ライフサイエンスコーパス: hyporesponsiveness

1 by using various techniques to achieve donor hyporesponsiveness.

2 enine (called 1V136) leads to subsequent TLR hyporesponsiveness.

3 ific memory cells is the cause of PS-induced hyporesponsiveness.

4 prolonged IL-12 treatment resulting in IL-12 hyporesponsiveness.

5 s largely abolishes IL-12 induction of IL-12 hyporesponsiveness.

6 leukin (IL)-10 overproduction, and CD4(+)Th1 hyporesponsiveness.

7 tivation, may play a role in adaptive immune hyporesponsiveness.

8 receptors (AR), as contributing to FL T cell hyporesponsiveness.

9 induction of the optimal level of macrophage hyporesponsiveness.

10 imary cause of hypoactivity, hypothermia and hyporesponsiveness.

11 and Thr399Ile) have been associated with LPS hyporesponsiveness.

12 suggesting that mature NK cells may acquire hyporesponsiveness.

13 (AMBP-1) appears to be responsible for this hyporesponsiveness.

14 une response signals to generate Ag-specific hyporesponsiveness.

15 ated with altered immune function, including hyporesponsiveness.

16 ytokine production, displaying a generalized hyporesponsiveness.

17 tivation, may play a role in adaptive immune hyporesponsiveness.

18 expression that is associated with iNKT cell hyporesponsiveness.

19 on to LV dysfunction through beta-adrenergic hyporesponsiveness.

20 the possible mechanism responsible for such hyporesponsiveness.

21 ylation of IRAK might all contribute to this hyporesponsiveness.

22 s analyzed with mechanisms of donor-specific hyporesponsiveness.

23 achieve stable chimerism and donor specific hyporesponsiveness.

24 e thymic tissue is able to induce xenogeneic hyporesponsiveness.

25 is in DBA/1 mice by induction of Ag-specific hyporesponsiveness.

26 sis (CML) assays demonstrated donor-specific hyporesponsiveness.

27 CD8(+) T cell response in a state of immune hyporesponsiveness.

28 L before LAM treatment abrogated LAM-induced hyporesponsiveness.

29 or B cells were required to induce iNKT cell hyporesponsiveness.

30 hus are unlikely to have a role in effecting hyporesponsiveness.

31 d potency of the Ag, were required to induce hyporesponsiveness.

32 dified immune cells and achieved immunologic hyporesponsiveness.

33 ther enteric glia are involved in epithelial hyporesponsiveness.

34 upon TCR stimulation and may lead to T cell hyporesponsiveness.

35 ted in human filariasis to understand immune hyporesponsiveness.

36 consisted of 36,450 patients; 1004 exhibited hyporesponsiveness.

37 on on protocol biopsy despite donor-specific hyporesponsiveness.

38 ion by inducing a state of peripheral T-cell hyporesponsiveness.

39 Oxidative stress can lead to T cell hyporesponsiveness.

40 tolerized mice exhibited xenodonor-specific hyporesponsiveness.

41 ls, which contributed to MDSC-induced T-cell hyporesponsiveness.

42 blocked at an immature stage associated with hyporesponsiveness.

43 state of active IL-10-mediated inflammatory hyporesponsiveness.

44 y response, followed by a secondary state of hyporesponsiveness, a so-called "tolerance." This hypore

45 -like T cell subset and indicate that T cell hyporesponsiveness, a state traditionally linked to tole

46 M receptors are responsible for producing AM hyporesponsiveness after hemorrhage.

47 rmine whether linezolid would reverse immune hyporesponsiveness after influenza infection in mice thr

48 key factor in the development of CD4+ T cell hyporesponsiveness after repeated parasite exposure invo

49 ed by lamina propria T cell (LPT) functional hyporesponsiveness after TCR engagement when compared wi

50 trategy of induction of alloantigen-specific hyporesponsiveness ("alloanergization") in donor bone ma

51 ures resulted in profound in vitro secondary hyporesponsiveness and 30-fold or greater protection fro

52 tosome infections are associated with T-cell hyporesponsiveness and a strong regulatory network.

53 renders them tolerogenic by inducing T-cell hyporesponsiveness and apoptosis.

54 eral T-cell compartment and exhibit profound hyporesponsiveness and decreased production of interleuk

55 This was associated with induction of T-cell hyporesponsiveness and enhanced T-cell apoptosis.

56 an the mean, respectively, the prevalence of hyporesponsiveness and hyper-responsiveness in these pat

57 When hyporesponsiveness and hyper-responsiveness to clopidogr

58 In addicted populations, both hyporesponsiveness and hyperresponsiveness of brain regi

59 nd in vitro, leading to Toll-like receptor 7 hyporesponsiveness and impaired IFN-alpha production.

60 odomain were previously associated with TLR4 hyporesponsiveness and increased susceptibility to bacte

61 pecific B cells in bone marrow, resulting in hyporesponsiveness and lack of long-term persistence of

62 mectomy on day -21, developed donor-specific hyporesponsiveness and maintained their cardiac grafts f

63 s that may be instrumental in general T-cell hyporesponsiveness and may contribute to the increased r

64 MF and DC is complex but contributes to the hyporesponsiveness and parasite persistence associated w

65 role in the cell-intrinsic program of T cell hyporesponsiveness and point to NR4A inhibition as a pro

66 ytokines and higher levels of erythropoietin hyporesponsiveness and poor clinical outcome, including

67 ith donor antigen resulted in donor-specific hyporesponsiveness and production of interleukin (IL)-10

68 AlloAg-pulsed Rapa DC induced T-cell hyporesponsiveness and promoted the generation of IL-10-

69 s resulted in secondary alloantigen-specific hyporesponsiveness and protection from graft-versus-host

70 These pigs developed in vitro donor-specific hyporesponsiveness and suppression.

71 ll defects may explain, in part, the vaccine hyporesponsiveness and susceptibility to bacterial infec

72 Our data demonstrate that KIR-mediated hyporesponsiveness and TGF-beta-mediated suppression are

73 ell subsets may provide a basis for antibody hyporesponsiveness and the limited effectiveness of 23vP

74 ulting in secondary mixed leukocyte reaction hyporesponsiveness and tolerance to alloantigen in vivo.

75 bal down-regulation of MHC-I induced NK cell hyporesponsiveness and tolerance to missing-self without

76 All demonstrated donor-specific hyporesponsiveness and were weaned from full-dose immuno

77 es that a soluble factor contributes to this hyporesponsiveness, and comparison of Peyer's patches an

78 e T and B cells, induction of cell-intrinsic hyporesponsiveness, and dominant regulatory cells mediat

79 ponses, induced stable GAD65-specific T cell hyporesponsiveness, and suppressed markedly control DC-i

80 e of memory B cells in 23vP-induced antibody hyporesponsiveness, and to identify the B-cell subtypes

81 nsiveness in vivo, but T cell depletion, not hyporesponsiveness, appears to be critical for anti-CD3

82 vestigations identified tumor-induced T-cell hyporesponsiveness as a form of clonal anergy, and they

83 -10 was observed to be critical in mediating hyporesponsiveness, as CD4+ cells from the sdLN of 4x mi

84 biasing iNKT cell Ags could induce iNKT cell hyporesponsiveness, as long as a minimum antigenic affin

85 CD4 T cells showed some hallmarks of hyporesponsiveness because TCR/CD28-mediated stimulation

86 ablishment of costimulation blockade induced hyporesponsiveness, but rather appears to be required fo

87 ent, all animals demonstrated donor-specific hyporesponsiveness by assays of direct alloresponse (cel

88 ic pathways are crucial for the induction of hyporesponsiveness by costimulation blockade.

89 Animals were monitored for donor-specific hyporesponsiveness by MLR and alloantibody determination

90 hese findings define the molecular basis for hyporesponsiveness by SHIP-deficient NK cells.

91 T-cell hyporesponsiveness can be caused by clonal anergy or ada

92 esponsiveness, a so-called "tolerance." This hyporesponsiveness can be induced by endotoxin stimulati

93 The immune hyporesponsiveness could be overcome if T cell help was

94 Ag-specific hyporesponsiveness could be reversed by the addition of

95 lymph node migratory capacity, induce T cell hyporesponsiveness, cross-present self-antigens to autor

96 rom, P<0.01), and equivalent beta-adrenergic hyporesponsiveness despite similar MI size.

97 The hyporesponsiveness did not depend on T or B lymphocytes,

98 falizumab may induce a unique type of T-cell hyporesponsiveness, directly induced by LFA-1 binding, w

99 This hyporesponsiveness does not involve CXCR4 modulation.

100 ed metabolic restrictions can mediate T cell hyporesponsiveness during cancer.

101 phosphorylation may be responsible for IL-6 hyporesponsiveness during sepsis.

102 forming growth factor (TGF)-beta in monocyte hyporesponsiveness during septic shock.

103 vent complications associated with secondary hyporesponsiveness during SIRS.

104 A window of hyporesponsiveness following influenza infection has bee

105 ied to the ease of measurement of lymphocyte hyporesponsiveness, has resulted in many attempts to und

106 receptor 4 (TLR4) associated with endotoxin hyporesponsiveness have decreased acute rejection over t

107 characterized in vitro as a pathway-specific hyporesponsiveness; however, this has not been demonstra

108 inhibits 1 degrees MLR and induces specific hyporesponsiveness in 2 degrees MLR, with both effects o

109 of many of the activated T cells, it induced hyporesponsiveness in a portion of the responding cells,

110 hibitor ARL 67156 partially overcomes T cell hyporesponsiveness in a subset of patient samples.

111 young and aged syngeneic hosts revealed that hyporesponsiveness in aged RTE was caused by a combinati

112 h in vivo CA treatment conferred Ag-specific hyporesponsiveness in BALB/c, NOD, DO11.10, and BDC-2.5

113 ect responsible for lipopolysaccharide (LPS) hyporesponsiveness in C3H/HeJ mice.

114 and the occurrence and severity of endotoxin hyporesponsiveness in children following elective cardia

115 imulatory molecules induce allogeneic T-cell hyporesponsiveness in coculture studies, mMDCs that expr

116 ction could partially account for the T cell hyporesponsiveness in filariasis.

117 Thus, the beta-AR hyporesponsiveness in human HF is mediated in large part

118 tional variants in the gene confer endotoxin-hyporesponsiveness in humans.

119 ty of Nippostrongylus brasiliensis to elicit hyporesponsiveness in lymph node T cells.

120 beta-adrenergic hyporesponsiveness in many cardiomyopathies is linked to

121 ot correlated with the development of T cell hyporesponsiveness in mixed lymphocyte culture.

122 bacterial components results in a status of hyporesponsiveness in otherwise reactive IEC.

123 ourse of the protocol, suggesting an adrenal hyporesponsiveness in participants with higher Pb concen

124 ajor mechanism underlying Ag-specific T cell hyporesponsiveness in patients with patent filarial infe

125 The overall hyporesponsiveness in skin from patients with background

126 Anergy is a state of long-term hyporesponsiveness in T cells that is characterized by a

127 en, with in vitro evidence of donor-specific hyporesponsiveness in the absence of donor macrochimeris

128 previously demonstrated profound Ag-specific hyporesponsiveness in the absence of NADPH oxidase-deriv

129 is not the main mechanism of donor-specific hyporesponsiveness in the direct pathway of allorecognit

130 patic DC induced alloantigen-specific T cell hyporesponsiveness in vitro, correlated with deficient T

131 ong-term acceptors maintained donor-specific hyporesponsiveness in vitro.

132 ed recovery of T cells and prolonged general hyporesponsiveness in vitro.

133 f both anti-CD3-induced T cell depletion and hyporesponsiveness in vivo, but T cell depletion, not hy

134 Immune hyporesponsiveness induced by 23vPPV in toddlers does no

135 istent with T cell anergy and similar to the hyporesponsiveness induced by administration of soluble

136 delivered siRNA prevented the development of hyporesponsiveness induced by repeated Ag stimulation in

137 The ensuing hyporesponsiveness is characterized by increases in both

138 The reason for this hyporesponsiveness is decreased or polarized expression

139 The IL-12 hyporesponsiveness is dependent on IL-12 concentration,

140 ication of antiplatelet nonresponsiveness or hyporesponsiveness is highly test specific, and does not

141 eonatal immune cells; however, the degree of hyporesponsiveness is highly variable and depends on the

142 Chemokine hyporesponsiveness is imposed upon T cells within hours

143 n, but the mechanism underlying the frequent hyporesponsiveness is incompletely understood.

144 hrough activating receptors, suggesting that hyporesponsiveness is responsible for self-tolerance.

145 ining T cells, demonstrating that FLN T cell hyporesponsiveness is reversible.

146 cular signaling circuitry that enforces this hyporesponsiveness is undefined.

147 ESA hyporesponsiveness may be useful in identifying potentia

148 Both tolerance and hyporesponsiveness occurred when the host was MHC I defi

149 plant recipients, donor-specific CD4+ T cell hyporesponsiveness occurs predominantly in CD4+ CD45RO+

150 We found that the hyporesponsiveness of AlvMs to IL-4 depended upon the lu

151 ein TCR transgenic mice, and showed that the hyporesponsiveness of autoantigen-reactive T cells from

152 This process contributes to the hyporesponsiveness of CD4(+) effector T cells and accumu

153 d-type LYP for binding to CSK and results in hyporesponsiveness of CD4(+) T cells to antigen stimulat

154 ce was capable of reversing the inflammatory hyporesponsiveness of GF mice in sterile inflammatory in

155 FasL is thus critical for both deletion and hyporesponsiveness of H-Y-reactive CD8+ T cells during p

156 trate that costimulation blockade can induce hyporesponsiveness of host CD4 T cells recognizing alloa

157 There was a reversible hyporesponsiveness of Ly49H(+) NK cells that extended to

158 M after CpG DNA pretreatment resulted in the hyporesponsiveness of macrophages that leads to the prot

159 CpG DNA/D-GalN-challenged mice is due to the hyporesponsiveness of macrophages to CpG DNA.

160 and ERK activation by acute alcohol leads to hyporesponsiveness of monocytes to LPS due to increased

161 We show that hyporesponsiveness of MUC1-Tg mice to this vaccine is a

162 However, signaling pathways that trigger hyporesponsiveness of phagocytes in clinically relevant

163 cross-linking FcgammaRIIA showed consistent hyporesponsiveness of platelets expressing the 276P/326Q

164 thways may partially underlie the documented hyporesponsiveness of PVN neurosecretory cells to certai

165 ortant new role for leptin in the anergy and hyporesponsiveness of regulatory T cells.

166 contrast to the partial clonal deletion and hyporesponsiveness of remaining T cells observed in CD28

167 The hyporesponsiveness of residual CD8+ T cells in mixed lym

168 ether this impairment may be associated with hyporesponsiveness of T cells to gamma-chain (gammac) cy

169 s demonstrate that the ex vivo proliferative hyporesponsiveness of Tgfb1(-/-) splenic lymphocytes is

170 insula during fear conditioning, as well as hyporesponsiveness of the dorsomedial prefrontal cortex

171 ermore, PLG formulation overcame an apparent hyporesponsiveness of the env DNA component in the combi

172 9H-activating receptor, which results in the hyporesponsiveness of the Ly49H(+) NK cell to stimulatio

173 that this cell-associated cytokine mediates hyporesponsiveness of the memory T cells in these microe

174 s responsible for the previously reported Ag hyporesponsiveness of these cells.

175 hods were used to estimate the effect of ESA hyporesponsiveness on allograft failure and all-cause mo

176 lls after primary antigen injection, and (2) hyporesponsiveness on reexposure to antigen.

177 was revealed by alloantigen-specific T-cell hyporesponsiveness on restimulation with the recipient i

178 receptor 4 (TLR4) associated with endotoxin hyporesponsiveness on the development of acute rejection

179 ion induces a state of donor-specific immune hyporesponsiveness or tolerance in some animal models.

180 administration of this TLR7 agonist induced hyporesponsiveness or tolerance to TLR2, -7, and -9 acti

181 The hyporesponsiveness partially dissipated without prolifer

182 ndependently of MHC-mediated inhibition, and hyporesponsiveness plays a role in self-tolerance of NK

183 cosal Ag exposure results in systemic T cell hyporesponsiveness, pre-existing systemic responses are

184 cytes pretreated with LPS exhibit a state of hyporesponsiveness, referred to as cross-tolerance, to b

185 marrow-derived cells could induce iNKT cell hyporesponsiveness, selective conditions, dependent on t

186 of corticosterone during a period of stress hyporesponsiveness suggest that these initial responses

187 The nature of this T-cell hyporesponsiveness suggests that T-cell responses may be

188 ions have been associated with immunological hyporesponsiveness that can affect responses to unrelate

189 by Jagged-1 promotes a novel form of T cell hyporesponsiveness that differs from anergy, whereby pri

190 ate that human liver DCs promote immunologic hyporesponsiveness that may contribute to hepatic tolera

191 In contrast to the observed Ag-specific hyporesponsiveness, the Ly-6A.2 transgenic CD4+ T cells

192 ons in immune function, in particular immune hyporesponsiveness, there have been only few studies tha

193 ls coated with anti-CTLA-4 Ab induced immune hyporesponsiveness through suppression of proinflammator

194 ions with polysaccharide (PS) vaccines cause hyporesponsiveness through undefined mechanisms.

195 stimulation through TLR7 induces a state of hyporesponsiveness (TLR tolerance) in both human and mou

196 age, children given 23vPPV exhibited immune hyporesponsiveness to a micro-23vPPV (20%) challenge dos

197 sure of monocytes/macrophages to LPS induces hyporesponsiveness to a second challenge with LPS, a phe

198 ficient hematopoietic cells failed to induce hyporesponsiveness to activating receptor stimulation, b

199 arly one-third of patients (including 3 with hyporesponsiveness to activating signals and 1 with mark

200 8-deficient platelets, resulting in a global hyporesponsiveness to agonists that signal through SFKs,

201 Recipients exhibit marked hyporesponsiveness to alloantigen in vitro.

202 tially acting as a barrier to attaining host hyporesponsiveness to an allograft.

203 y resembles resting memory cells, exhibiting hyporesponsiveness to anti-CD3 stimuli, lower proliferat

204 Patients with diabetes often show hyporesponsiveness to antiplatelet therapies, and it has

205 In aggregate, the data indicate that hyporesponsiveness to BCR cross-linking associated with

206 nsitivity, which contrasts with the vascular hyporesponsiveness to catecholamines.

207 of IRAK-1 was responsible for the macrophage hyporesponsiveness to CpG DNA.

208 Hyporesponsiveness to degranulation in NK cells was not

209 Local and systemic hyporesponsiveness to dietary antigens, classically refe

210 s allogeneic T-cell responses and results in hyporesponsiveness to donor and third party alloantigens

211 to third party alloantigen, yet may promote hyporesponsiveness to donor antigen.

212 The primary CTL hyporesponsiveness to donor B-LCL could not be reversed

213 In all animals assessed, in vitro hyporesponsiveness to donor hematopoietic cells persiste

214 ystemic insult is associated with subsequent hyporesponsiveness to endotoxin (as measured by ex vivo

215 Specific hyporesponsiveness to epitopes encoded in the peptide-Ig

216 overproduction of cytokines may account for hyporesponsiveness to erythropoietic therapy in patients

217 tients on hemodialysis with inflammation and hyporesponsiveness to ESA therapy.

218 a indicate that the gingival epithelial cell hyporesponsiveness to FimA is attributable to the lack o

219 -treated graft recipients transferred un- or hyporesponsiveness to hBPAG2 to other mice and demonstra

220 ajor factors determining human fetal NK cell hyporesponsiveness to HLA class I-negative target cells

221 under the prion promoter, results in immune hyporesponsiveness to human Abeta, in terms of both anti

222 sive locus and is associated with lymphocyte hyporesponsiveness to IL-12.

223 High phagocytic activity along with hyporesponsiveness to inflammatory insults and lack of a

224 Mechanistic studies revealed specific hyporesponsiveness to IRBP without immune deviation, no

225 f NF-kappaB ODN DC-treated animals exhibited hyporesponsiveness to islet antigens with low production

226 low expression of MIF may be predisposed to hyporesponsiveness to lipopolysaccharide and gram-negati

227 o-2 cell lines, is characterized by relative hyporesponsiveness to LPS and diminished expression of T

228 recurrent bacterial infections and profound hyporesponsiveness to LPS and IL-1, we previously identi

229 or exposure of 3E10/TLR2 cells to LPS led to hyporesponsiveness to LPS, LAM, and STF, indicating that

230 at in human monocytes, acute alcohol induces hyporesponsiveness to LPS, resulting in decreased TNF-al

231 atory and antimicrobial responses, including hyporesponsiveness to LPS.

232 lobulin; mTg) loaded multi-ligand DCs caused hyporesponsiveness to mTg challenge, suppression of auto

233 es augmented Foxp3(+) Treg cells and induced hyporesponsiveness to NOD-derived pancreatic beta-cell a

234 R1/2 signaling pathway may account for human hyporesponsiveness to OspA vaccination.

235 matic reactions (LARs) followed by bronchial hyporesponsiveness to peptide, inhibition of the allerge

236 ole or S-methyl-L-thiocitrulline reverts the hyporesponsiveness to phenylephrine and increases the va

237 dothelial dysfunction, including endothelial hyporesponsiveness to prototypical angiogenic growth fac

238 sess specific mechanisms of immunoregulatory hyporesponsiveness to repeated LPS exposure.

239 oped to overcome the T-independent response, hyporesponsiveness to repeated vaccination, and poor imm

240 Hyporesponsiveness to restimulation was not due to apopt

241 However, BCR signal-mediated hyporesponsiveness to SDF-1 is associated with phosphory

242 main self-tolerant and exhibit a generalized hyporesponsiveness to stimulation through activating rec

243 anergy induction does not appear to abrogate hyporesponsiveness to stimulation.

244 ure of macrophages to LPS induces a state of hyporesponsiveness to subsequent challenge with LPS.

245 unity, and initial exposure to 3D-EC confers hyporesponsiveness to subsequent exposure to immunogenei

246 LPS tolerance is a state of hyporesponsiveness to subsequent LPS challenge and is ac

247 robacterial LPS induces a state of transient hyporesponsiveness to subsequent LPS exposure, termed en

248 epeated exposure to a TLR agonist can induce hyporesponsiveness to subsequent TLR stimulation.

249 gand (FasL)-mediated apoptosis, resulting in hyporesponsiveness to subsequent vaccination.

250 KG mice have impaired T cell development and hyporesponsiveness to TCR stimulation, markedly reduced

251 Ptpra(-/-) fibroblasts exhibited hyporesponsiveness to TGF-beta, manifested by diminished

252 Decreased survival is accompanied by hyporesponsiveness to the B cell survival factor BLyS (a

253 ons induced by whole allergens and bronchial hyporesponsiveness to the peptides on the second injecti

254 y inhibits cell surface trafficking, confers hyporesponsiveness to TLR1 agonists, and protects agains

255 NFkappaB activity, absent p38 activity, and hyporesponsiveness to TLR2 and TLR4 agonists.

256 The hyporesponsiveness to TLR7 restimulation was associated

257 to LPS with down-regulation of MTP1, despite hyporesponsiveness to tumor necrosis factor-alpha signal

258 ut not two latter models, tumors induced CTL hyporesponsiveness to tumor-unrelated antigens.

259 gnals capable of inducing vasodilatation and hyporesponsiveness to vasoconstrictors in the splanchnic

260 s of nitric oxide synthase 1 blockade in the hyporesponsiveness to vasoconstrictors.

261 , and it is characterized by hypotension and hyporesponsiveness to vasoconstrictors.

262 ypotension, cardiac depression, and vascular hyporesponsiveness to vasopressor treatment.

263 and are not associated with the induction of hyporesponsiveness ("tolerance") in the skin or lung.

264 the frequency of Th1/Th17 cells, and induces hyporesponsiveness toward donor antigens.

265 al Th2 profile skewing and ex vivo recipient hyporesponsiveness toward donor-derived antigen as well

266 ontrast, prior implantation of 3D-EC induced hyporesponsiveness toward subsequent injection of EC-TCP

267 sful strategy to induce alloantigen-specific hyporesponsiveness towards stem cells in the CNS, which

268 ily kinase Lck is required to confer the BCR hyporesponsiveness typical of CD5+ B-1 cells and appears

269 specific activation receptors that result in hyporesponsiveness unless modulated by self-major histoc

270 bogluconate counteracted CD20 mAb-induced NK hyporesponsiveness, unveiling an unrecognized role for C

271 B cells, which in turn may contribute to the hyporesponsiveness upon BCR stimulation.

272 degrees MLR does not affect the induction of hyporesponsiveness upon restimulation.

273 IL-10 induced LPS hyporesponsiveness using the same mechanisms, i.e., ubiq

274 Hemorrhage-induced AM hyporesponsiveness was accompanied by the decreased expr

275 The HSC-induced T-cell hyporesponsiveness was associated with enhanced T-cell a

276 al of CD4(+)CD25(+) T cells, indicating that hyporesponsiveness was due to anergy and not due to acti

277 This hyporesponsiveness was evident even in the presence of I

278 Th2 cell hyporesponsiveness was evident within 10 d of initiation

279 Such MC hyporesponsiveness was induced antigen-specifically and

280 The hyporesponsiveness was more pronounced in CD28(-/-) and

281 ith Ag-pulsed macrophages demonstrating that hyporesponsiveness was not due to a direct effect of H.

282 This hyporesponsiveness was not observed when the antigen was

283 No evidence of mucosal hyporesponsiveness was observed after MACPS priming in t

284 In functional assays, hyporesponsiveness was observed for TAP-deficient NK cel

285 In one animal, general in vitro hyporesponsiveness was observed, with subsequent death f

286 ESA hyporesponsiveness was primarily defined as a monthly ES

287 T-cell hyporesponsiveness was reversed by depleting CD25(+) cel

288 Hyporesponsiveness was reversed by exogenous interleukin

289 ents to induce durable GAD65-specific T cell hyporesponsiveness was reversed once the control of glyc

290 This hyporesponsiveness was spontaneously reversible after wi

291 investigate the neural basis of this stress hyporesponsiveness we examined the changes in the restra

292 cells (CD4/CD45RA ) and in vitro xenogeneic hyporesponsiveness were observed.

293 cine-zipper domain of Foxp3 causes a loss of hyporesponsiveness when compared with wild-type Foxp3 up

294 airway hyperresponsiveness (AHR), but caused hyporesponsiveness when initiated before i.p. sensitizat

295 K cells mimics IL-12 priming, inducing IL-12 hyporesponsiveness, whereas transfection of miR-132, -21

296 val, inducing a robust and transferable host hyporesponsiveness, while administration of an ACK2 (ant

297 characterized by profound Ag-specific T cell hyporesponsiveness with impaired IFN-gamma and IL-2 prod

298 prolonged incubation resulted in a state of hyporesponsiveness with no reactivation of the cells by

299 ssays in both groups revealed donor-specific hyporesponsiveness with vigorous third-party reactivity.

300 o a single dose (1x), results in CD4+ T cell hyporesponsiveness within the skin-draining lymph nodes