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 owing an Ag encounter, yet remain viable and hyporesponsive.

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

5 independent SMG trNK cells are intrinsically hyporesponsive.

6 10 donors, G-CD4 cells were more strikingly hyporesponsive.

7 ells by trogocytosis, rendering the NK cells hyporesponsive.

8 vation receptor by trogocytosis renders them hyporesponsive.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 Hyporesponsive cells showed no alteration in expression

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

47 LPS-hyporesponsive cells, primary macrophages, and polymorph

48 ntial mechanism for TH2 development in these hyporesponsive cells.

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

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

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

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

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

54 -1 cells express CD5 but not Lck and are not hyporesponsive; however, within the peritoneum, these B-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 This hyporesponsive phenotype was determined to be a conseque

95 The hyporesponsive phenotype was not a consequence of altere

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

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

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

99 tion mutations and human naturally occurring hyporesponsive polymorphisms map.

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

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

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

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

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

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

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

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

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

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

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

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

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

113 This hyporesponsive state persisted for at least 2 months and

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

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

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

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

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

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

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

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

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

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

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

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

126 ains intrahepatic NK cells in a functionally hyporesponsive state.

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

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

129 Both hyporesponsive states manifested a block in IkappaB degr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 ibit autoimmunity because they are generally hyporesponsive to stimulation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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