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1  capsules of SCID mice (ie, mice with severe combined immunodeficiency).
2 h protection occurred without causing severe combined immunodeficiency.
3 erize an inflammatory disease evocative of a combined immunodeficiency.
4 ations associated with multiple atresia with combined immunodeficiency.
5 ncy is a rare, but life-threatening, primary combined immunodeficiency.
6 mbined immunodeficiency, Omenn syndrome, and combined immunodeficiency.
7 tenuated MM tumor growth in mice with severe combined immunodeficiency.
8 who displayed an unusual progressive form of combined immunodeficiency.
9 inflammatory bowel disease-like disorder and combined immunodeficiency.
10 s with gene therapy for ADA-deficient severe combined immunodeficiency.
11 esting conditions in mice and a patient with combined immunodeficiency.
12 1-null mutant mice on a background of severe combined immunodeficiency.
13  myelokathexis (WHIM) syndrome, a human rare combined immunodeficiency.
14 idered LCK a candidate gene in patients with combined immunodeficiency.
15 rigel, and formed tumors in mice with severe combined immunodeficiency.
16 assays in nonobese diabetic mice with severe combined immunodeficiency.
17 ch is mutated in humans with X-linked severe combined immunodeficiency.
18  subsequently received a diagnosis of severe combined immunodeficiency.
19 ciency is associated with a novel variant of combined immunodeficiency.
20 vels of IgE are features of some variants of combined immunodeficiency.
21 1 leads to a severe clinical presentation of combined immunodeficiency.
22 ns and null mutations in mice lead to severe combined immunodeficiency.
23 om 9 patients with genetically confirmed PNP-combined immunodeficiency, 10,000 DBS samples from healt
24 4%) an autoinflammatory disorder, 14 (15%) a combined immunodeficiency, 3 (3%) an innate immune defec
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 order of purine metabolism leading to severe combined immunodeficiency (ADA-SCID).
31 of immune manifestations, such as late-onset combined immunodeficiency and autoimmunity.
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
35 allosal agenesis, cataracts, cardiomyopathy, combined immunodeficiency and hypopigmentation.
36 enting with a much more complex phenotype of combined immunodeficiency and immune dysregulation.
37             Mutations associated with severe combined immunodeficiency and Omenn syndrome had signifi
38 oal of defining the true incidence of severe combined immunodeficiency and providing early treatment
39 patients presented from early childhood with combined immunodeficiency and severe autoimmune disease.
40 ted disorders, including MIA associated with combined immunodeficiency and very early onset inflammat
41 y immunodeficiencies (PIDs) including severe combined immunodeficiency and Wiskott-Aldrich syndrome a
42 jected intraperitoneally (ie, in CB17 severe combined immunodeficiencies) and significantly increased
43 osa-associated lymphoid tissue 1 (MALT1) for combined immunodeficiencies, and tetratricopeptide repea
44                                   Background Combined immunodeficiencies are marked by inborn errors
45         Omenn syndrome (OS) is a rare severe combined immunodeficiency associated with autoimmunity a
46 y reported a novel syndrome characterized by combined immunodeficiency associated with severe develop
47 lifornia established the incidence of severe combined immunodeficiency at 1 in 66,250 live births.
48 Orai1 Ca2+ channels lead to a form of severe combined immunodeficiency, auto-immunity, muscle hypoton
49  heart) was tested in infarcted SCID (severe combined immunodeficiency)-Beige mice.
50 given intranasally or i.p. to newborn severe combined immunodeficiency-beige mice exposed to 90% O2 f
51 ridium parasites from 6 of 7 infected severe combined immunodeficiency-beige mice, and the parasites
52 t is a common finding in infants with severe combined immunodeficiency but is not typically observed
53  Janus kinase 3 (JAK3) are a cause of severe combined immunodeficiency, but hypomorphic JAK3 defects
54 overy occurred in VLP-dosed mice with severe combined immunodeficiency, but not in wild-type mice dep
55  T-cell deficiencies in patients with severe combined immunodeficiency by replacing resident thymus c
56 ed via osmotic pump in an intratibial severe combined immunodeficiency CAG myeloma model or in a syst
57 cy CAG myeloma model or in a systemic severe combined immunodeficiency CAG-heparanase model of aggres
58                                       Severe combined immunodeficiency can be caused by loss-of-funct
59                                     Profound combined immunodeficiency can present with normal number
60 tor of cytokinesis 8 (DOCK8) deficiency is a combined immunodeficiency caused by autosomal recessive
61 I3K-delta) syndrome (APDS) is a rare primary combined immunodeficiency caused by either dominant gain
62 s emerged as a convincing therapy for severe combined immunodeficiency caused by ILR2G mutation (SCID
63 n dedicator of cytokinesis 8 (DOCK8) cause a combined immunodeficiency characterized by atopy, recurr
64 ations in DOCK8 have been reported to have a combined immunodeficiency characterized by cutaneous vir
65       DOCK8 mutations result in an inherited combined immunodeficiency characterized by increased sus
66 ytokine receptor subunit give rise to severe combined immunodeficiency characterized by lack of T and
67                              Patients with a combined immunodeficiency characterized by normal number
68 g c-Rel protein expression in a patient with combined immunodeficiency characterized by susceptibilit
69 ovirus incidence was compared between severe combined immunodeficiency children with (n = 10) and wit
70 on of disease phenotypes for X-linked severe combined immunodeficiency, chronic granulomatous disease
71 n dedicator of cytokinesis 8 (DOCK8) cause a combined immunodeficiency (CID) also classified as autos
72                                              Combined immunodeficiency (CID) is a T-cell defect frequ
73                                              Combined immunodeficiency (CID) is characterized by seve
74                                              Combined immunodeficiency (CID) refers to inborn errors
75 I1 and STIM1 genes that abolish SOCE cause a combined immunodeficiency (CID) syndrome that is accompa
76 onical NF-kappaBeta pathways, resulting in a combined immunodeficiency (CID) without endocrine or ect
77 truction that is sometimes associated with a combined immunodeficiency (CID), leading to increased su
78 o present with autologous circulating T-cell combined immunodeficiency (CID).
79                                              Combined immunodeficiencies (CIDs) and "atypical" SCID s
80                                              Combined immunodeficiencies (CIDs) are diseases of defec
81                                              Combined immunodeficiencies (CIDs) form a heterogeneous
82  this review we describe peculiarities about combined immunodeficiencies (CIDs) in the Middle East.
83        Further, the nonobese diabetic severe combined immunodeficiency common gamma chain knockout-bo
84                                          PNP-combined immunodeficiency complies with the criteria for
85                 Newborn screening for severe combined immunodeficiency detects athymic patients, alth
86  decrease in survival and developed a severe combined immunodeficiency disease (SCID) affecting B, T,
87      The approach to the diagnosis of severe combined immunodeficiency disease (SCID) and related dis
88 ead to an autosomal recessive form of severe combined immunodeficiency disease (SCID).
89 nt with WHIM syndrome, an autosomal dominant combined immunodeficiency disease caused by gain-of-func
90     PET experiments were performed in severe combined immunodeficiency disease mice inoculated with p
91                         Patients with severe combined immunodeficiency disease who have matched sibli
92           Children with clinical features of combined immunodeficiencies, especially with early-onset
93 s with specific forms of PID, such as severe combined immunodeficiency, for over 10 years.
94 s of anti-CD3epsilon mAb treatment in severe combined immunodeficiency forms characterized by poor th
95 healthy donors were injected into NOD-severe combined immunodeficiency gammac(-/-) mice, followed by
96                     Nonobese diabetic-severe combined immunodeficiency-gammac(-/-) mice were injected
97 ells proliferate in nonobese diabetes/severe combined immunodeficiency/gammac(null) mice under the in
98 tients with atypical presentations of severe combined immunodeficiency gene mutations presents an opp
99 nt advances and newborn screening for severe combined immunodeficiency, has resulted in improved outc
100 ts with adenosine deaminase deficient severe combined immunodeficiency have identified neutropenia, a
101 -infected humanized nonobese diabetic severe combined immunodeficiency (HU-NOD/SCID) mice were genera
102 prevented bone destruction in vivo in severe combined immunodeficiency-hu mice.
103   Although its complete defect causes severe combined immunodeficiency (ie, T(-)B(-) severe combined
104  and engraftment in nonobese diabetic/severe combined immunodeficiency IL-2gamma(null) (NSG) mice com
105                  We report here the cause of combined immunodeficiency in 4 patients from 2 different
106            We studied the molecular basis of combined immunodeficiency in a patient who presented wit
107 In 6.5 years of newborn screening for severe combined immunodeficiency in California, 3,252,156 infan
108 encoding gamma(c) results in X-linked severe combined immunodeficiency in humans, and gamma(c) family
109 in patients with MIA and MIA associated with combined immunodeficiency include abnormalities of enter
110 hosts as well as in nonobese diabetic/severe combined immunodeficiency/interleukin 2Rgamma(null) mice
111 e immune-deficient (nonobese diabetic/severe combined immunodeficiency/interleukin-2 gammac receptor(
112 efore, we created a nonobese diabetic/severe combined immunodeficiency/interleukin-2 receptor-gamma-n
113 on by transplanting nonobese diabetic/severe combined immunodeficiency/interleukin-2 receptor-gamma-n
114 arly onset of bone marrow failure leading to combined immunodeficiency is associated with microcephal
115 mbined immunodeficiency (ie, T(-)B(-) severe combined immunodeficiency), its suboptimal activity is a
116 eplacement for Hemophilia B, X-linked Severe Combined Immunodeficiency, Leber's Congenital Amaurosis
117 T cells in a spectrum including leaky severe combined immunodeficiency (LS) and Omenn syndrome (OS).
118 rowth in vitro, and tumorigenicity in severe combined immunodeficiency mice (all P < 0.05).
119 lls, leading to increased survival of severe combined immunodeficiency mice after transplantation of
120 al liver cells into nonobese diabetic/severe combined immunodeficiency mice allows for the long-term
121 after subcutaneous transplantation in severe combined immunodeficiency mice and differentiated into S
122 d copper-DOTA-conatumumab was done in severe combined immunodeficiency mice bearing Colo205 xenograft
123                        In female CB17 severe combined immunodeficiency mice bearing Colo205 xenograft
124 by PET and ex vivo biodistribution in severe combined immunodeficiency mice bearing H2009 tumor (huma
125 o experiments, 6- to 12-wk-old female severe combined immunodeficiency mice bearing M21 xenografts (h
126 4)-BBN: for in vivo GRPR blockade) in severe combined immunodeficiency mice bearing PC-3 xenografts.
127 n erythrocytes into nonobese diabetic/severe combined immunodeficiency mice extends blood circulation
128 s transplanted onto nonobese diabetic/severe combined immunodeficiency mice faithfully recapitulated
129   Finally, YT cells transplanted into severe combined immunodeficiency mice had an invasive behavior.
130                 Six nonobese diabetic severe combined immunodeficiency mice received transplanted hum
131 ed the development of diabetes in NOD severe combined immunodeficiency mice receiving diabetogenic sp
132 transplantation in Non-obese diabetic/severe combined immunodeficiency mice that the HAGE knockdown i
133 ion in xenotolerant nonobese diabetic/severe combined immunodeficiency mice through intrasplenic or i
134 ted nonobese diabetic background with severe combined immunodeficiency mice to assess suppressive fun
135                     Nonobese diabetic/severe combined immunodeficiency mice transplanted with leukemi
136        The tumorigenicity of cells in severe combined immunodeficiency mice was augmented to a larger
137                                  Male severe combined immunodeficiency mice were subcutaneously impla
138 nized urokinase plasminogen activator/severe combined immunodeficiency mice were used to establish ch
139 lanted with MSCs in nonobese diabetic severe combined immunodeficiency mice with a significantly high
140 mproved survival of nonobese diabetic/severe combined immunodeficiency mice with HL-60 leukemia.
141 eased tumour volumes and mortality of severe combined immunodeficiency mice xenografted with PC3 and
142 nced MM cells were then injected into severe combined immunodeficiency mice, and tumor growth in s.c.
143            In a xenograft analysis of severe combined immunodeficiency mice, cisplatin also efficient
144 as not observed in non-obese diabetic/severe combined immunodeficiency mice, indicating the immune re
145         In a tumor xenograft model in severe combined immunodeficiency mice, inoculation of human HCC
146  immunocompromised non-obese diabetic/severe combined immunodeficiency mice, supporting an oncogenic
147 MB-231 cell-derived mammary tumors in severe combined immunodeficiency mice, we show here for the fir
148 sts and in aggressive tumor growth in severe combined immunodeficiency mice.
149  day prior to graft implantation into severe combined immunodeficiency mice.
150 s the tumorigenicity of A549 cells in severe combined immunodeficiency mice.
151 nhibited cholangiocarcinoma growth in severe combined immunodeficiency mice.
152 ro and in engrafted nonobese diabetic-severe combined immunodeficiency mice.
153 the choroids of six nude rats and six severe combined immunodeficiency mice.
154 hen transplanted to nonobese diabetic/severe combined immunodeficiency mice.
155 ansfer, delayed diabetes onset in NOD.severe combined immunodeficiency mice.
156  the tumorigenicity of MCF-7 cells in severe combined immunodeficiency mice.
157 n PBMC cultures and in PBMC-engrafted severe combined immunodeficiency mice.
158 the skeletal muscle of dystrophic mdx/severe combined immunodeficiency mice.
159 agar assays and xenograft analysis of severe combined immunodeficiency mice.
160 -L1-negative, and mixed tumor-bearing severe combined immunodeficiency mice.
161 1 nu/nu and LNCaP tumor-bearing CB-17 severe combined immunodeficiency mice.
162  suppressed tumor xenograft growth in severe combined immunodeficiency mice.
163 subcutaneously into nonobese diabetic severe combined immunodeficiency mice.
164                                 SCID (severe combined immunodeficiency) mice underwent left anterior
165           When xenografted into SCID (severe combined immunodeficiency) mice, the expression of muPAR
166 found in NOD/SCID (non-obese diabetic/severe combined immunodeficiency) mice.
167                       In human artery-severe combined immunodeficiency mouse chimeras, in which patie
168 ation into diabetic nonobese diabetic-severe combined immunodeficiency mouse kidneys.
169 lence in human skin xenografts in the severe combined immunodeficiency mouse model in vivo.
170 ly in infected skin xenografts in the severe combined immunodeficiency mouse model of VZV pathogenesi
171             Using a nonobese diabetic/severe combined immunodeficiency mouse model, those antibodies
172 ftment in NOD-SCID (nonobese diabetic-severe combined immunodeficiency) mouse myocardium increased ca
173 h experimental systemic infections of severe combined immunodeficiency Mus musculus with the bacteriu
174 ith a synthetic LAT gene bearing this severe combined immunodeficiency mutation.
175 cell lymphopenic infants had variant SCID or combined immunodeficiency (n = 6), genetic syndromes ass
176 he renal capsule of nonobese diabetic severe combined immunodeficiency (NOD SCID) mice with MSCs isol
177 +) progenitors into nonobese diabetic/severe combined immunodeficiency (NOD-SCID) mice resulted in th
178 xpressing tumors in nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice with partially
179 induced diabetes in nonobese diabetic severe combined immunodeficiency (NOD/SCID) mice.
180 il dystrophy, accounting for the nude/severe combined immunodeficiency (nu/SCID) phenotype in humans
181 entified in patients and are associated with combined immunodeficiencies of varying severity.
182 ided into 3 main categories: T(-)B(-) severe combined immunodeficiency, Omenn syndrome, and combined
183 been reported to be associated with either a combined immunodeficiency or common variable immunodefic
184 uses T(-)B(+) natural killer-positive severe combined immunodeficiency or T-cell lymphopenia with sev
185 ystem since it did not occur in nude, severe combined immunodeficiency, or T-cell depleted mice.
186 ons or autoimmunity, they represent profound combined immunodeficiency (P-CID), for which outcome dat
187 xpression of Bcl2 does not rescue the severe combined immunodeficiency phenotype in Ku70-deficient mi
188  We describe a pedigree affected by a severe combined immunodeficiency phenotype with absent T cells
189 lex are now recognized as the cause of novel combined immunodeficiency phenotypes, which all share ab
190                A 14-year-old boy with severe combined immunodeficiency presented three times to a med
191  of STAT1 can be associated with progressive combined immunodeficiency, quite distinct from the limit
192 eficiency presents with a varied spectrum of combined immunodeficiency, ranging from a T(-)B(-)NK(+)
193 ular, and clinical features of many types of combined immunodeficiencies remain unknown.
194 ntains a rare CD34(-) population with severe combined immunodeficiency-repopulating capacity.
195 ectasia and a class of Radiosensitive-Severe Combined Immunodeficiency (RS-SCID), respectively, funct
196 n therefore results in radiosensitive severe combined immunodeficiency (RS-SCID).
197 -lymphocyte-independent protection of severe combined immunodeficiency SCID mice from disseminated ca
198                         A subgroup of severe combined immunodeficiencies (SCID) is characterized by l
199 , wild-type (WT) and C3H animals with severe combined immunodeficiency (SCID animals) were inoculated
200 on of adenosine deaminase (ADA) cause severe combined immunodeficiency (SCID) and affect many other c
201 TEMIS deficiency usually present with severe combined immunodeficiency (SCID) and cellular radiosensi
202 cell transplantation in children with severe combined immunodeficiency (SCID) and other primary immun
203 opulation-based newborn screening for severe combined immunodeficiency (SCID) and related disorders h
204                                       Severe combined immunodeficiency (SCID) and X-linked agammaglob
205                                       Severe combined immunodeficiency (SCID) arises from different g
206                                       Severe combined immunodeficiency (SCID) can be cured by using a
207 e show that over 90% of patients with severe combined immunodeficiency (SCID) can be genetically-char
208                                       Severe combined immunodeficiency (SCID) carries a poor prognosi
209 g gene 1 (RAG1) deficiency results in severe combined immunodeficiency (SCID) caused by a complete la
210                                       Severe combined immunodeficiency (SCID) comprises a group of di
211                                       Severe combined immunodeficiency (SCID) comprises a heterogeneo
212 pathology of Omenn syndrome and leaky severe combined immunodeficiency (SCID) has not been previously
213                      The inclusion of severe combined immunodeficiency (SCID) in a Europe-wide screen
214 cular dysgenesis (RD), a rare form of severe combined immunodeficiency (SCID) in humans.
215                                       Severe combined immunodeficiency (SCID) is a life-threatening d
216                  Early recognition of severe combined immunodeficiency (SCID) is a pediatric emergenc
217             Adenosine deaminase (ADA)-severe combined immunodeficiency (SCID) is caused by genetic va
218                                       Severe combined immunodeficiency (SCID) is characterized by arr
219                                       Severe combined immunodeficiency (SCID) is characterized by sev
220 ne deaminase (ADA) cause a subtype of severe combined immunodeficiency (SCID) known as severe combine
221 was determined in LNCaP tumor-bearing severe combined immunodeficiency (SCID) mice after sacrifice at
222 essing SDF-1alpha were xenografted on severe combined immunodeficiency (SCID) mice.
223 oft agar and enhanced tumor growth in severe combined immunodeficiency (SCID) mice.
224 by transfer of their splenocytes into severe combined immunodeficiency (SCID) mice.
225 phagy in human skin xenografts in the severe combined immunodeficiency (SCID) mouse model of VZV path
226 RARalpha2-overexpressing MM tumors in severe combined immunodeficiency (SCID) mouse model.
227 at least a month in both nude rat and severe combined immunodeficiency (SCID) mouse xenograft models
228 onobese diabetic (NOD) mice, NOD with severe combined immunodeficiency (scid) mutation (SCID) mice, a
229 iver cells in nonobese diabetic (NOD)/severe combined immunodeficiency (SCID) or NOD/SCID/gammac(-/-)
230 nonimmunologic outcomes in cohorts of severe combined immunodeficiency (SCID) patients with either RA
231                                       Severe combined immunodeficiency (SCID) represents congenital d
232                                       Severe combined immunodeficiency (SCID) represents the most let
233 sis is an autosomal recessive form of severe combined immunodeficiency (SCID) that usually manifests
234 um (PIDTC) is enrolling children with severe combined immunodeficiency (SCID) to a prospective natura
235                 Newborn screening for severe combined immunodeficiency (SCID) using assays to detect
236                                       Severe combined immunodeficiency (SCID) with a complete absence
237 that impair Rag2 function can lead to severe combined immunodeficiency (SCID), a condition characteri
238  position found in some patients with severe combined immunodeficiency (SCID), and the double mutant
239 l reconstitution in many infants with severe combined immunodeficiency (SCID), but correction of B-ce
240 een identified, often associated with severe combined immunodeficiency (SCID), consistent with the re
241 to young horses (foals) affected with severe combined immunodeficiency (SCID), followed by challenge
242 cal profound T-cell dysfunction (TD), severe combined immunodeficiency (SCID), has been carefully def
243 vical spinal cords of adult mice with severe combined immunodeficiency (SCID), human pluripotent stem
244 ansplantation (HCT) for patients with severe combined immunodeficiency (SCID), including survival, T-
245 evant per se because in patients with severe combined immunodeficiency (SCID), infections caused by o
246 (ADA) deficiency, a cause of X-linked severe combined immunodeficiency (SCID), is a case in point.
247 und primary immunodeficiency disease, severe combined immunodeficiency (SCID), is fatal in infancy un
248                 The most severe form, severe combined immunodeficiency (SCID), presents with profound
249 tural history of patients treated for severe combined immunodeficiency (SCID), Wiskott-Aldrich syndro
250 te lymphocyte development and lead to severe combined immunodeficiency (SCID), XLF mutations cause a
251                                  In a severe combined immunodeficiency (SCID)-hu murine model of huma
252  in ORAI1 or STIM1 genes present with severe combined immunodeficiency (SCID)-like disease.
253 pathway result in radiation-sensitive severe combined immunodeficiency (SCID).
254 G) xenografts maintained in mice with severe combined immunodeficiency (SCID).
255 ion-based newborn screening (NBS) for severe combined immunodeficiency (SCID).
256 abesia microti infection in mice with severe combined immunodeficiency (SCID).
257 f adenosine deaminase (ADA)-deficient severe combined immunodeficiency (SCID).
258 nation, hence loss of DNA-PK leads to severe combined immunodeficiency (SCID).
259 e plasma in young horses (foals) with severe combined immunodeficiency (SCID).
260 gnificant proportion of patients with severe combined immunodeficiency (SCID).
261 ansplantation (HSCT) in patients with severe combined immunodeficiency (SCID).
262 n-2 gamma-chain receptor (IL2RG)/JAK3 severe combined immunodeficiency (SCID).
263 ic metabolic disease characterized by severe combined immunodeficiency (SCID).
264 the generation of a marmoset model of severe combined immunodeficiency (SCID).
265  B-lymphocytes and are diagnosed with severe combined immunodeficiency (SCID).
266 rabian and 1 Arabian-pony cross) with severe combined immunodeficiency (SCID).
267 development, clinically presenting as severe combined immunodeficiency (SCID).
268 immunodeficiencies including X-linked severe combined immunodeficiency (SCID-X1) and adenine deaminas
269                              X-linked severe combined immunodeficiency (SCID-X1) caused by mutations
270                              X-linked severe-combined immunodeficiency (SCID-X1) has been treated by
271                              X-linked Severe Combined Immunodeficiency (SCID-X1) is a genetic disease
272 tem-cell transplantation for X-linked severe combined immunodeficiency (SCID-X1) often fails to recon
273 ials involving children with X-linked severe combined immunodeficiency (SCID-X1), a Moloney murine le
274  vectors for gene therapy of X-linked severe combined immunodeficiency (SCID-X1), we have evaluated n
275 for the correction of canine X-linked severe combined immunodeficiency (SCID-X1).
276 hy donors and a subject with X-linked severe combined immunodeficiency (SCID-X1).
277  use in a clinical trial for X-linked severe combined immunodeficiency (SCID-X1).
278 in vivo in hairless outbred mice with severe combined immunodeficiency (SHO-Prkdc(scid)Hr(hr)).
279 phopenia, patients with ADA-deficient severe combined immunodeficiency showed a partial block in cent
280 nically mild initial presentation could be a combined immunodeficiency, so as to provide appropriate
281  A patient with multiorgan autoinflammation, combined immunodeficiency, subclinical amylopectinosis,
282 that inactivate Artemis cause a human severe combined immunodeficiency syndrome associated with cellu
283 mutations are responsible for a rare primary combined immunodeficiency syndrome associated with sever
284  inflammation, muscle weakness, and a severe combined immunodeficiency syndrome.
285 ast, hypomorphic Artemis mutations result in combined immunodeficiency syndromes of varying severity,
286 shed tumors (ie, in nonobese diabetic-severe combined immunodeficiencies) that were derived from CD44
287 a spectrum of phenotypes ranging from severe combined immunodeficiency to immune dysregulation.
288  We performed a multicenter survey of severe combined immunodeficiency transplantation centers in Nor
289 h adenosine deaminase (ADA)-deficient severe combined immunodeficiency using 2 slightly different ret
290 ntified through newborn screening for severe combined immunodeficiency using the T-cell receptor exci
291  neutrophil infiltration in mice with severe combined immunodeficiency, which is accompanied by stron
292                         Most defects lead to combined immunodeficiency with a range of severity.
293  in AK2 cause reticular dysgenesis, a severe combined immunodeficiency with agranulocytosis, lymphope
294 ciency should be considered in patients with combined immunodeficiency with B cell, T cell, and fibro
295 ntified in patients with a recessive form of combined immunodeficiency with defects in T, B, and NK c
296                                              Combined immunodeficiency with multiple intestinal atres
297 ciency should be considered in patients with combined immunodeficiency with T-cell abnormalities.
298 e bone marrow transplant for X-linked severe combined immunodeficiency, with no recovery of T lymphoc
299 n complex 1B (ARPC1B) subunit of Arp2/3 show combined immunodeficiency, with symptoms of immune dysre
300                              X-linked severe combined immunodeficiency (X-SCID) is an immune disorder

 
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