ライフサイエンスコーパス: lymphopenia

1 S), a rare immunodeficiency characterized by lymphopenia.

2 d expression of lymphocyte related genes and lymphopenia.

3 row cellularity, erythroid anemia and B cell lymphopenia.

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

5 ocyte development resulting in severe T-cell lymphopenia.

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

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

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

9 omeostatic cytokine exposure during neonatal lymphopenia.

10 ntaneous T cell activation and severe T cell lymphopenia.

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

12 injection to mice also significantly induced lymphopenia.

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

14 stigated the role of C5a receptors in septic lymphopenia.

15 alters immune cell trafficking, and induces lymphopenia.

16 onsible for spontaneous T cell apoptosis and lymphopenia.

17 /ShcFFF mice also had significant peripheral lymphopenia.

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

19 osuppression through the induction of T-cell lymphopenia.

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

21 ngraftment and correction of neutropenia and lymphopenia.

22 ve chronic immune activation rather than CD4 lymphopenia.

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

24 s of RATG were independent of posttransplant lymphopenia.

25 2, HR = 0.6) despite its potential to induce lymphopenia.

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

27 0 (1/19,900 [0.005%]) had significant T-cell lymphopenia.

28 This caused a peripheral T cell lymphopenia.

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

30 main-associated protein 6 upregulation and B lymphopenia.

31 s that were associated with neutrophilia and lymphopenia.

32 re more or less likely to develop anemia and lymphopenia.

33 to be discontinued due to high toxicity and lymphopenia.

34 ith the development of hemorrhagic fever and lymphopenia.

35 Seventy-three percent of patients had lymphopenia.

36 lly S1P(1) functional antagonists that cause lymphopenia.

37 as discontinued because of high toxicity and lymphopenia.

38 s not the primary cause of peripheral T cell lymphopenia.

39 immune system in models of radiation induced lymphopenia.

40 xpected adverse events of rash and transient lymphopenia.

41 worse lasting for 8 or more days, except for lymphopenia.

42 th cardiac and splenic irradiation models of lymphopenia.

43 n-gamma and differential T and B cell subset lymphopenia.

44 spontaneous NK cell death and severe NK cell lymphopenia.

45 investigated whether plateletpheresis causes lymphopenia.

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

51 he control group), anemia (11.8% vs. 19.7%), lymphopenia (15.1% vs. 10.7%), and pneumonia (13.7% vs.

52 dverse events were neutropenia (28% vs 15%), lymphopenia (17% vs 10%), and stomatitis (13% vs 16%).

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 adverse events were thrombocytopenia (31%), lymphopenia (24%), anemia (21%), and neutropenia (21%).

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

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

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

61 4 adverse events included neutropenia (34%), lymphopenia (32%), infection (22%), and cardiac events (

62 5%), chills (45%), hyperbilirubinemia (34%), lymphopenia (34%), infusion-related reactions (34%), and

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

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

65 by a subset of inflammatory monocytes(5,6), lymphopenia(7,8) and T cell exhaustion(9,10).

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

67 quent in the CE+V arm than the CE+P arm: CD4 lymphopenia (8% v 0%; P = .06) and neutropenia (49% v 32

68 %), hand-foot syndrome (11%), diarrhea (8%), lymphopenia (8%), and leukopenia (6%).

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

70 he most common grade 3-4 adverse events were lymphopenia (98 [77%] of 127 patients in the radiotherap

71 owledged by a decrease of spleen's weight, a lymphopenia, a decrease of major histocompatibility comp

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

73 In HLH patients, severe and transient lymphopenia, activated NK cell phenotype (eg, increased

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

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

76 Lymphopenia (ALC<0.75 x10 3cells/uL) at one month was as

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

78 dead at Day 28.Conclusions: Profound global lymphopenia and a "chemokine signature" were observed in

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

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

81 develop pneumonia generally associated with lymphopenia and a severe inflammatory response due to un

82 inflammation-induced immunosuppression with lymphopenia and alterations of CD4+ T-cell functions tha

83 in cardiac and splenic irradiation models of lymphopenia and assessed the severity of radiation-induc

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

85 ytokines and severe CD4(+) and CD8(+) T-cell lymphopenia and coagulopathy.

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

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

88 s, in which it correlated to relative B cell lymphopenia and duration of disease.

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

90 raphic and laboratory abnormalities, such as lymphopenia and elevated lactate dehydrogenase, are comm

91 T cell maturation, caused peripheral T cell lymphopenia and enhanced complement susceptibility.

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

93 lymphocytes undergo apoptosis, resulting in lymphopenia and immunosuppression.

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

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

96 induce S1P(1)-desensitizing effects, such as lymphopenia and lung vascular leakage.

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

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

99 oreover, the knockout models showed distinct lymphopenia and neutrophilia, different from the full SG

100 chromosome 2p11.2 are associated with T-cell lymphopenia and probable thymic hypoplasia in human subj

101 17 consecutive patients with profound B-cell lymphopenia and prolonged COVID-19 symptoms, negative im

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

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

104 is based on simple criteria, such as chronic lymphopenia and/or history of corticosteroid boluses cou

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

106 ith a positive skin biopsy had elevated ACE, lymphopenia, and bihilar lymphadenopathy on CXR.

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

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

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

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

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

112 0 in the hematopoietic system causes anemia, lymphopenia, and postnatal lethality.

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

114 bined immunodeficiency with agranulocytosis, lymphopenia, and sensorineural deafness that requires he

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

116 1.0-3.4, p=0.039]) and presenting findings (lymphopenia [aOR 1.9, 95%CI 1.1-3.5, p=0.033], abnormal

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

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

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

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

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

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

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

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

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

126 receptor excision circles (TRECs) and T cell lymphopenia at birth, who carried heterozygous loss-of-f

127 s an important genetic determinant of T cell lymphopenia at birth.

128 Lymphopenia at COVID-19 diagnosis was associated with hi

129 p-value <0.001) compared to patients without lymphopenia at one month.

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

131 should be considered in SOT recipients with lymphopenia, BK-related infections and rituximab exposur

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

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

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

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

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

137 deficient T cells contributing to the T cell lymphopenia characteristic of this primary immunodeficie

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

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

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

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

142 using radiation chimeras we find that T cell lymphopenia depends on T cell-intrinsic expression of th

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

144 The common treatment-related AEs included lymphopenia, diarrhea, and elevated transaminases.

145 Lymphopenia did not parallel the observed spleen alterat

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

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

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

149 ngitudinal analysis showed persistent T cell lymphopenia during infancy, often associated with nail d

150 4 related toxicities were transient fevers, lymphopenia, elevated liver enzymes, and fatigue.

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

152 Also, in the spleen, T lymphopenia, especially after in vitro restimulation wit

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

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

155 Alemtuzumab produced profound lymphopenia followed by gradual T cell and more rapid B

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

157 Lymphopenia following PPCI is associated with poor progn

158 s with WAS manifest increased DNA damage and lymphopenia from cell death, yet how WASp influences DNA

159 atment-related toxicities included transient lymphopenia (group A, n = 1; group B, n = 1), pain (grou

160 All subjects with elevated ACE and lymphopenia had evidence of systemic sarcoidosis.

161 unophenotypes that included selective T-cell lymphopenia had overlapping microdeletions at chromosome

162 Lymphopenia has been associated with an increased risk o

163 Induction of lymphopenia has been exploited therapeutically to improv

164 02), CD8(+) (P < 0.0001), and B (P < 0.0001) lymphopenia, higher HLA-DR expression on monocytes (P <

165 Patients showed typical lymphopenia, higher prothrombotic profile, and higher ma

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

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

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

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

170 BACKGROUNDIdiopathic CD4 lymphopenia (ICL) is defined by persistently low CD4+ ce

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

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

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

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

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

176 vival in vitro, likely playing a role in CD4 lymphopenia in conjunction with its induced IL-7 recepto

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

178 is associated with CD4(+) and CD8(+) T-cell lymphopenia in healthy platelet donors.

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

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

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

182 arked defects in thymocyte egress and T cell lymphopenia in peripheral lymphoid organs in vivo.

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

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

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

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

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

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

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

190 ytokine levels (IL-6, IL-10, and TNF-alpha), lymphopenia (in CD4+ and CD8+ T cells), and decreased IF

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

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

193 ac2(+/E62K) mice phenocopy the T- and B-cell lymphopenia, increased neutrophil F-actin, and excessive

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

195 By contrast, profound lymphopenia induced by loss of lymphocyte S1P(1) provide

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

197 ggest that premature CD4(+) T-cell aging and lymphopenia induced spontaneous peripheral T-cell prolif

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

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

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

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

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

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

204 Lymphopenia-induced proliferation (LIP) occurs when reso

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

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

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

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

209 Lymphopenia induces T cells to undergo cell divisions as

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

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

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

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

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

219 The trigger for septic lymphopenia is unknown.

220 ologic laboratory abnormalities were common (lymphopenia, leukopenia, anemia, 98% each; neutropenia,

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

222 Five of nine patients had lymphopenia (<1.0 x 109 cells per L).

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

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

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

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

227 mutations resulting in severe T- and B-cell lymphopenia, myeloid dysfunction, and recurrent respirat

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

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

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

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

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

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

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

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

236 amma, in the onset of myeloproliferation and lymphopenia of A20 deficient mice.

237 drome presenting with persistent CD4+ T cell lymphopenia of unknown origin, and opportunistic infecti

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

239 0 patients), nausea (11 of 30 patients), and lymphopenia or diarrhoea (ten of 30 patients).

240 els of cardiac and splenic radiation-induced lymphopenia or gastrointestinal mucosal injury.

241 Patients may present with lymphopenia or pancytopenia at diagnosis.

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

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

244 atologic or lung malignancies, peri-COVID-19 lymphopenia, or baseline neutropenia had worse COVID-19

245 g the role of key immune cells, the cause of lymphopenia, organ-specific immunology, the dynamics of

246 .001), CMV infection (P = .001), and severe lymphopenia (P = .001) were significantly higher in case

247 1218/mm3 +/- 34; P = 0.001) including a CD4+ lymphopenia (P = 0.01).

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

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

250 Lymphopenia present in 74.2% of patients on admission da

251 th exhibited increased inflammatory markers, lymphopenia, pro-inflammatory cytokines, and high anti-r

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

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

254 t for confounding variables, the presence of lymphopenia remained statistically significantly associa

255 persistently low immunoglobulin M levels and lymphopenia, respectively.

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

257 Here we show lymphopenia, selective loss of CD4+ T cells, CD8+ T cell

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

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

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

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

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

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

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

265 Lymphopenia, thrombocytopenia, and elevation in inflamma

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

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

268 [27%] in cohort 1, five [20%] in cohort 2), lymphopenia (two [8%] in each cohort), and increased gam

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

270 Those found to have selective T-cell lymphopenia underwent testing with chromosomal microarra

271 Sensitivity of lymphopenia was 23.7%, with specificity 96.5% and AUC 0.

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

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

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

275 Persistent lymphopenia was defined as an absolute lymphocyte count

276 Lymphopenia was observed in 40 subjects, of whom 18 (45.

277 blood and lungs, whereas CD4 and CD8 T-cell lymphopenia was observed in the 2 compartments.

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

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

280 Lymphopenia was shown to predict bacteremia better than

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

282 Lymphopenia was the most common grade 3 or worse adverse

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

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

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

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

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

288 Combined elevated ACE and lymphopenia were strongly suggestive of systemic sarcoid

289 The common thread linking these patients is lymphopenia, which largely reflects a decline in the num

290 hile effective, it causes significant T-cell lymphopenia, which may increase risk of infection.

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

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

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

294 , especially herpetic, infections and T-cell lymphopenia with impaired T-cell but not B-cell prolifer

295 t to determine the cause of selective T-cell lymphopenia with inverted kappa/lambda ratio in several

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

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

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

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

300 myeloid cell activation, cytokine storm, and lymphopenia, with unknown immunopathological mechanisms.