4 who displayed an unusual progressive form of combined immunodeficiency.
5 inflammatory bowel disease-like disorder and combined immunodeficiency.
6 s with gene therapy for ADA-deficient severe combined immunodeficiency.
7 1-null mutant mice on a background of severe combined immunodeficiency.
8 myelokathexis (WHIM) syndrome, a human rare combined immunodeficiency.
9 idered LCK a candidate gene in patients with combined immunodeficiency.
10 rigel, and formed tumors in mice with severe combined immunodeficiency.
11 assays in nonobese diabetic mice with severe combined immunodeficiency.
12 ch is mutated in humans with X-linked severe combined immunodeficiency.
13 subsequently received a diagnosis of severe combined immunodeficiency.
14 ciency is associated with a novel variant of combined immunodeficiency.
15 vels of IgE are features of some variants of combined immunodeficiency.
16 process defective in human and mouse severe combined immunodeficiency.
17 infant hospitalized in Minnesota with severe combined immunodeficiency.
18 sensitivity to ionizing radiation and severe combined immunodeficiency.
19 is defective in humans with X-linked severe combined immunodeficiency.
20 ns and null mutations in mice lead to severe combined immunodeficiency.
21 h protection occurred without causing severe combined immunodeficiency.
22 erize an inflammatory disease evocative of a combined immunodeficiency.
23 ations associated with multiple atresia with combined immunodeficiency.
24 om 9 patients with genetically confirmed PNP-combined immunodeficiency, 10,000 DBS samples from healt
25 ated in human radiosensitive T(-)B(-) severe combined immunodeficiency, a syndrome characterized by t
26 ed with adenosine deaminase-deficient severe combined immunodeficiency (ADA-SCID) and set out to eval
27 ast, 39 adenosine deaminase-deficient severe combined immunodeficiency (ADA-SCID) patients have been
28 cult' conditions [adenosine deaminase-severe combined immunodeficiency (ADA-SCID), major histocompati
29 at destroy the immune system, causing severe combined immunodeficiency (ADA-SCID), often referred to
30 denosine deaminase deficiency-related severe combined immunodeficiency (ADA-SCID), Shwachman-Bodian-D
32 ify the genetic alteration in a patient with combined immunodeficiency and characterize human caspase
33 ecessive CD70 deficiency is a novel cause of combined immunodeficiency and EBV-associated diseases, r
34 l case of an RSV-infected infant with severe combined immunodeficiency and effectively no adaptive im
36 hese features are consistent with the severe combined immunodeficiency and mild extraimmunological sy
37 oal of defining the true incidence of severe combined immunodeficiency and providing early treatment
38 patients presented from early childhood with combined immunodeficiency and severe autoimmune disease.
39 ted disorders, including MIA associated with combined immunodeficiency and very early onset inflammat
40 jected intraperitoneally (ie, in CB17 severe combined immunodeficiencies) and significantly increased
41 osa-associated lymphoid tissue 1 (MALT1) for combined immunodeficiencies, and tetratricopeptide repea
42 osis of adenosine deaminase-deficient severe combined immunodeficiency, and consanguinity were associ
45 y reported a novel syndrome characterized by combined immunodeficiency associated with severe develop
46 lifornia established the incidence of severe combined immunodeficiency at 1 in 66,250 live births.
48 given intranasally or i.p. to newborn severe combined immunodeficiency-beige mice exposed to 90% O2 f
50 ridium parasites from 6 of 7 infected severe combined immunodeficiency-beige mice, and the parasites
51 t is a common finding in infants with severe combined immunodeficiency but is not typically observed
52 Janus kinase 3 (JAK3) are a cause of severe combined immunodeficiency, but hypomorphic JAK3 defects
53 overy occurred in VLP-dosed mice with severe combined immunodeficiency, but not in wild-type mice dep
54 T-cell deficiencies in patients with severe combined immunodeficiency by replacing resident thymus c
55 ed via osmotic pump in an intratibial severe combined immunodeficiency CAG myeloma model or in a syst
56 cy CAG myeloma model or in a systemic severe combined immunodeficiency CAG-heparanase model of aggres
59 tor of cytokinesis 8 (DOCK8) deficiency is a combined immunodeficiency caused by autosomal recessive
60 s emerged as a convincing therapy for severe combined immunodeficiency caused by ILR2G mutation (SCID
61 n dedicator of cytokinesis 8 (DOCK8) cause a combined immunodeficiency characterized by atopy, recurr
62 ations in DOCK8 have been reported to have a combined immunodeficiency characterized by cutaneous vir
64 ytokine receptor subunit give rise to severe combined immunodeficiency characterized by lack of T and
66 ovirus incidence was compared between severe combined immunodeficiency children with (n = 10) and wit
67 on of disease phenotypes for X-linked severe combined immunodeficiency, chronic granulomatous disease
68 n dedicator of cytokinesis 8 (DOCK8) cause a combined immunodeficiency (CID) also classified as autos
72 I1 and STIM1 genes that abolish SOCE cause a combined immunodeficiency (CID) syndrome that is accompa
73 onical NF-kappaBeta pathways, resulting in a combined immunodeficiency (CID) without endocrine or ect
74 truction that is sometimes associated with a combined immunodeficiency (CID), leading to increased su
79 this review we describe peculiarities about combined immunodeficiencies (CIDs) in the Middle East.
82 equivocal evidence that children with severe combined immunodeficiency could be cured by gene transfe
85 V-CTLs both in vitro and in vivo in a severe combined immunodeficiency disease (SCID) mouse model and
87 nt with WHIM syndrome, an autosomal dominant combined immunodeficiency disease caused by gain-of-func
88 PET experiments were performed in severe combined immunodeficiency disease mice inoculated with p
92 s of anti-CD3epsilon mAb treatment in severe combined immunodeficiency forms characterized by poor th
93 healthy donors were injected into NOD-severe combined immunodeficiency gammac(-/-) mice, followed by
95 ells proliferate in nonobese diabetes/severe combined immunodeficiency/gammac(null) mice under the in
96 tients with atypical presentations of severe combined immunodeficiency gene mutations presents an opp
97 nt advances and newborn screening for severe combined immunodeficiency, has resulted in improved outc
98 ts with adenosine deaminase deficient severe combined immunodeficiency have identified neutropenia, a
99 -infected humanized nonobese diabetic severe combined immunodeficiency (HU-NOD/SCID) mice were genera
102 and engraftment in nonobese diabetic/severe combined immunodeficiency IL-2gamma(null) (NSG) mice com
104 tor ARTEMIS cause radiation-sensitive severe combined immunodeficiency in humans and may increase sus
105 in patients with MIA and MIA associated with combined immunodeficiency include abnormalities of enter
106 hosts as well as in nonobese diabetic/severe combined immunodeficiency/interleukin 2Rgamma(null) mice
107 e immune-deficient (nonobese diabetic/severe combined immunodeficiency/interleukin-2 gammac receptor(
108 efore, we created a nonobese diabetic/severe combined immunodeficiency/interleukin-2 receptor-gamma-n
109 on by transplanting nonobese diabetic/severe combined immunodeficiency/interleukin-2 receptor-gamma-n
110 arly onset of bone marrow failure leading to combined immunodeficiency is associated with microcephal
111 eplacement for Hemophilia B, X-linked Severe Combined Immunodeficiency, Leber's Congenital Amaurosis
112 T cells in a spectrum including leaky severe combined immunodeficiency (LS) and Omenn syndrome (OS).
114 lls, leading to increased survival of severe combined immunodeficiency mice after transplantation of
115 al liver cells into nonobese diabetic/severe combined immunodeficiency mice allows for the long-term
116 after subcutaneous transplantation in severe combined immunodeficiency mice and differentiated into S
117 d copper-DOTA-conatumumab was done in severe combined immunodeficiency mice bearing Colo205 xenograft
119 by PET and ex vivo biodistribution in severe combined immunodeficiency mice bearing H2009 tumor (huma
120 o experiments, 6- to 12-wk-old female severe combined immunodeficiency mice bearing M21 xenografts (h
121 4)-BBN: for in vivo GRPR blockade) in severe combined immunodeficiency mice bearing PC-3 xenografts.
122 n erythrocytes into nonobese diabetic/severe combined immunodeficiency mice extends blood circulation
123 s transplanted onto nonobese diabetic/severe combined immunodeficiency mice faithfully recapitulated
124 Finally, YT cells transplanted into severe combined immunodeficiency mice had an invasive behavior.
125 gnificantly prolonged the survival of severe combined immunodeficiency mice inoculated with LCLs.
126 ers in the injured skeletal muscle of severe combined immunodeficiency mice more effectively than CD5
128 transplantation in Non-obese diabetic/severe combined immunodeficiency mice that the HAGE knockdown i
129 ion in xenotolerant nonobese diabetic/severe combined immunodeficiency mice through intrasplenic or i
130 ted nonobese diabetic background with severe combined immunodeficiency mice to assess suppressive fun
133 nized urokinase plasminogen activator/severe combined immunodeficiency mice were used to establish ch
134 lanted with MSCs in nonobese diabetic severe combined immunodeficiency mice with a significantly high
135 mproved survival of nonobese diabetic/severe combined immunodeficiency mice with HL-60 leukemia.
136 eased tumour volumes and mortality of severe combined immunodeficiency mice xenografted with PC3 and
137 nced MM cells were then injected into severe combined immunodeficiency mice, and tumor growth in s.c.
139 as not observed in non-obese diabetic/severe combined immunodeficiency mice, indicating the immune re
141 immunocompromised non-obese diabetic/severe combined immunodeficiency mice, supporting an oncogenic
142 ferent genogroup, are inoculated into severe combined immunodeficiency mice, the order of severity of
143 ffeensis strains were inoculated into severe combined immunodeficiency mice, the order of the severit
144 MB-231 cell-derived mammary tumors in severe combined immunodeficiency mice, we show here for the fir
163 were performed in Mec-1-bearing SCID (severe combined immunodeficiency) mice, a new animal model of h
169 ly in infected skin xenografts in the severe combined immunodeficiency mouse model of VZV pathogenesi
171 ftment in NOD-SCID (nonobese diabetic-severe combined immunodeficiency) mouse myocardium increased ca
172 h experimental systemic infections of severe combined immunodeficiency Mus musculus with the bacteriu
174 cell lymphopenic infants had variant SCID or combined immunodeficiency (n = 6), genetic syndromes ass
175 he renal capsule of nonobese diabetic severe combined immunodeficiency (NOD SCID) mice with MSCs isol
176 +) progenitors into nonobese diabetic/severe combined immunodeficiency (NOD-SCID) mice resulted in th
177 Here, we show that nonobese diabetic severe combined immunodeficiency (NOD/SCID) beta(2) microglobul
178 nto immunodeficient nonobese diabetic severe combined immunodeficiency (NOD/SCID) mice leads to the d
179 xpressing tumors in nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice with partially
182 n transplanted into nonobese diabetic/severe combined immunodeficiency (NOD/SCID) recipient mice, FA-
184 ided into 3 main categories: T(-)B(-) severe combined immunodeficiency, Omenn syndrome, and combined
185 uses T(-)B(+) natural killer-positive severe combined immunodeficiency or T-cell lymphopenia with sev
186 ystem since it did not occur in nude, severe combined immunodeficiency, or T-cell depleted mice.
187 esent a model for radiation-sensitive severe combined immunodeficiency, our findings suggest that the
188 ons or autoimmunity, they represent profound combined immunodeficiency (P-CID), for which outcome dat
189 xpression of Bcl2 does not rescue the severe combined immunodeficiency phenotype in Ku70-deficient mi
190 We describe a pedigree affected by a severe combined immunodeficiency phenotype with absent T cells
191 lex are now recognized as the cause of novel combined immunodeficiency phenotypes, which all share ab
193 of STAT1 can be associated with progressive combined immunodeficiency, quite distinct from the limit
194 eficiency presents with a varied spectrum of combined immunodeficiency, ranging from a T(-)B(-)NK(+)
197 ectasia and a class of Radiosensitive-Severe Combined Immunodeficiency (RS-SCID), respectively, funct
199 -lymphocyte-independent protection of severe combined immunodeficiency SCID mice from disseminated ca
201 , wild-type (WT) and C3H animals with severe combined immunodeficiency (SCID animals) were inoculated
202 on of adenosine deaminase (ADA) cause severe combined immunodeficiency (SCID) and affect many other c
203 TEMIS deficiency usually present with severe combined immunodeficiency (SCID) and cellular radiosensi
204 nd severely impaired dissemination in severe combined immunodeficiency (SCID) and immunocompetent mic
205 cell transplantation in children with severe combined immunodeficiency (SCID) and other primary immun
206 opulation-based newborn screening for severe combined immunodeficiency (SCID) and related disorders h
211 g gene 1 (RAG1) deficiency results in severe combined immunodeficiency (SCID) caused by a complete la
214 pathology of Omenn syndrome and leaky severe combined immunodeficiency (SCID) has not been previously
227 ant prolonged survival in a xenograft severe combined immunodeficiency (SCID) mouse model of dissemin
228 phagy in human skin xenografts in the severe combined immunodeficiency (SCID) mouse model of VZV path
230 at least a month in both nude rat and severe combined immunodeficiency (SCID) mouse xenograft models
231 onobese diabetic (NOD) mice, NOD with severe combined immunodeficiency (scid) mutation (SCID) mice, a
232 iver cells in nonobese diabetic (NOD)/severe combined immunodeficiency (SCID) or NOD/SCID/gammac(-/-)
233 nonimmunologic outcomes in cohorts of severe combined immunodeficiency (SCID) patients with either RA
236 um (PIDTC) is enrolling children with severe combined immunodeficiency (SCID) to a prospective natura
239 that impair Rag2 function can lead to severe combined immunodeficiency (SCID), a condition characteri
240 position found in some patients with severe combined immunodeficiency (SCID), and the double mutant
241 l reconstitution in many infants with severe combined immunodeficiency (SCID), but correction of B-ce
242 een identified, often associated with severe combined immunodeficiency (SCID), consistent with the re
243 to young horses (foals) affected with severe combined immunodeficiency (SCID), followed by challenge
244 cal profound T-cell dysfunction (TD), severe combined immunodeficiency (SCID), has been carefully def
245 vical spinal cords of adult mice with severe combined immunodeficiency (SCID), human pluripotent stem
246 ansplantation (HCT) for patients with severe combined immunodeficiency (SCID), including survival, T-
247 evant per se because in patients with severe combined immunodeficiency (SCID), infections caused by o
248 (ADA) deficiency, a cause of X-linked severe combined immunodeficiency (SCID), is a case in point.
249 und primary immunodeficiency disease, severe combined immunodeficiency (SCID), is fatal in infancy un
251 tural history of patients treated for severe combined immunodeficiency (SCID), Wiskott-Aldrich syndro
252 te lymphocyte development and lead to severe combined immunodeficiency (SCID), XLF mutations cause a
271 immunodeficiencies including X-linked severe combined immunodeficiency (SCID-X1) and adenine deaminas
275 ials involving children with X-linked severe combined immunodeficiency (SCID-X1), a Moloney murine le
276 vectors for gene therapy of X-linked severe combined immunodeficiency (SCID-X1), we have evaluated n
281 phopenia, patients with ADA-deficient severe combined immunodeficiency showed a partial block in cent
282 nically mild initial presentation could be a combined immunodeficiency, so as to provide appropriate
283 A patient with multiorgan autoinflammation, combined immunodeficiency, subclinical amylopectinosis,
284 that inactivate Artemis cause a human severe combined immunodeficiency syndrome associated with cellu
285 mutations are responsible for a rare primary combined immunodeficiency syndrome associated with sever
287 ast, hypomorphic Artemis mutations result in combined immunodeficiency syndromes of varying severity,
288 shed tumors (ie, in nonobese diabetic-severe combined immunodeficiencies) that were derived from CD44
289 We performed a multicenter survey of severe combined immunodeficiency transplantation centers in Nor
291 h adenosine deaminase (ADA)-deficient severe combined immunodeficiency using 2 slightly different ret
292 anglion (DRG) xenografts in mice with severe combined immunodeficiency using multiscale correlative i
293 neutrophil infiltration in mice with severe combined immunodeficiency, which is accompanied by stron
294 l killer cell-sufficient patient with severe combined immunodeficiency, whom we found had mutations i
295 ciency should be considered in patients with combined immunodeficiency with B cell, T cell, and fibro
297 ciency should be considered in patients with combined immunodeficiency with T-cell abnormalities.
298 tion in a clinical trial for X-linked severe combined immunodeficiency (X-SCID) has prompted safety c
300 ore immunity to infants with X-linked severe combined immunodeficiency (XSCID) caused by mutations in
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