ライフサイエンスコーパス: SCID

1 SCID disorders are split into groups based on their pres

2 SCID has been associated with impaired purine nucleotide

3 SCID mice were also more insulin sensitive with increase

4 SCID mice were infected with 1.1-1.5 x 108 B. microti-in

5 SCID mice with human HCT116 cancer xenografts were image

6 SCID mice with human PC3 prostate cancer xenografts (Gro

7 SCID mice, which lack an adaptive immune system due to t

8 SCID was detected in a newborn before the onset of infec

9 SCID-beige mice injected via the tail vein with ERK clon

10 ional young adult Arabian-pony crosses and 1 SCID foal were then inoculated with plasma containing on

11 etic stem cell transplantation (HSCT) and 14 SCID-X1 patients treated with gene therapy over the same

12 conducted on LNCaP tumor-bearing male CB-17 SCID mice.

13 n a mouse model of chronic infection, 5 of 6 SCID/beige mice (83.3%) were cured after treatment with

14 tivity (IC50 = 10 nM) and oral activity in a SCID mouse model of Pf infection with an ED50 of 100 and

15 progenitor T cells, which is in line with a SCID phenotype at the level of early T cell development

16 rst, we gathered available information about SCID diagnostic and therapeutic guidelines, then we deve

17 dynamics and diversity in a cohort of 15 ADA-SCID children treated with gammaretroviral vectors and f

18 y caused by adenosine deaminase defects (ADA-SCID).

19 dicines Agency approved gene therapy for ADA-SCID patients without a suitable bone marrow donor.

20 icient severe combined immunodeficiency (ADA-SCID) patients have been treated with 4 distinct gammare

21 ausing severe combined immunodeficiency (ADA-SCID), often referred to as the "bubble boy" disease.

22 ta, in combination with results of other ADA-SCID gene therapy trials, suggest that disease backgroun

23 atment of choice for ADA-deficient SCID (ADA-SCID) is hematopoietic stem cell transplant from an HLA-

24 of gene therapy (GT) in 18 patients with ADA-SCID for whom an HLA-identical family donor was not avai

25 observed in more than 100 patients with ADA-SCID who received gammaretrovirus- or lentivirus-mediate

26 immune deficiency seen in patients with ADA-SCID, patients should be followed for specific noninfect

27 Eight additional SCID mice bearing HCT116 xenografts in dorsal skinfold w

28 vivo proof of concept was established in an SCID mouse model of malaria, after oral administration (

29 In an SCID mouse xenograft model, low-dose metronomic paclitax

30 agnosis while still asymptomatic by using an SCID newborn screening test, allowing early initiation o

31 further extended to in vivo Swiss albino and SCID mice models also revalidated the anti-carcinogenic

32 is can lead to both megaloblastic anemia and SCID in MTHFD1 deficiency.

33 ablish infection in both immunocompetent and SCID mice and has been proposed to facilitate evasion of

34 odeficiency (scid) mutation (SCID) mice, and SCID bearing a null mutation in the IL-2 common gamma ch

35 rangements in mice transplanted with Artemis-SCID cells.

36 In human artery-SCID chimeras, PD-1 blockade exacerbated vascular inflam

37 g a group of disorders collectively known as SCID.

38 TEMIS) have been described to cause atypical SCID, Omenn syndrome, Hyper IgM syndrome and inflammator

39 ned immunodeficiencies (CIDs) and "atypical" SCID show reduced, not absent T-cell immunity.

40 of 51 had a genetic diagnosis of "atypical" SCID and 14 of 51 of CID.

41 as performed in 143B and OS-17 tumor-bearing SCID mice and followed by radioimmunotherapy (RIT) with

42 ol groups (n = 6-7) using C4-2 tumor-bearing SCID mice by evaluating tumor growth and survival over 6

43 ing immunocompetent hosts into tumor-bearing SCID-NOD immunocompromised mice attenuated tumor growth

44 CB17 SCID mice infected with R. typhi(GFPuv) succumb to the i

45 l PET imaging studies were performed in CB17 SCID and LNCaP xenograft-bearing SHO mice, respectively,

46 In the spleen and liver of infected CB17 SCID mice, the bacteria are detectable by immunofluoresc

47 and immune reconstitution in 13 consecutive SCID-X1 patients having undergone haploidentical hematop

48 d is not informative for adenosine deaminase-SCID, whereas hypomorphic mutations lead to less severe

49 mmunodeficiency caused by gammac-deficiency (SCID X1) and adenosine deaminase (ADA) deficiency.

50 including severe combined immune deficiency (SCID), autoimmunity, and inflammation.

51 including severe combined immune deficiency (SCID), Wiskott-Aldrich syndrome (WAS), and chronic granu

52 X-linked severe combined immune deficiency (SCID-X1) lacking a matched sibling donor may have better

53 The treatment of choice for ADA-deficient SCID (ADA-SCID) is hematopoietic stem cell transplant fr

54 Ten subjects with confirmed ADA-deficient SCID and no available matched sibling or family donor we

55 efficacy from gene therapy for ADA-deficient SCID, with an excellent clinical safety profile.

56 with mutations in DCLRE1C (Artemis-deficient SCID), there is no optimal approach that uses standard d

57 in both severe combined immunity-deficient (SCID) and muMT mice indicates that peritoneal B cells al

58 denosine deaminase-deficient (ADA-deficient) SCID when combined with reduced intensity conditioning (

59 In streptozotocin-induced diabetic SCID/beige mice, the injection of 750 rat islet equivale

60 conditioning in infants with newly diagnosed SCID-X1 had low-grade acute toxic effects and resulted i

61 ioning in eight infants with newly diagnosed SCID-X1.

62 n screening has been effective in diagnosing SCID patients early in life, there is an urgent need to

63 a severe combined immunodeficiency disease (SCID) affecting B, T, and natural killer cells, with an

64 reduced in trigenic mice (Tie2(cre)/Osx(f/f)/SCID) with endothelial-specific deletion of osteoblast c

65 ant OSX compared with bigenic mice (Osx(f/f)/SCID).

66 nts leading to efficacy in the P. falciparum SCID mouse malaria model.

67 a undetectable in vivo using a P. falciparum SCID mouse model.

68 ID during 2000-2009, diagnostic criteria for SCID, and the pilot project of newborn screening for SCI

69 dy of infants identified by means of NBS for SCID who received care at the University of California,

70 Newborn screening (NBS) for SCID permits identification of affected infants before d

71 ing (NGS)-based multigene-targeted panel for SCID and other severe PIDDs requiring rapid therapeutic

72 ore than 800 subjects on PIDTC protocols for SCID, and enrollment in the studies on WAS and CGD is un

73 d the pilot project of newborn screening for SCID in the Navajo Nation.

74 rly in countries where newborn screening for SCID is not universally available and delayed diagnosis

75 to pose the greatest threat to survival for SCID patients.

76 less, the first attempts of gene therapy for SCID X1 were associated with insertional mutagenesis cau

77 nfirmed over the long term, gene therapy for SCID-X1 appears to be an equal, if not superior, alterna

78 e development of autologous cell therapy for SCID-X1 subjects.

79 es of hematopoietic cell transplantation for SCID during 2000-2009, diagnostic criteria for SCID, and

80 ementary determining region 3 sequences from SCID and OS iPSC-derived cells, whereas control iPSCs yi

81 ins give rise to a phenotypic spectrum, from SCID to extreme growth failure, with deficiencies in cer

82 he in vivo prostate regeneration assay, host SCID mice carrying Src(Y529F)-transduced regeneration ti

83 tment of a previously unknown cause of human SCID.

84 geted to generate a zebrafish model of human SCID.

85 ormal and IPF fibroblasts and in a humanized SCID mouse model of IPF employing both short interfering

86 Moreover, in a humanized SCID mouse model, CD19(+) CD5(-) B cells were more effec

87 In the humanized SCID mouse, local injection of Netrin-1 into skin enhanc

88 ctober 2016, 32 patients with NBS-identified SCID and leaky SCID from California and other states wer

89 -linked sSevere cCombined iImmunodeficiency (SCID-X1) using targeted integration of a cDNA into the e

90 nfection even in severely immunocompromised- SCID or inducible NO synthase-, CD40-, or IL-12-deficien

91 esent with severe combined immunodeficiency (SCID) and cellular radiosensitivity, but hypomorphic mut

92 ients with severe combined immunodeficiency (SCID) can be genetically-characterized.

93 clusion of severe combined immunodeficiency (SCID) in a Europe-wide screening program is currently de

94 re form of severe combined immunodeficiency (SCID) in humans.

95 Severe combined immunodeficiency (SCID) is characterized by arrested T-lymphocyte producti

96 Severe combined immunodeficiency (SCID) is characterized by severely impaired T-cell devel

97 subtype of severe combined immunodeficiency (SCID) known as severe combined immune deficiency caused

98 or-bearing severe combined immunodeficiency (SCID) mice after sacrifice at defined time points up to

99 cytes into severe combined immunodeficiency (SCID) mice.

100 fts in the severe combined immunodeficiency (SCID) mouse model of VZV pathogenesis, and observed that

101 Severe combined immunodeficiency (SCID) represents congenital disorders characterized by a

102 Severe combined immunodeficiency (SCID) represents the most lethal form of primary immunod

103 ve form of severe combined immunodeficiency (SCID) that usually manifests in newborns.

104 ldren with severe combined immunodeficiency (SCID) to a prospective natural history study.

105 Severe combined immunodeficiency (SCID) with a complete absence of T cells was observed in

106 iated with severe combined immunodeficiency (SCID), consistent with the requirement for NHEJ during V

107 vere form, severe combined immunodeficiency (SCID), presents with profound deficiencies of T cells, B

108 ients with severe combined immunodeficiency (SCID).

109 L2RG)/JAK3 severe combined immunodeficiency (SCID).

110 terized by severe combined immunodeficiency (SCID).

111 t model of severe combined immunodeficiency (SCID).

112 nosed with severe combined immunodeficiency (SCID).

113 ross) with severe combined immunodeficiency (SCID).

114 senting as severe combined immunodeficiency (SCID).

115 -sensitive severe combined immunodeficiency (SCID).

116 mice with severe combined immunodeficiency (SCID).

117 ients with severe combined immunodeficiency (SCID).

118 X-linked Severe Combined Immunodeficiency (SCID-X1) is a genetic disease that leaves newborns at hi

119 r X-linked severe combined immunodeficiency (SCID-X1) often fails to reconstitute immunity associated

120 completely abolished in the immunodeficient SCID/beige (bg) variant.

121 Using immunodeficient SCID mice, we focused on targeting human brain tumors wi

122 studied in severe combined immunodeficient (SCID) mice inoculated with activated hPBMCs in Matrigel.

123 Severe combined immunodeficient (SCID) mice were infected and treated with sulfadiazine t

124 culation of severe combined immunodeficient (SCID) mice yielded isolates from 5 of 5 samples, but 0 o

125 utants from severe combined immunodeficient (SCID) patient cells showed a failure to sustain progress

126 manized uPA/severe combined immunodeficient (SCID)/beige mice challenged with HBV in vivo, immune ind

127 suppression, and flow chamber assays and in SCID mice with human intestinal xenografts.

128 n increased frequency of immature T cells in SCID pigs.

129 delta locus rearrangements, were detected in SCID and OS-derived T-lineage cells, consistent with a p

130 correction of chemically induced diabetes in SCID-Beige mice for 3 months.

131 DeltagD(-/+gD1) elicited no disease in SCID mice, whereas 1000-fold lower doses of wild-type vi

132 es employing cell-sorted skin equivalents in SCID/NOD mice demonstrated enhanced transepidermal water

133 ne resulting in a 3-fold greater exposure in SCID mice.

134 ired for the development of lung fibrosis in SCID mice humanized with IPF lung fibroblasts.

135 ive techniques to measure kidney function in SCID mice with adriamycin-induced nephropathy.

136 Furthermore, in SCID mice transplanted with neural progenitors derived f

137 Hypothyroidism was generated in SCID-beige mice using an iodine-deficient diet containin

138 acers revealed uptake in activated hPBMCs in SCID mice.

139 tient-derived xenografts tumors implanted in SCID mice.

140 injecting 5.5 MBq of 99mTc-anti-CD56 mAb in SCID mice bearing ARO tumor xenografts in the right thig

141 We determined that Bxv1 was also present in SCID mice that were used for in vivo propagation of Endo

142 e were able to enhance anti-TB protection in SCID mice, and the transfer of vaccine-primed B cells al

143 ing mutations in human IL-2Rgammac result in SCID, a primary immunodeficiency characterized by greatl

144 raft tumors were implanted subcutaneously in SCID mice.

145 bcutaneous model of colon (HCT-116) tumor in SCID-bg mice showed that the activity of 1 and 2 signifi

146 MFD-1 was tumorigenic in SCID mouse and proliferative and invasive in 3D cultures

147 oduce estrogen-dependent xenograft tumors in SCID mice, we also observed lower ERalpha protein levels

148 hen ectopic human xenograft LNCaP tumours in SCID mice were treated with SDT using the systemically-a

149 ells and the growth of a Panc-1 xenograft in SCID mice.

150 C infection model in human gut xenografts in SCID mice and used it to study the role of T3SS in the p

151 ion mice developed an interferon-independent SCID phenotype with a T-cell, B-cell, and natural killer

152 on during HCV infection because HCV-infected SCID/Alb-uPA mice accumulated higher plasma ketones whil

153 passive transfer of immune sera to infected SCID mice.

154 3.5 months post-implantation into SCID mice, the micro-computed tomography imaging showed

155 ine-primed T cells from Jh(-/-) KO mice into SCID mice only provided suboptimal protection.

156 by subcutaneous transplantation of skin into SCID/beige or athymic nude mice at 2 independent sites.

157 ism, and quality of life (QoL) of IL2RG/JAK3 SCID patients >2 years post-HSCT at our center.

158 IL2RG/JAK3 SCID survivors free from immunoglobulin replacement have

159 patients with NBS-identified SCID and leaky SCID from California and other states were treated, and

160 mutations can cause milder phenotypes (leaky SCID).

161 including the diagnosis of typical vs leaky SCID/Omenn syndrome, diagnosis via family history or new

162 Most of the patients with leaky SCID were compound heterozygous for 1 loss-of-function a

163 patients with typical SCID and 32 with leaky SCID, Omenn syndrome, or reticular dysgenesis.

164 proteins and are often associated with leaky SCID.

165 The infant had "leaky" SCID (i.e., a form of SCID in which a minimal degree of

166 ells implanted into the femoral bone of male SCID mice caused massive bone loss and stimulation of mo

167 .071 +/- 0.035 mm, SCID: 0.137 +/- 0.032 mm, SCID/bg: 0.804 +/- 0.039 mm; P < 0.001).

168 ge luminal diameter, WT: 0.071 +/- 0.035 mm, SCID: 0.137 +/- 0.032 mm, SCID/bg: 0.804 +/- 0.039 mm; P

169 Using a human MM/SCID mice model, the combination of bortezomib and SP101

170 e combined immunodeficiency (scid) mutation (SCID) mice, and SCID bearing a null mutation in the IL-2

171 in the Artemis gene that cause T(-)B(-)NK(+) SCID in pigs.

172 y were shown to be affected by T(-)B(-)NK(+) SCID, representing, to our knowledge, the first example

173 ons had thymic hypoplasia, causing a T-B+NK+ SCID phenotype, whereas the hair and nails of these mice

174 ad a presentation consistent with T-/loB+NK+ SCID, with normal hair and nails, distinct from the clas

175 l administration of CLH001 to BALB/c and NOD SCID gamma (NSG) mice resulted in complete survival with

176 g cells were adoptively transferred into NOD SCID gammaC-deficient mice, which were given isotype or

177 of 143B cells injected into the tibia of NOD SCID gamma mice.

178 n transplanted into non-obese diabetic (NOD)-SCID-gamma (NSG) mice with detectable levels of gene cor

179 EC313, for the treatment for UFs using a NOD-SCID mouse model.

180 ly increased the survival of PEL bearing NOD-SCID mice in an orthotopic xenograft model as compared w

181 abetic/severe combined immunodeficiency (NOD-SCID) mice resulted in the formation of microvessels der

182 burden in BLCL-engrafted immunodeficient NOD-SCID/Il2rg(-/-) mice.

183 [(55)Co]Co-DOTATATE by PET/CT imaging in NOD-SCID mice bearing subcutaneous somatostatin receptor-exp

184 reventing metastasis and angiogenesis in NOD-SCID mice, while being non-toxic in vivo.

185 e to form a tumor with only 100 cells in NOD-SCID or immunocompetent mice.

186 ved tumors and xenografts established in NOD-SCID or nude mice, low MCPIP1 levels correlated strongly

187 and in their capacity to metastasize in NOD-SCID-Il2rg(-/-) (NSG) mice.

188 s to high titers in human lung grafts in NOD-SCID/gamma mice, resulting in a robust inflammatory resp

189 estigated by using hu-spl-PBMC-NSG mice, NOD-SCID-IL2rgamma(-/-) (NSG) mice intrasplenically injected

190 firmed in the adoptive transfer model of NOD-SCID mice where tolDCs delayed diabetes onset.

191 Here we made use of the NOD-SCID-IL-2Rgamma(-/-) xenograft model and lentiviral cell

192 nd Srsf10, but not Ptbp2, in the PLNs of NOD.SCID mice.

193 e only observed in xenografts grown in a NOD/SCID IL2 receptor gamma (NOG) knockout mouse strain tran

194 interleukin-3, and stem cell factor in a NOD/SCID-IL2Rgamma(null) background (NSGS mice), we demonstr

195 the radiation-depleted bone marrow of a NOD/SCID/IL2rg(-/-) (NSG) mouse on which a patient's tumor i

196 Using ICG-001 in a NOD/SCID/IL2Rgamma(-/-) mouse model of engrafted human chron

197 intravenously into immune-competent and NOD/SCID mice, and lung metastases were quantified.

198 GSI treatment of MM tumor-bearing NOD/SCID/gammac-/- mice increased BCMA expression on tumor c

199 stablish glucose homeostasis in diabetic NOD/SCID mice.

200 loped in streptozotocin-induced diabetic NOD/SCID mice.

201 mune system mice were made by engrafting NOD/SCID/IL2Rgammanull (NSG) mice with human hematopoietic s

202 ) (NSIN) mice by knocking out Foxn1 from NOD/SCID/IL2rg(-/-) (NSI) mice using the CRISPR/Cas9 system.

203 ted human islets in the liver of healthy NOD/SCID mice.

204 tly milder hemotoxicity in the humanized NOD/SCID mouse model engrafted with red blood cells from G6P

205 a P. falciparum infection in a humanized NOD/SCID mouse model system.

206 abetic/severe combined immunodeficiency (NOD/SCID) mice with partially reconstituted immune systems w

207 abetic severe combined immunodeficiency (NOD/SCID) mice.

208 iabetic/severe combined immunodeficient (NOD/SCID) mice bearing human PSMA(+) PC3 PIP and PSMA(-) PC3

209 and transplantation into immunodeficient NOD/SCID/interleukin 2 receptor gamma chain null mice.

210 y formation and orthotopic GBM growth in NOD/SCID mice and decelerates the progression of low-grade a

211 pheral blood mononuclear cells (PBMC) in NOD/SCID mice harboring xenografts of MDA-MB-231, a triple-n

212 Death occurred later in NOD/SCID mice receiving REH cells depleted of CD9 for transp

213 2 knockdown invasive MDA-MB-231 cells in NOD/SCID mice, and compared parental and bone-derived varian

214 h ability of AGS gastric cancer cells in NOD/SCID mice.

215 potent in vivo antileukemic activity in NOD/SCID mouse xenograft models of relapsed and chemotherapy

216 mutant ER-expressing tumor xenografts in NOD/SCID-gamma mice after oral or subcutaneous administratio

217 engrafted at a markedly higher level in NOD/SCID/IL-2 receptor gamma chain-null (NSG) mice compared

218 significant delay in AML progression in NOD/SCID/IL2Rg(null) mice, but the persistence of adoptively

219 y assays as well as adoptive transfer in NOD/SCID/IL2Rgamma mice were used to assess for pathogen-spe

220 Interestingly, NOD/SCID mice, which have a deficiency in T, B, and NK cells

221 To examine these mechanisms, NOD/SCID IL-2 RG(-/-) humanized mice were either directly in

222 disease (GvHD) model of humanized mice (NOD/SCID/IL-2Rgammac(-/-) [NSG] mice).

223 udy, we generated a novel strain of nude NOD/SCID/IL2rg(-/-) (NSIN) mice by knocking out Foxn1 from N

224 astatic nodule formation in the lungs of NOD/SCID mice.

225 itting diodes (LED) prior to infusion of NOD/SCID-IL2Rgamma(-/-) mice.

226 In particular, NOD/SCID/IL2rg(-/-) mice can support the growth of various t

227 V-1(WT)) and HTLV-1(p12KO) We found that NOD/SCID/gamma(C) (-/-) c-kit(+) mice engrafted with human t

228 tive T cells in HIV-infected brain using NOD/SCID/IL-2rcgamma(-/-) mice reconstituted with human PBMC

229 en human B-cell lymphoma in a xenogeneic NOD/SCID/IL2rg(null) mouse model.

230 ted, and 42 patients with NBS-identified non-SCID T-cell lymphopenia were followed.

231 ore sensitive to ionizing radiation than non-SCID piglets, eliminating the RAG1 and RAG2 genes.

232 cterizes a group of patients with nontypical SCID T-cell deficiencies from a therapeutic perspective.

233 he nude/severe combined immunodeficiency (nu/SCID) phenotype in humans and mice.

234 ir and nails, distinct from the classic nude/SCID phenotype in individuals with autosomal-recessive F

235 ge, the first example of naturally occurring SCID in pigs.

236 entification of JAK3 mutations as a cause of SCID.

237 Early detection of SCID could reduce the cost of treatment by euro50,000-10

238 s study compares human T-cell development of SCID vs OS patients, and elucidates important difference

239 Early diagnosis of SCID through population-based screening of newborns can

240 subcutaneous pockets on the dorsal flanks of SCID mice.

241 The infant had "leaky" SCID (i.e., a form of SCID in which a minimal degree of immune function is pre

242 ng experiments were performed on 2 groups of SCID mice inoculated subcutaneously with increasing numb

243 Genetic heterogeneity of SCID frequently delays the diagnosis; a specific diagnos

244 and potentially saved by early management of SCID.

245 were coinjected into the mammary fat pad of SCID mice.

246 Rescue of SCID fibroblast radiosensitivity by human Artemis protei

247 he poorly vascularized subcutaneous space of SCID-Beige mice.

248 eted cell lines showed prolonged survival of SCID mice, suggesting a possible implication for overexp

249 tive family history or clinical suspicion of SCID or other severe PIDD identified deleterious mutatio

250 We performed transplantation of SCID CD34(+) bone marrow stem/progenitor cells into an o

251 development caused by various major types of SCID.

252 ell responses, as demonstrated by the use of SCID mice.

253 plantation of tumor cells into B6.CB17-Prkdc SCID mice.

254 nsitive severe combined immunodeficiency (RS-SCID).

255 cell transplantation for radiation-sensitive SCID suggest that minimizing exposure to alkylating agen

256 rest in thymic development caused by several SCID mutations.

257 ncies (median 45%) in CD34(+) HSPCs from six SCID-X1 patients and demonstrate rescue of lymphopoietic

258 ensity S. Typhi transposon library in hu-SRC-SCID mice to identify virulence loci using transposon-di

259 with human hematopoietic stem cells (hu-SRC-SCID) are susceptible to lethal S. Typhi infection.

260 h for confirming a diagnosis of BMD but that SCID mouse inoculation could be a useful complement to P

261 The SCID pig can be an important biomedical model, but these

262 pression of interferon-stimulated genes, the SCID phenotype was not reversed in STING V154M/WT IFNAR

263 rowth was significantly less frequent in the SCID mice treated with anti-CXCL9 serum than in mice tre

264 F invasion into coimplanted cartilage in the SCID mouse model of RA.

265 ZV infection of human skin xenografts in the SCID mouse model of VZV pathogenesis showed both that pC

266 e erythrocytic stage of P. falciparum in the SCID mouse model with an ED90 of 11.7 mg/kg when dosed o

267 ated cartilage invasion were examined in the SCID mouse model.

268 dium berghei malaria model as well as in the SCID mouse P. falciparum model.

269 eved nearly half the patency observed in the SCID/bg mouse (NK Ab: 0.356 +/- 0.151 mm, Asp/Pla: 0.452

270 ltaMLD, the virus remained active within the SCID mouse brain and showed widespread infection of norm

271 us mutations as the molecular basis for this SCID phenotype.

272 cells are sufficient to transfer TEC H/P to SCID recipients.

273 ls both in vitro and in an adoptive transfer SCID model of pulmonary fibrosis.

274 f in vivo platelet counts in the transferred SCID mice suggesting that anti-CD20 therapy significantl

275 nvisaged as an alternative strategy to treat SCID diseases.

276 nical development of genome editing to treat SCID-Xl.

277 not establish infection in anti-Ly6G-treated SCID and C3H/HeN mice (depletion of neutrophils).

278 was detected for mutations causing a typical SCID phenotype.

279 to 2014, including 68 patients with typical SCID and 32 with leaky SCID, Omenn syndrome, or reticula

280 phoma and Hodgkin lymphoma cells and in vivo SCID mouse models.

281 tion caused human multisystem anomalies with SCID and also revealed a prethymic role for BCL11B in he

282 In experiments with SCID mice infected with S. pneumoniae, we found passive

283 on protocols for NBS identified infants with SCID, as well as infants with other T-lymphopenic disord

284 Eight infants with SCID-X1 were followed for a median of 16.4 months.

285 hly efficient production of founder NHP with SCID phenotypes, with promises of multiple pre-clinical

286 For treatment costs, patients with SCID admitted to the national reference center for prima

287 assessing the risk of aGVHD in patients with SCID and designing the approach for GVHD prophylaxis.

288 standardized clinical care for patients with SCID during the time between diagnosis and definitive tr

289 ze supportive clinical care of patients with SCID from diagnosis to definitive treatment, reduce dise

290 anting CD34(+) stem cells from patients with SCID into a xenograft mouse model provides previously un

291 nal retrospective review of 74 patients with SCID undergoing transplantation between 1988 and 2014.

292 th posttransplantation GVHD in patients with SCID.

293 alists involved in the care of patients with SCID.

294 tegy on the supportive care of patients with SCID.

295 The proband presented with SCID, megaloblastic anemia, and neurologic abnormalities

296 lls, confirming correction of the cellular X-SCID phenotype.

297 X-linked severe combined immunodeficiency (X-SCID) is an immune disorder caused by mutations in the I

298 ntiation at the T cell progenitor stage in X-SCID cells.

299 To model X-SCID in vitro, we generated a mouse embryonic stem cell

300 y stronger antitumor activity in a xenograft SCID mouse model and depletes B cells in cynomolgus monk