ライフサイエンスコーパス: hyporesponsive

1 astric mucosa, they have been reported to be hyporesponsive.

2 of IL-6, the central cytokine compartment is hyporesponsive.

3 CD28(-/-), and Bcl-x(L)-transgenic mice were hyporesponsive.

4 10 donors, G-CD4 cells were more strikingly hyporesponsive.

5 owing an Ag encounter, yet remain viable and hyporesponsive.

6 ges remain immunologically and metabolically hyporesponsive.

7 independent SMG trNK cells are intrinsically hyporesponsive.

8 ells by trogocytosis, rendering the NK cells hyporesponsive.

9 vation receptor by trogocytosis renders them hyporesponsive.

10 (BM), and the existing T cells seemed to be hyporesponsive.

11 for self HLA are therefore "unlicensed" and hyporesponsive.

12 oward a Th1 response, but these cells remain hyporesponsive.

13 s lacking receptors for self MHC class I are hyporesponsive.

14 se phenotypes in patients with lymphopenia: "hyporesponsive" (23.2%), "hypercytokinemic" (36.4%), and

15 ay 4 after initiation of G-CSF (G-PBMC) were hyporesponsive (31.5% +/- 9.2% response, P = .003) compa

16 to their advantage, we hypothesize that the hyporesponsive 602S variant may confer protection by ena

17 l of local inflammatory reactions and become hyporesponsive after prolonged TLR4 activation by bacter

18 ture responsive NK cells from WT mice became hyporesponsive after transfer to MHC I-deficient mice, w

19 and observed that Sostdc1(-/-) NK cells are hyporesponsive against MHC class I-deficient cell target

20 zed perturbations, with two possible regimes-hyporesponsive and hyperresponsive-and the transition be

21 Paradoxically, RA T cells are hyporesponsive and proliferate poorly to antigens and mi

22 DCs and DCs) derived from cord blood induced hyporesponsive and regulatory CD4+ T cells.

23 In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in th

24 lpha-GalCer) results in the acquisition of a hyporesponsive (anergic) phenotype by these cells.

25 Patients' proliferation hyporesponsive (anergic) T cells had increased expressio

26 process of tolerization in which they become hyporesponsive/anergic to antigenic stimulation.

27 baseline or near baseline, with two of five hyporesponsive animals becoming unresponsive to Ag.

28 to other chronic viral infections in which a hyporesponsive antigen-specific T cell repertoire preven

29 ve T cells were initially activated but were hyporesponsive at the single cell level.

30 and inflammatory cytokine production in LPS-hyporesponsive C3H/HeJ and wild-type control C3H/HeOuJ m

31 While LPS-hyporesponsive C3H/HeJ macrophages failed to respond to

32 th HIV-LTR-luciferase and TLR4 cDNA from LPS-hyporesponsive C3H/HeJ mice abrogates LPS-induced HIV tr

33 rt also inhibit signaling and cells from LPS-hyporesponsive C3H/HeJ mice fail to exhibit this transpo

34 4) pg/ml) were required to stimulate the LPS-hyporesponsive C3H/HeJ mice peritoneal macrophages such

35 responsive C3H/OuJ mice and not from the LPS-hyporesponsive C3H/HeJ mice, a finding that is consisten

36 immunodeficient mouse strains, including LPS-hyporesponsive C3H/HeJ mice, muMT(-) (B-cell-deficient)

37 In LPS-hyporesponsive C3H/HeJ mice, only NDV induces this chemo

38 In LPS-hyporesponsive C3H/HeJ mice, PECAM-1 and MIP-2 were not

39 ot able to induce NO from lipopolysaccharide-hyporesponsive C3H/HeJ mouse peritoneal macrophages, but

40 dotoxin-responsive (C3Heb/FeJ) and endotoxin-hyporesponsive (C3H/HeJ) macrophages.

41 phages from LPS-responsive (C3H/HeN) and LPS-hyporesponsive (C3H/HeJ) mice internalized LPS with simi

42 ages and splenocytes from lipopolysaccharide-hyporesponsive (C3H/HeJ) mice.

43 charide (LPS)-responsive (C3H/HeOuJ) and LPS-hyporesponsive (C3H/HeJ) mouse strains infected with the

44 Mice circulating hyporesponsive CD4 T cells also fail to reject skin allo

45 eg) cell response, and to the development of hyporesponsive CD4+ T cells at the infection site, the p

46 fraction of these patients, an aberrant and hyporesponsive CD56(-)CD16(+)p75/AIRM1(-) NK-cell subset

47 on NK cells accounted for the generation of hyporesponsive CD56(dim) NK cells with limited degranula

48 The proportion of these hyporesponsive cells increases considerably with age.

49 Furthermore, IL-12-hyporesponsive cells regain responsiveness of IFN-gamma

50 Hyporesponsive cells showed no alteration in expression

51 RNA and protein expression were increased in hyporesponsive cells, and overexpression of Tollip in IE

52 LPS-hyporesponsive cells, primary macrophages, and polymorph

53 ntial mechanism for TH2 development in these hyporesponsive cells.

54 s upon M. tuberculosis infection, inducing a hyporesponsive cellular state.

55 lls exist in only two states, responsive and hyporesponsive, corresponding to cells that express or f

56 the RAPA-treated chimeras that the remaining hyporesponsive DLI-derived CD4+ T cells secrete large am

57 rt that persistence of the hypoinflammatory (hyporesponsive) effector immune cells during late sepsis

58 d tissue, thereby reversing or replacing the hyporesponsive endotoxin-tolerant cells that occur and p

59 d tumours(3-5), in part because they enter a hyporesponsive ('exhausted' or 'dysfunctional') state(6-

60 -1 cells express CD5 but not Lck and are not hyporesponsive; however, within the peritoneum, these B-

61 model recapitulates a clinical outcome of a hyporesponsive HPA stress axis, an important feature of

62 to a SCID mouse footpad, CD4(+) T cells were hyporesponsive in DTH to donor type HLA-B Ags and deriva

63 ssing subset of the CD4 memory population is hyporesponsive in many in vitro assays.

64 cytes from growth factor-treated donors were hyporesponsive in mixed leukocyte culture and in respons

65 bond formation and maintenance but is often hyporesponsive in people with anxiety or depression.

66 Y-redirected T cells proved hyporesponsive in peripheral lymphoid organs, whereas th

67 NK cells rendered hyporesponsive in this manner were deficient in the abil

68 hocyte phenotype with increasing age that is hyporesponsive in vitro led us to examine the possibilit

69 cells were equally responsive or moderately hyporesponsive; in two of 10 donors, G-CD4 cells were mo

70 dynia after SNI with the exception of stress-hyporesponsive LEW rats, despite all strains displaying

71 aride (LPS) responsiveness (lps(n)) and from hyporesponsive (lps(d)) fibroblasts have led to the find

72 fluorescently labeled LPS in cells from LPS-hyporesponsive (Lpsd) mice.

73 enotypically distinct population of FCRL4(+) hyporesponsive memory B cells (MBCs) was reported to be

74 In both LPS-responsive and -hyporesponsive mice given endotoxin-containing HEL, B ce

75 on of IL-9 was markedly reduced in bronchial hyporesponsive mice, and the level of expression was det

76 In marked contrast, in LPS-hyporesponsive mice, splenic DC show little gain in C4H3

77 in also decline in P(+) E. coli-infected LPS-hyporesponsive mice.

78 ty(r)) and C3H/HeJ (lipopolysaccharide [LPS]-hyporesponsive) mice.

79 the missense mutant Tlr4(P712H) found in LPS-hyporesponsive mouse strain (C3H/HeJ) inhibits LPS-induc

80 PH was attenuated in all lipopolysaccharide-hyporesponsive mouse strains studied (e.g., C3H/HeJ, Tlr

81 In contrast, hyporesponsive mutated CLL clones may have developed int

82 sfer to MHC I-deficient mice, whereas mature hyporesponsive NK cells from MHC I-deficient mice became

83 ins a significant population of functionally hyporesponsive NK cells that express high levels of the

84 cytokine stimulation restored reactivity of hyporesponsive NK cells through mTOR activation.

85 , by maintaining a greater percentage of the hyporesponsive NKG2A(+)Ly49(-) NK cells in the liver.

86 om BUF that received UVB-treated LEW SC were hyporesponsive on MLC stimulation by donor LEW alloantig

87 r these immunizations: C3H/HeJ, which is LPS hyporesponsive, or C3H/HeOuJ, which is LPS responsive.

88 ected to stressful stimuli during the stress hyporesponsive period exhibit varied neuroendocrine and

89 rmination coincides with a declining "stress hyporesponsive period" when corticosterone release is at

90 This 'stress hyporesponsive period' (SHRP) is thought to be at least

91 terone (CORT) are observed during the stress-hyporesponsive period.

92 T cell response to persistent Ag contains a hyporesponsive phase following an initial expansion and

93 estigated whether the germfree state and its hyporesponsive phenotype alter host resistance to an inf

94 We also demonstrated that the SMG NK cell hyporesponsive phenotype during murine CMV infection is

95 the wild-type allele of TLR4 rescues the LPS hyporesponsive phenotype in either primary airway epithe

96 the maintenance of the tolerance-associated hyporesponsive phenotype in T cells.

97 ive response in vitro, suggesting that their hyporesponsive phenotype is not directly mediated by CD4

98 ls in rejectors, which was associated with a hyporesponsive phenotype of activated effector T cells.

99 inase amplification loop may account for the hyporesponsive phenotype of CD19-deficient B cells.

100 This hyporesponsive phenotype of iNKT cells required IL-12 ex

101 Therefore, we examined whether the hyporesponsive phenotype of intestinal macrophages is pr

102 Overall, DNMAML T cells acquired a hyporesponsive phenotype that blocked cytokine productio

103 This hyporesponsive phenotype was determined to be a conseque

104 The hyporesponsive phenotype was not a consequence of altere

105 lls are induced to express Lck and acquire a hyporesponsive phenotype.

106 LPS responsiveness is a hallmark of the LPS-hyporesponsive phenotype.

107 nventional (CV) mice, and this was dubbed a "hyporesponsive phenotype." Taking into account that the

108 tion mutations and human naturally occurring hyporesponsive polymorphisms map.

109 st that exhaustion markers contribute to the hyporesponsive profile of lepromatous patients, and that

110 signaling pathways paradoxically results in hyporesponsive rather than hyperresponsive NK cells.

111 microchimerism increased with FEV1 for the 1 hyporesponsive recipient; for the other 6 recipients, bo

112 these cells to be either hyperresponsive or hyporesponsive, resulting in a changed immune response t

113 SWS is ideal for replay given hyporesponsive sensory systems, and thus reduced interfe

114 ent to promote Abeta degradation rescued the hyporesponsive state and olfactory behavior.

115 esults demonstrate that Tregs maintain their hyporesponsive state by suppressing the induction and pr

116 Peanut OIT induces a hyporesponsive state in basophils that is consistent wit

117 microenvironment, which may contribute to a hyporesponsive state in liver DC.

118 The molecular mechanisms underlying this hyporesponsive state in T cells are not fully understood

119 Induction of a hyporesponsive state in tumor Ag-specific T cells is one

120 Adaptive tolerance is a hyporesponsive state in which lymphocyte Ag receptor sig

121 transferred T cells could be induced and the hyporesponsive state maintained in the absence of CTLA-4

122 regulators of T cell signaling leading to a hyporesponsive state of T cells.

123 The hyporesponsive state of the T cells is not reversed by t

124 This hyporesponsive state persisted for at least 2 months and

125 ore activated, the adaptive immunity is in a hyporesponsive state reflected in alterations in CD4+CD2

126 tion with IgG1 anti-CD20, the FVIII-specific hyporesponsive state remained.

127 , exposure of AMs to tobacco smoke induces a hyporesponsive state similar to endotoxin tolerance as m

128 in the absence of costimulation results in a hyporesponsive state termed anergy.

129 ivide after activation exist in a profoundly hyporesponsive state that is refractory to both TCR/CD28

130 ing by maintaining alloreactive T cells in a hyporesponsive state, but has also been implicated in pr

131 The requirements for the induction of this hyporesponsive state, however, remain poorly defined.

132 ast, the Th2-biasing Ag OCH did not induce a hyporesponsive state, nor did cytokine-driven iNKT cell

133 ated to anergy in lymphocytes (GRAIL) in the hyporesponsive state.

134 ns alive for an extended period of time in a hyporesponsive state.

135 T cell activation and are associated with a hyporesponsive state.

136 ssion was isolated to the hepatocytes in the hyporesponsive state.

137 patocyte-derived NO may be protective in the hyporesponsive state.

138 ater in life when the network converted to a hyporesponsive state.

139 ains intrahepatic NK cells in a functionally hyporesponsive state.

140 , donor-reactive T and B cells remained in a hyporesponsive state.

141 Both hyporesponsive states manifested a block in IkappaB degr

142 anergy is a tolerance mechanism defined as a hyporesponsive status of antigen-specific T cells upon p

143 e IFN-beta production and acquire an M2-like hyporesponsive status.

144 itive subjects were more commonly female and hyporesponsive subjects were more often male (p = 0.016)

145 Peripheral blood monocytes from hyporesponsive subjects, compared with sensitive subject

146 g 6.5 micrograms or less of LPS, whereas 11 "hyporesponsive" subjects maintained an FEV1 >/= 90% of t

147 B10 recipients induced alloantigen-specific hyporesponsive T cell proliferation and prolonged subseq

148 and ability to induce alloantigen-specific, hyporesponsive T cell proliferation was not associated w

149 erences between T cell dysfunction and other hyporesponsive T cell states and discuss the spatio-temp

150 T gene expression, a program associated with hyporesponsive T cell states like anergy or exhaustion,

151 OVA-specific T cells result in induction of hyporesponsive T cells but also that these T cells could

152 These Ag-specific hyporesponsive T cells were subsequently able to activel

153 hich within 7-14 days produces 20-40 million hyporesponsive T cells.

154 cells to form a complex set of noncanonical hyporesponsive T helper cell subsets that lack the infla

155 tion of these cells before transfer revealed hyporesponsive Th1 function.

156 his suggests that heterozygous carriage of a hyporesponsive TLR9 allele is not associated with comple

157 Although several hyporesponsive TLR9 variants have been reported, their f

158 ection, the liver's ability to switch from a hyporesponsive to a proinflammatory environment is media

159 ic DCs rendered alloantigen-specific T cells hyporesponsive to a subsequent challenge with donor immu

160 In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist.

161 ee mice had a less mature phenotype and were hyporesponsive to activation with the antigen alpha-gala

162 ically, GATA-3-deficient CD8(+) T cells were hyporesponsive to Ag stimulation due to a defect in the

163 sed in Nur77-GFP(HI) cells, these cells were hyporesponsive to agonist TCR stimulation compared with

164 t CD45RC(-) T cells from tolerant hosts were hyporesponsive to alloantigen and suppressed the prolife

165 ipheral blood mononuclear cells (G-PBMC) are hyporesponsive to alloantigen compared with control PBMC

166 und that CD4+ T cells become profoundly more hyporesponsive to alloantigen restimulation with prolong

167 cl-2 mice remained deficient in B1 cells and hyporesponsive to anti-Igs, thymus-independent type 1 Ag

168 Circulating and intratumoral DN3 MBCs were hyporesponsive to antigen stimulation, had low antibody

169 secretion of naive T cells and rendered them hyporesponsive to antigenic restimulation, resulting in

170 Additionally, iNKT cells were hyporesponsive to antigenic stimulation in vivo.

171 In chronic infection, T cells become hyporesponsive to antigenic stimulation to prevent immun

172 We found that T(S) cells were hyporesponsive to antigenic stimuli in vivo and unable t

173 e liver conventional myeloid DCs (mDCs) were hyporesponsive to ATP, compared with their splenic count

174 ry receptors and activation markers, and are hyporesponsive to B-cell receptor (BCR) restimulation in

175 reased ability to internalize Ags, they were hyporesponsive to bacterial LPS: relative to control DC,

176 deficient NK cells, Clr-b(-/-) NK cells were hyporesponsive to both NK1.1 (NKR-P1C)-stimulated and IL

177 a spontaneous mutation in TLR4 (P712H) were hyporesponsive to both pneumolysin alone and the combina

178 (FL)-infiltrating CD8+ and CD4+ T cells are hyporesponsive to CD3/CD28 costimulation.

179 Circulating B cells in cirrhotics were hyporesponsive to CD40/TLR9 activation, as characterized

180 ithin the CD4(+) cells in vivo, but they are hyporesponsive to classical T cell receptor (TCR) stimul

181 iota by rendering lamina propria macrophages hyporesponsive to commensal bacteria through the down-re

182 loit GRK2/3 functional domains to render ASM hyporesponsive to contractile agents while increasing re

183 K-M was not sufficient to render macrophages hyporesponsive to CpG DNA but was required for induction

184 report a novel TLR9 allele, R892W, which is hyporesponsive to CpG ODN and acts as a dominant-negativ

185 ld-derived inbred mouse strain, MOLF/Ei, are hyporesponsive to CpG ODN but are fully responsive to ba

186 ficient hosts, natural killer (NK) cells are hyporesponsive to cross-linking of activation receptors.

187 manized mice were quantitatively reduced and hyporesponsive to cytokine and polyclonal stimulation.

188 ver transplantation, and only a minority are hyporesponsive to donor alloantigen.

189 ), we found both patients to be specifically hyporesponsive to donor compared with third-party B-LCL

190 Several chimeric recipients have become hyporesponsive to donor-major histocompatibility complex

191 In contrast, PBMC from tolerant chimeras hyporesponsive to donor-type cells could not be stimulat

192 re, vasa deferentia from t-PA-null mice were hyporesponsive to EFS (P<0.0001) but were normalized by

193 mutations in toll-like receptor 4 (TLR4) are hyporesponsive to endotoxin.

194 Five of nine were hyporesponsive to equine Ig, generating titers 50- to 25

195 atients with CKD who are on hemodialysis are hyporesponsive to erythropoiesis-stimulating agents (ESA

196 The remaining H-Y-specific T cells were hyporesponsive to H-Y as assayed by decreased proliferat

197 Reduced SHP-2 activity renders NK cells hyporesponsive to IL-15, which is associated with suppre

198 s, eventually resulting in T cells that were hyporesponsive to IL-2.

199 , resulting in miR-155(-/-) Th17 cells being hyporesponsive to IL-23.

200 Although Rpl22-deficient pro-B cells are hyporesponsive to IL-7, a key cytokine required for earl

201 in animals injected with MalE-OVA alone were hyporesponsive to in vitro Ag restimulation and did not

202 that developed in these mice appeared to be hyporesponsive to K(b), demonstrating that expression of

203 n vivo, and whose leukocytes were profoundly hyporesponsive to LPS and IL-1 in vitro.

204 n the cytoplasmic fraction and the cells are hyporesponsive to LPS in an unprimed condition.

205 ithelial cell line did not express CD14, was hyporesponsive to LPS stimulation, and demonstrated poor

206 Furthermore, the airways of KO mice were hyporesponsive to methacholine challenge at baseline and

207 dent cells also contribute to making the gut hyporesponsive to microorganisms.

208 d [Ca2+]i signaling, thus making these cells hyporesponsive to mitogen.

209 mal animals, lack CD5+ B cells (B1), and are hyporesponsive to mitogenic anti-Igs and thymus-independ

210 the human MUC1 gene (MUC1-Tg) are similarly hyporesponsive to MUC1.

211 l epithelial cells appear to be functionally hyporesponsive to normal intestinal flora, human intesti

212 ced with the MBAE-1-102-IgG recombinant, are hyporesponsive to p1-102.

213 a nonlupus systemic autoimmune disease, were hyporesponsive to P2X7 stimulation and resistant to P2X7

214 hypothalamic-pituitary-adrenal (HPA) axis is hyporesponsive to psychogenic stressors.

215 lymphocytes, those from Tgfb1(-/-) mice are hyporesponsive to receptor-mediated mitogenic stimulatio

216 Tg361 CD4 T cells, but instead renders them hyporesponsive to rechallenge with alloantigen.

217 ells activated by allogeneic rapa-ECs became hyporesponsive to restimulation in an alloantigen-specif

218 the final patient TIL infusion product, were hyporesponsive to restimulation with MART-1 peptide-puls

219 T cells recovered from RPE cocultures were hyporesponsive to restimulation with splenic APC and Ag,

220 These CD4(+)CD25(+) T cells are hyporesponsive to secondary alloantigen stimulation and

221 Rip2-deficient cells were also hyporesponsive to signalling through interleukin (IL)-1

222 They are hyporesponsive to signalling through the B cell receptor

223 iniature swine SLA(dd) T cells were rendered hyporesponsive to specific allogeneic Ag after coculturi

224 >mature B cell developmental pathway and are hyporesponsive to stimulation through the BCR.

225 T-cell anergy is a state of T cells that is hyporesponsive to stimulation via the T-cell receptor an

226 IFN-gamma revealed that IL-2(-/-) mice were hyporesponsive to stimulation with anti-CD3 or parasite

227 These cells were CD62L(low) and hyporesponsive to stimulation with cognate Ag but demons

228 Treg cell lines were markedly hyporesponsive to stimulation with dendritic cells and w

229 pDC and monocytes/macrophages rapidly became hyporesponsive to stimulation with SIV-encoded TLR ligan

230 f E-selectin expression but were found to be hyporesponsive to stimulation with the specific TLR2 lig

231 ibit autoimmunity because they are generally hyporesponsive to stimulation.

232 vities in LPS-tolerized cells remain low and hyporesponsive to subsequent LPS or LTA challenges.

233 T cells primed with alcohol-treated DCs were hyporesponsive to subsequent stimulation with the same d

234 timulation through TLRs renders immune cells hyporesponsive to subsequent stimulation with TLR ligand

235 ted in the presence of HLA-DQA1 are rendered hyporesponsive to subsequent stimuli.

236 ereas mice carrying an AD-HIES mutation were hyporesponsive to systemic anaphylaxis models.

237 cells from transgenic mice were functionally hyporesponsive to Talpha146-162 in terms of proliferatio

238 not educate fetal NK cells but rendered them hyporesponsive to target cells lacking HLA class I.

239 chromatosis donor-derived Vdelta2+ cells are hyporesponsive to TCR stimulation in terms of ROS produc

240 ed by CD4(+) T cells and thereby render them hyporesponsive to TCR stimulation.

241 Thus, 129/J mice are hyporesponsive to the preprodynorphin activating effects

242 plenic B cells from c-Abl-deficient mice are hyporesponsive to the proliferative effects of B cell Ag

243 earlier behavioral finding that 129 mice are hyporesponsive to the rewarding effects of heroin.

244 sal bacteria, the colonic mucosa is normally hyporesponsive to these potentially proinflammatory sign

245 ed fibroblasts from AKT2-deficient mice were hyporesponsive to TLR signals, in contrast to these from

246 ents with ligamentum flavum hypertrophy were hyporesponsive to TLR2 signals.

247 Macrophages from Treml4(-/-) mice were hyporesponsive to TLR7 agonists and failed to produce ty

248 nt activation, CD19-deficient mice (that are hyporesponsive to transmembrane signals) and mice overex

249 B lymphocytes from CD19-deficient mice are hyporesponsive to transmembrane signals, while B lymphoc

250 ever, CD19-deficient (CD19(-/-)) B cells are hyporesponsive to transmembrane signals, while Lyn-defic

251 ies revealed PD-L1-deficient recipients were hyporesponsive toward alloantigen, despite increased num

252 Despite this, human lung NK cells were hyporesponsive toward target cell stimulation, even afte

253 rs than the control monkey and significantly hyporesponsive when compared with a monkey that had reje

254 f costimulation are rendered anergic and are hyporesponsive when presented with Ag in the presence of

255 re unresponsive to MHC I-deficient cells and hyporesponsive when stimulated through activating recept

256 kemia causes T cells to become activated and hyporesponsive with increased PD-1 and TIM3 expression s

257 nse to suboptimal activation, T cells become hyporesponsive, with a severely reduced capacity to prol