ライフサイエンスコーパス: lymphopenia

1 alters immune cell trafficking, and induces lymphopenia.

2 onsible for spontaneous T cell apoptosis and lymphopenia.

3 /ShcFFF mice also had significant peripheral lymphopenia.

4 S), a rare immunodeficiency characterized by lymphopenia.

5 e CD8 T cells to MP CD8 T cells during acute lymphopenia.

6 osuppression through the induction of T-cell lymphopenia.

7 ue, as well as with more generalized splenic lymphopenia.

8 ngraftment and correction of neutropenia and lymphopenia.

9 ve chronic immune activation rather than CD4 lymphopenia.

10 ed the rates of detection of non-SCID T-cell lymphopenia.

11 s of RATG were independent of posttransplant lymphopenia.

12 2, HR = 0.6) despite its potential to induce lymphopenia.

13 d expression of lymphocyte related genes and lymphopenia.

14 r breaching self-tolerance in the setting of lymphopenia.

15 0 (1/19,900 [0.005%]) had significant T-cell lymphopenia.

16 This caused a peripheral T cell lymphopenia.

17 ilia, a loss of reticulocytes, and a massive lymphopenia.

18 main-associated protein 6 upregulation and B lymphopenia.

19 s that were associated with neutrophilia and lymphopenia.

20 ths, respectively) and profound naive T-cell lymphopenia.

21 bited rapid reconstitution after TBI-induced lymphopenia.

22 ) T cells in the setting of selective T cell lymphopenia.

23 row cellularity, erythroid anemia and B cell lymphopenia.

24 cell fraction, and B-cell and CD8(+) T-cell lymphopenia.

25 results, especially in the setting of marked lymphopenia.

26 ife span in vivo were found to contribute to lymphopenia.

27 of regulatory CD4(+) T cells in response to lymphopenia.

28 cell development, accounting for circulating lymphopenia.

29 normalities, hyperimmunoglobulin E, and Th17 lymphopenia.

30 8 total) included fatigue, hypertension, and lymphopenia.

31 grade 3 toxicities included hypokalemia and lymphopenia.

32 ncreased lymphocyte loss resulting in T-cell lymphopenia.

33 PFAPA flares also manifested a relative lymphopenia.

34 the TCR at the cell surface and selective T lymphopenia.

35 ocyte development resulting in severe T-cell lymphopenia.

36 , with 22 (88%) patients having grade 3 or 4 lymphopenia.

37 aricella, cutaneous warts, and CD4(+) T-cell lymphopenia.

38 P5 has a key role in BB-DR rat and NOD mouse lymphopenia.

39 omeostatic cytokine exposure during neonatal lymphopenia.

40 ntaneous T cell activation and severe T cell lymphopenia.

41 r, depression, anorexia, petechial rash, and lymphopenia.

42 injection to mice also significantly induced lymphopenia.

43 ke Ly-6C(+)CD44(hi) phenotype in response to lymphopenia.

44 stigated the role of C5a receptors in septic lymphopenia.

45 Neutropenia (1-146 cells/muL), lymphopenia (0-270 cells/muL), and thrombocytopenia (150

46 utropenia (30%), thrombocytopenia (22%), and lymphopenia (11%).

47 most common of any-grade adverse events were lymphopenia (12 [100%]) and gastrointestinal disorders (

48 rapy were hypertension (21%), fatigue (16%), lymphopenia (14%), and hyperglycemia (14%).

49 mia, leukopenia, and neutropenia (19% each); lymphopenia (14%); and thrombocytopenia (10%).

50 penia (121 [74%] of 164 vs 55 [34%] of 164), lymphopenia (149 [94%] of 158 vs 53 [33%] of 161), neutr

51 de 3-4 events, the most common of which were lymphopenia (15 [21%]) and neutropenia (14 [19%]).

52 xicities included neutropenia (29 patients), lymphopenia (16 patients), leucopenia (13 patients), and

53 ncluded neutropenia (8), leukopenia (5), and lymphopenia (2).

54 ent grade 3/4 hematologic abnormalities were lymphopenia (20% v 11%), anemia (9% v 8%), and neutropen

55 ded neutropenia (70%), leukopenia (36%), and lymphopenia (20%).

56 at group vs 118 [31%] in the placebo group), lymphopenia (202 [53%] vs 150 [40%]), diarrhoea (97 [26%

57 events were thrombocytopenia (25 patients), lymphopenia (24), neutropenia (17), leucopenia (ten), an

58 quent grade 3 to 4 adverse events (AEs) were lymphopenia (25%) and fatigue (14%).

59 erse effects were nausea (29%) and transient lymphopenia (26%).

60 the following adverse events versus placebo: lymphopenia (27 [8%] patients vs 0 patients), increased

61 ade 3 or worse in the safety population were lymphopenia (31 [12%] in the cilengitide group vs 26 [10

62 Es) possibly related to carfilzomib included lymphopenia (43%), thrombocytopenia (32%), hypertension

63 Grade 3/4 AEs included lymphopenia (48.1%), neutropenia (32.7%), thrombocytopen

64 ticipated grade 3 to 4 toxicities, including lymphopenia (53%) and thrombocytopenia (18%).

65 Grade 3 to 4 toxicities included lymphopenia (77%), neutropenia (33%), thrombocytopenia (

66 %), hand-foot syndrome (11%), diarrhea (8%), lymphopenia (8%), and leukopenia (6%).

67 The most frequent grade 3/4 toxicities were lymphopenia (82%), neutropenia (47%), and opportunistic

68 Pak2 gene in mice resulted in severe T cell lymphopenia accompanied by marked defects in development

69 nificant independent predictor of persistent lymphopenia (adjusted odds ratio, 2.70 [95% CI, 1.10, 6.

70 lted in splenocyte apoptosis and significant lymphopenia after 3 d, which was not observed in C5aR1(-

71 events were: thrombocytopenia, anaemia, and lymphopenia (all for patient number 2; anaemia and lymph

72 osis of SCID and other disorders with T-cell lymphopenia, allowing prompt and effective treatment and

73 in T-PPAR Teff function were not elicited by lymphopenia alone but also required the additional activ

74 Our results confirmed lymphopenia and a deficiency in naive T and B cells in A

75 elial-specific manner, creates a circulating lymphopenia and a higher percentage of effector T cells

76 In GSD-1b subjects, we found lymphopenia and a reduced capacity of T cells to engage

77 S1P) receptor agonist that induces sustained lymphopenia and accumulates in the CNS, represents a new

78 The association between lymphopenia and autoimmunity is recognized, but the unde

79 Both patients had CD4(+) T-cell lymphopenia and decreased lymphocyte proliferation to mi

80 fection is associated with a progressive CD4 lymphopenia and defective HIV-specific CD8 responses kno

81 e defects (eg, adult-onset idiopathic T-cell lymphopenia and early-onset autoimmunity might be due to

82 icity in arm 2 (34% v 53%; P < .001), mostly lymphopenia and fatigue.

83 Patients commonly have lymphopenia and Ig-production abnormalities.

84 t ADAP dampens naive CD8 T cell responses to lymphopenia and IL-15, and they demonstrate a novel Ag-i

85 lymphocytes undergo apoptosis, resulting in lymphopenia and immunosuppression.

86 l-specific dynamin 2 deficiency had profound lymphopenia and impaired egress from lymphoid organs.

87 sregulation, leading to a variable degree of lymphopenia and increased T-cell differentiation.

88 Profound lymphopenia and lack of early antiviral therapy were ass

89 that patients with ICL, despite gut mucosal lymphopenia and local tissue inflammation, have preserve

90 The patient displayed CD4(+) T-cell lymphopenia and low levels of CD4 and CD8 expression on

91 preemptive therapy era (n = 233) showed only lymphopenia and mechanical ventilation as significant ri

92 rly after HSCT can exploit both the state of lymphopenia and minimal residual disease for generating

93 adenosine deaminase (ADA) can cause profound lymphopenia and result in the clinical presentation of s

94 the risk of plasma/serum RSV RNA detection; lymphopenia and steroid use did not.

95 ic antibody-mediated T(Reg) depletion during lymphopenia and the consequent synergistic enhancement o

96 t is impaired, leading to a state of chronic lymphopenia and to a significant increase in the number

97 plasia, which results in a peripheral T cell lymphopenia and unusual T helper cell skewing.

98 ose of 18.9 MBq/mouse induced only transient lymphopenia and weight loss (<10% baseline weight).

99 thought to contribute to age-related T cell lymphopenias and hinder T cell recovery after bone marro

100 4 immunocompromised hosts had idiopathic CD4 lymphopenia, and 1 had human immunodeficiency virus/AIDS

101 set invasive bacterial and viral infections, lymphopenia, and defective T-cell, B-cell, and natural k

102 ing protein Gimap5 exhibit peripheral T cell lymphopenia, and Gimap5 can bind to Bcl-2.

103 ties were fatigue, thrombocytopenia, anemia, lymphopenia, and leukopenia.

104 agic fever with a deficient immune response, lymphopenia, and lymphocyte apoptosis.

105 ity included female sex, elevated bilirubin, lymphopenia, and mechanical ventilation; grade 3/4 acute

106 T cells, occurs independently of Nef-induced lymphopenia, and most likely results from multiple mecha

107 yndrome of monocytopenia, B-cell and NK-cell lymphopenia, and mycobacterial, fungal, and viral infect

108 0 in the hematopoietic system causes anemia, lymphopenia, and postnatal lethality.

109 ukopenia including neutropenia, B and T cell lymphopenia, and progression to bone marrow failure.

110 ible with laboratory findings of leukopenia, lymphopenia, and thrombocytopenia.

111 ed defects in BM hematopoiesis, resulting in lymphopenia, anemia, and thrombocytosis.

112 ity through the restriction of virus-induced lymphopenia, apoptosis-independent NK cell death, and lo

113 of regulatory CD4(+) T cells in response to lymphopenia appears to be primarily controlled by IL-2.

114 cytosis, and leukopenia, with pronounced pan-lymphopenia as demonstrated by flow cytometric analysis

115 c) mice), XLF deficiency leads to a profound lymphopenia associated with a severe defect in V(D)J rec

116 r data suggest that one of the mechanisms of lymphopenia associated with lethal H5N1 virus infection

117 ytopenia and B- and natural killer (NK)-cell lymphopenia associated with opportunistic infections and

118 duction of colibactin by E. coli exacerbates lymphopenia associated with septicemia and could impair

119 uirements for Tfh cell development change in lymphopenia-associated autoimmune settings.

120 strate that homeostatic proliferation drives lymphopenia-associated autoimmunity in humans.

121 a role in Teff proliferation and survival in lymphopenia-associated autoimmunity.

122 ma in CD4(+) T cells in two murine models of lymphopenia-associated autoimmunity.

123 polyclonal T cells, insufficient to prevent lymphopenia-associated expansion of subsequently adminis

124 ated that negative effects of posttransplant lymphopenia at 1 month (<1,000/muL) were significant reg

125 c cell transplantation is slow, resulting in lymphopenia at the time of DLI.

126 S1P1 is responsible for the peripheral blood lymphopenia believed to be key to its efficacy.

127 dverse events reported, with neutropenia and lymphopenia both occurring in 41% of patients and leukop

128 complete responses (CR) despite significant lymphopenia (Brincidofovir vs cidofovir; CR = 13 (80%) v

129 l strategies for newborn screening of B-cell lymphopenia by measuring immunoglobulin kappa chain-dele

130 e usefulness of detection of non-SCID T-cell lymphopenias by the same screening remains to be determi

131 This lymphopenia cannot be suppressed by deletion of p53 or c

132 Investigation revealed B-cell lymphopenia (CD19(+) range, 0.016-0.22 x 10(9)/L) and pa

133 dysregulation in patients with PHTS included lymphopenia, CD4(+) T-cell reduction, and changes in T-

134 named 'XMEN syndrome', characterized by CD4 lymphopenia, chronic EBV infection, and EBV-related lymp

135 We propose that HCs, possibly induced by lymphopenia, decrease the signaling threshold for TCR ac

136 Patients with mutated NIK exhibit B-cell lymphopenia, decreased frequencies of class-switched mem

137 ith a complete lack of B lymphocytes, T-cell lymphopenia, defective hematopoiesis, and developmental

138 in patients with congenital neutropenia and lymphopenia despite the absence of hypogammaglobulinemia

139 Lymphopenia did not parallel the observed spleen alterat

140 ed proportions of CD8(+) T cells and reduced lymphopenia-driven proliferation and memory-type convers

141 whether neonate-specific mechanisms prevent lymphopenia-driven T cell activation.

142 was associated with a peripheral CD4+ T cell lymphopenia due to defective thymocyte maturation.

143 Lymphopenia during hospitalization normalizes in majorit

144 4 related toxicities were transient fevers, lymphopenia, elevated liver enzymes, and fatigue.

145 Lymphopenia, eosinophilia, low numbers of naive CD8(+) T

146 xploitable in the treatment of patients with lymphopenia, especially in the case of chronic viral dis

147 sis of SCID and other conditions with T-cell lymphopenia, facilitating management and optimizing outc

148 ia (five [10%] and two [10%], respectively), lymphopenia (five [10%] and two [10%], respectively), pn

149 ere neutropenia (five [28%] of 18 patients), lymphopenia (five [28%]), anaemia (four [22%], and throm

150 TBI-induced lymphopenia followed by docetaxel treatment improved the

151 Alemtuzumab induction produced profound lymphopenia followed by repopulation, during which naive

152 Lymphopenia following PPCI is associated with poor progn

153 T cell lymphopenia has also been shown to be a barrier to CD4(+

154 Lymphopenia has been associated with an increased risk o

155 Induction of lymphopenia has been exploited therapeutically to improv

156 different families) presenting with profound lymphopenia, hypogammaglobulinemia, fluctuating monocyto

157 Idiopathic CD4 lymphopenia (ICL) is a rare heterogeneous immunological

158 Idiopathic CD4(+) lymphopenia (ICL) is a rare syndrome characterized by lo

159 Idiopathic CD4 lymphopenia (ICL) is a rare syndrome defined by low CD4

160 Idiopathic CD4 lymphopenia (ICL) is an immunodeficiency disorder of unc

161 hopenic conditions, including idiopathic CD4 lymphopenia (ICL), which is characterized by CD4 lymphop

162 a in 18 (10%), hypophosphataemia in 16 (9%), lymphopenia in 25 (14%), oral mucositis in 19 (11%), and

163 enia was observed in 70%, leukopenia in 59%; lymphopenia in 45%; and elevated levels of lactate dehyd

164 e incidence, causes, and follow-up of T-cell lymphopenia in a large diverse population.

165 is, which could contribute to the congenital lymphopenia in A-T.

166 T cell-lymphopenia in association with VEGFR2 blockade resulted

167 ymic ablation was evaluated by the degree of lymphopenia in blood samples collected at 4 weeks of age

168 Although FTY720 produced lymphopenia in both control and PT-S1P1-null mice, it re

169 was associated with both CD3 and CD4 T-cell lymphopenia in deteriorating patients.

170 eucopenia was noted in six patients, grade 4 lymphopenia in five, grade 4 neutrophils in five, and gr

171 utic opportunity for treating sepsis-induced lymphopenia in humans.

172 hanism(s) by which lethal H5N1 viruses cause lymphopenia in mammalian hosts remains poorly understood

173 ematopoietic stem cells corrected the T cell lymphopenia in mice after bone marrow transplantation.

174 However, this long lasting lymphopenia in patients with a previously normal immune

175 ortality and an increased risk of persistent lymphopenia in patients with sepsis, and it may be an ea

176 cell development and gives rise to a severe lymphopenia in peripheral organs, while also leading to

177 ion of histones prevented the development of lymphopenia in sepsis.

178 producing colibactin induced a more profound lymphopenia in septicemic mice, compared with the isogen

179 Remarkably, the B cell lymphopenia in the absence of ASCIZ can also be fully su

180 ocyte responses, T lymphocyte apoptosis, and lymphopenia in the absence of direct infection of T lymp

181 hopenia (ICL), which is characterized by CD4 lymphopenia in the absence of human immunodeficiency vir

182 uesters lymphocytes within SLO, resulting in lymphopenia in the blood and lymph.

183 aftment and tolerance without the hazards of lymphopenia in the challenging nonhuman primate islet al

184 verse events occurred in four (5%) patients: lymphopenia in two patients, blood creatine phosphokinas

185 deficient CD8 T cells are hyperresponsive to lymphopenia in vivo and exhibit enhanced activation of S

186 tation, we explored the possibility that the lymphopenia in WS arises from defects at the HSPC level.

187 l interventions for SCID and non-SCID T-cell lymphopenia included immunoglobulin infusions, preventiv

188 atory infections, progressive airway damage, lymphopenia, increased circulating transitional B cells,

189 go homeostatic proliferation during times of lymphopenia induced by certain viral infections or cause

190 mpared to free drugs, importantly, reversing lymphopenia induced by FTY720.

191 rface IL-15 expression is upregulated during lymphopenia induced by total body irradiation (TBI), cyc

192 ssue is the duration and significance of the lymphopenia induced.

193 ration of cognitive ability in aged mice, by lymphopenia-induced homeostasis-driven proliferation of

194 our laboratory demonstrated Ag-independent, lymphopenia-induced homeostatic proliferation to be a co

195 hile preserving the slow homeostatic form of lymphopenia-induced peripheral expansion that repopulate

196 Similarly, in lymphopenia-induced proliferating CD8 T cells, whereby n

197 TRAF6-activating factor capable of enhancing lymphopenia-induced proliferation (LIP) in vivo, and tha

198 In adult mice, lymphopenia-induced proliferation (LIP) leads to T cell

199 Lymphopenia-induced proliferation (LIP) occurs when reso

200 ouble-deficient (45RAGKO) mice, we show that lymphopenia-induced proliferation (LIP) of CD45-sufficie

201 mbining in vivo and mathematical modeling of lymphopenia-induced proliferation (LIP) of two distinct

202 otably the result of a cell-extrinsic-driven lymphopenia-induced proliferation as wild-type cells tra

203 IL-7-dependent manner, but failed to undergo lymphopenia-induced proliferation.

204 function in a model of chronic infection, or lymphopenia-induced proliferation.

205 for CD45 on innate immune cells in promoting lymphopenia-induced T cell proliferation and suggest tha

206 However, it is well recognized that lymphopenia induces compensatory proliferation of immune

207 Lymphopenia induces T cells to undergo cell divisions as

208 ment, in the context of chemotherapy-induced lymphopenia, induces a novel CD4(+) T cell population ch

209 clinical phenotype associating T- and B-cell lymphopenia, intermittent neutropenia, and atrial septal

210 ese results describe a new pathway of septic lymphopenia involving complement and extracellular histo

211 Although lymphopenia is a hallmark of severe infection with highl

212 Sepsis-induced lymphopenia is a major cause of morbidities in intensive

213 Peritransplant lymphopenia is a powerful prognostic factor for the recu

214 Peritransplant lymphopenia is a powerful prognostic factor for the recu

215 tioning-induced inflammatory stimuli, T cell lymphopenia is a risk factor for GVHD in mixed chimeras

216 recovery of CD4 T cells from sepsis-induced lymphopenia is accompanied by alterations to the composi

217 We demonstrate in this study that T cell lymphopenia is an independent risk factor for GVHD follo

218 The clonal response to lymphopenia is extremely diverse, and it is unknown whet

219 fferentially dictated by the manner in which lymphopenia is induced.

220 f TGF-beta signals, an added trigger such as lymphopenia is needed to drive overt autoimmune disease.

221 Transient lymphopenia is one hallmark of sepsis, and emergent data

222 The lymphopenia is the result of rapid apoptosis of newly ex

223 The trigger for septic lymphopenia is unknown.

224 high doses of radiation (>10 Gy) can lead to lymphopenia, lower radiation doses (2-4 Gy) represent a

225 gression analysis, peritransplant persistent lymphopenia (<1000/muL before LT and <500/muL at 2 weeks

226 gression analysis, peritransplant persistent lymphopenia (<1000/muL before LT and <500/muL at 2 weeks

227 Furthermore, severe pretransplant lymphopenia (<500/muL) was an independent prognostic fac

228 l repopulation following alemtuzumab-induced lymphopenia may contribute to its long-lasting suppressi

229 those without reactivation to have prolonged lymphopenia (median, 95 versus 22 days; P = 0.01) and to

230 T-cell impairment (n = 12), secondary T-cell lymphopenia (n = 9), or preterm birth (n = 8).

231 ), febrile neutropenia (n=1), anaemia (n=2), lymphopenia (n=1), diarrhoea (n=2), hypoalbuminaemia (n=

232 utropenia (n=27), febrile neutropenia (n=7), lymphopenia (n=4), diarrhoea (n=6), and hypokalaemia (n=

233 nsferase (n=6), hypophosphataemia (n=6), and lymphopenia (n=6).

234 At day 0, the degree of cytoreduction (lymphopenia, neuthropenia, and thrombocytopenia) achieve

235 odepleting chemotherapy regimen and included lymphopenia, neutropenia, and thrombocytopenia (21 [100%

236 pairment is a key mechanism underpinning the lymphopenia observed in mice and likely in WS patients.

237 de 3 or 4 neutropenia, thrombocytopenia, and lymphopenia occurred in 1%, 2%, and 9%, respectively, of

238 Lymphopenia occurred in 19 (6%) patients in the fingolim

239 , pulmonary hypertension (one of eight), and lymphopenia (one of eight).

240 tients with ICL, patients with secondary CD4 lymphopenia or 60 healthy subjects.

241 0 patients), nausea (11 of 30 patients), and lymphopenia or diarrhoea (ten of 30 patients).

242 Patients may present with lymphopenia or pancytopenia at diagnosis.

243 our results imply that any setting of T cell lymphopenia or reduced CD40 function, including B cell r

244 igns of systemic disease, such as arthritis, lymphopenia, or antinuclear antibodies.

245 1218/mm3 +/- 34; P = 0.001) including a CD4+ lymphopenia (P = 0.01).

246 mic development but profound and progressive lymphopenia particularly within the T cell compartment.

247 susceptibility were noted along with T-cell lymphopenia, particularly of CD8(+) T cells, and reduced

248 Despite the severe peripheral B-cell lymphopenia, patients with ADA-deficient severe combined

249 Lymphopenia present in 74.2% of patients on admission da

250 Posttransplantation lymphopenia promoted massive expansion of MCMV-specific

251 Six patients without lymphopenia received 12.5 mg/kg cyclophosphamide 4 days

252 Rag1 (Rag1(C/C)) or Rag2 (Rag2(C/C)) exhibit lymphopenia, reflecting impaired V(D)J recombination and

253 Radiation-induced lymphopenia (RIL) is associated with treatment of differ

254 nts were neutropenia (eight [62%] patients), lymphopenia (seven [54%] patients), and thrombocytopenia

255 human immunodeficiency characterized by CD4 lymphopenia, severe chronic viral infections, and defect

256 ndicate that achieving optimal recovery from lymphopenia should aim to improve early Treg reconstitut

257 irus dissemination to extrapulmonary organs, lymphopenia, significantly elevated levels of proinflamm

258 poietic cells also showed a loss of HSCs and lymphopenia, suggesting a cell intrinsic effect.

259 y and most importantly reduce FTY720-induced lymphopenia, suggesting its potential use in clinical ca

260 enetic disease characterized by neutropenia, lymphopenia, susceptibility to infections, and myelokath

261 ts with SCID or other forms of severe T-cell lymphopenia (TCL) have been detected, and no infants wit

262 events were thrombocytopenia (13 patients), lymphopenia (ten), neutropenia (nine), leucopenia (seven

263 They had more lymphopenia than control KTRs (1020/mm3 +/- 32 vs 1218/m

264 required development of an assay for T-cell lymphopenia that could be performed on dried bloodspots

265 y of homeostatic proliferation stimulated by lymphopenia, the effects of specific depleting agents on

266 unctional exhaustion of mature monocytes and lymphopenia, the hallmarks of immune suppression after e

267 antitumor efficacy engendered by TMZ-induced lymphopenia, there was a treatment related increase in t

268 nia (five in group 3 and six in group 4) and lymphopenia (three in group 3 and four in group 4).

269 ed with Marburg hemorrhagic fever, including lymphopenia, thrombocytopenia, marked liver damage, and

270 lgias, abdominal pain, anorexia, leukopenia, lymphopenia, thrombocytopenia, or elevated liver enzymes

271 eased to 76% of 114 participants with marked lymphopenia (total lymphocyte count [TLC] </=1200 cells/

272 [27%] in cohort 1, five [20%] in cohort 2), lymphopenia (two [8%] in each cohort), and increased gam

273 red in more than one patient in cycle 1 were lymphopenia (two), and neutropenia (eight).

274 s, and the prognostic relevance of post-PPCI lymphopenia was assessed by Cox proportional hazards reg

275 In the retrospective cohort, lymphopenia was associated with a lower rate of survival

276 Lymphopenia was cell intrinsic and, in the case of T cel

277 Persistent lymphopenia was defined as an absolute lymphocyte count

278 y CD4(+) T cell proliferation in response to lymphopenia was guided by classical homeostatic resource

279 ermined at experiment termination, and blood lymphopenia was measured 3 and 24 h after the last injec

280 nd CD11b(+)Gr1(+) MDSC following TBI-induced lymphopenia was measured in B16 melanoma tumor-bearing m

281 Significant T-cell lymphopenia was observed in the mucosal tissue of patien

282 At the cellular level, lymphopenia was present in patients with ICH at admissio

283 Lymphopenia was shown to predict bacteremia better than

284 muL versus 500-1,000/muL versus >1,000/muL), lymphopenia was significantly associated with higher rat

285 possible relationship between colibactin and lymphopenia, we examined the effects of transient infect

286 ants with SCID and other diagnoses of T-cell lymphopenia were classified.

287 penia (all for patient number 2; anaemia and lymphopenia were dose-limiting toxicities); hyperglycaem

288 When non-HIV causes of CD4 lymphopenia were excluded, the probability rose to 99.2%

289 patients with NBS-identified non-SCID T-cell lymphopenia were followed.

290 oimmune arthritis develops in the setting of lymphopenia when Foxp3(+)CD4(+) regulatory T cells are i

291 h active treatment versus placebo apart from lymphopenia, which was a severe event in 10 (5%) patient

292 1)-selective agonists that induce reversible lymphopenia while persisting in the CNS may be effective

293 ral blood (PB) anaemia, myelomonocytosis and lymphopenia, while the number of phenotypic HSCs increas

294 ive thymic T-cell development and selection, lymphopenia with homeostatic proliferation, and lack of

295 odel, we suggest a more quantitative view of lymphopenia with respect to the factors that promote LIP

296 e severe combined immunodeficiency or T-cell lymphopenia with severe viral infections.

297 All patients developed lymphopenia, with 22 (88%) patients having grade 3 or 4

298 s effect was exacerbated under conditions of lymphopenia, with the formation of potent memory T cells

299 openic throughout), despite full reversal of lymphopenia within each dosing interval.

300 We hypothesized that sustained lymphopenia would not be required for efficacy and that