ライフサイエンスコーパス: hyporesponsiveness

1 expression that is associated with iNKT cell hyporesponsiveness.

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

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

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

5 induction of the optimal level of macrophage hyporesponsiveness.

6 imary cause of hypoactivity, hypothermia and hyporesponsiveness.

7 and Thr399Ile) have been associated with LPS hyporesponsiveness.

8 suggesting that mature NK cells may acquire hyporesponsiveness.

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

10 une response signals to generate Ag-specific hyporesponsiveness.

11 ytokine production, displaying a generalized hyporesponsiveness.

12 on to LV dysfunction through beta-adrenergic hyporesponsiveness.

13 L before LAM treatment abrogated LAM-induced hyporesponsiveness.

14 the possible mechanism responsible for such hyporesponsiveness.

15 ylation of IRAK might all contribute to this hyporesponsiveness.

16 s analyzed with mechanisms of donor-specific hyporesponsiveness.

17 achieve stable chimerism and donor specific hyporesponsiveness.

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

19 e thymic tissue is able to induce xenogeneic hyporesponsiveness.

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

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

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

23 t recipients also demonstrated allo-specific hyporesponsiveness.

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

25 tes the induction of antigen-specific T-cell hyporesponsiveness.

26 ther enteric glia are involved in epithelial hyporesponsiveness.

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

28 ted in human filariasis to understand immune hyporesponsiveness.

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

30 on on protocol biopsy despite donor-specific hyporesponsiveness.

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

32 Oxidative stress can lead to T cell hyporesponsiveness.

33 tolerized mice exhibited xenodonor-specific hyporesponsiveness.

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

35 blocked at an immature stage associated with hyporesponsiveness.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 When hyporesponsiveness and hyper-responsiveness to clopidogr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 -10 was observed to be critical in mediating hyporesponsiveness, as CD4+ cells from the sdLN of 4x mi

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

78 injection of OVA induced Ag-specific T cell hyporesponsiveness, as manifested by decreased T cell pr

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

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

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

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

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

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

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

86 This suggests that hyporesponsiveness can be induced in CD4 T cells, but no

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

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

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

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

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

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

93 This hyporesponsiveness does not involve CXCR4 modulation.

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

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

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

97 A window of hyporesponsiveness following influenza infection has bee

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

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

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

101 ne of the laboratory findings, including LPS hyporesponsiveness, immunologic parameters, and inflamma

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

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

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

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

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

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

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

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

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

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

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

113 To determine the reason for LPS hyporesponsiveness in IEC, we examined the expression of

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

115 beta-adrenergic hyporesponsiveness in many cardiomyopathies is linked to

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

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

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

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

120 The overall hyporesponsiveness in skin from patients with background

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

122 imerism and lead to long-term donor-specific hyporesponsiveness in the absence of a cytoreductive con

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

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

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

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

127 ow) that induced alloantigen-specific T cell hyporesponsiveness in vitro.

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

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

130 Immune hyporesponsiveness induced by 23vPPV in toddlers does no

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

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

133 The ensuing hyporesponsiveness is characterized by increases in both

134 The reason for this hyporesponsiveness is decreased or polarized expression

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

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

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

138 Chemokine hyporesponsiveness is imposed upon T cells within hours

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

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

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

142 cular signaling circuitry that enforces this hyporesponsiveness is undefined.

143 ESA hyporesponsiveness may be useful in identifying potentia

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

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

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

147 nsiveness in RAW264.7 cells and suggest that hyporesponsiveness of C3H/HeJ mice to LPS is attributed

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

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

150 with heart failure is partly attributable to hyporesponsiveness of cyclic guanosine monophosphate (cG

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

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

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

154 The hyporesponsiveness of Ly-6A.2 transgenic CD4+ T cells is

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 propria is a basal state contributing to the hyporesponsiveness of the intestinal immune response.

170 9H-activating receptor, which results in the hyporesponsiveness of the Ly49H(+) NK cell to stimulatio

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

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

173 P-gp(high) subset may thus contribute to the hyporesponsiveness of this age-dependent, anergic memory

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

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

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

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

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

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

180 The hyporesponsiveness partially dissipated without prolifer

181 ifferences in costimulation blockade-induced hyporesponsiveness persist in the absence of CD4(+) T ce

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 Thus, thymocyte glucocorticoid hyporesponsiveness resulted in loss of cells capable of

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

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

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

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

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

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

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

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 The GS-sensitive increase in Qaw and its hyporesponsiveness to albuterol in asthmatic subjects ma

202 Recipients exhibit marked hyporesponsiveness to alloantigen in vitro.

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

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

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

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

207 illary muscle studies revealed isoproterenol hyporesponsiveness to be unaltered by NO synthase (NOS)

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

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

210 Hyporesponsiveness to degranulation in NK cells was not

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

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

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

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

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

216 Specific hyporesponsiveness to epitopes encoded in the peptide-Ig

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

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

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

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

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

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

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

238 Hyporesponsiveness to restimulation was not due to apopt

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 The hyporesponsiveness to TLR7 restimulation was associated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

273 Donor-specific hyporesponsiveness was demonstrated by cell-mediated lym

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

275 This hyporesponsiveness was evident even in the presence of I

276 Th2 cell hyporesponsiveness was evident within 10 d of initiation

277 Such MC hyporesponsiveness was induced antigen-specifically and

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

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

280 This hyporesponsiveness was not observed when the antigen was

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

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

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

284 ESA hyporesponsiveness was primarily defined as a monthly ES

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

286 Hyporesponsiveness was reversed by exogenous interleukin

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

288 This hyporesponsiveness was spontaneously reversible after wi

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

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

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

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

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

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

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

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

297 n inducing long-term antigen-specific T-cell hyporesponsiveness with rAd-transduced DC.

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

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

300 t and therefore we would predict that T cell hyporesponsiveness would develop predominantly in the CD