ライフサイエンスコーパス: immune suppression

1 conventional immune-modulatory agents, or no immune suppression).

2 lays a prominent role in activating systemic immune suppression.

3 atic autonomic hyperreflexia and post-injury immune suppression.

4 ecial emphasis on therapeutic resistance and immune suppression.

5 nisms and those not directly associated with immune suppression.

6 pathology in CVN-AD mice is driven by local immune suppression.

7 has a prominent role in activating systemic immune suppression.

8 ammation, while inducing several pathways of immune suppression.

9 of hyperinflammation, as well as protracted immune suppression.

10 we tested its role in apoptotic cell-driven immune suppression.

11 me particles/kg under transient or sustained immune suppression.

12 ls from TNF-induced apoptosis and not due to immune suppression.

13 lated N-glycans in inducing the IgM-mediated immune suppression.

14 umans and mice and contribute to age-related immune suppression.

15 reas device in diabetic primates without any immune suppression.

16 s MDSC expansion is accompanied by sustained immune suppression.

17 ease burden, without the need for drug-based immune suppression.

18 r functions of inflammation, modulation, and immune suppression.

19 immune responses without requiring systemic immune suppression.

20 Fel d 1-ILIT involved multiple mechanisms of immune suppression.

21 totic death in contributing to cytopenia and immune suppression.

22 sidered the major mediator of B cell-induced immune suppression.

23 ings suggest involvement in tumor-associated immune suppression.

24 ained for more than 1 year in the absence of immune suppression.

25 a benefit of diminishing iatrogenic systemic immune suppression.

26 tastatic dissemination, and the induction of immune suppression.

27 incidence of MCC among persons with systemic immune suppression.

28 stemness-associated transcription factor, in immune suppression.

29 cells, aberrant vasculature, and noteworthy immune suppression.

30 ata presented herein indicate that AD causes immune suppression.

31 esponding increase in splenic leucopenia and immune suppression.

32 ent that polarizes inflammatory cells toward immune suppression.

33 engages these MyD88 structural elements for immune suppression.

34 antigen-specific signaling in Treg-mediated immune suppression.

35 molecule directly affected cell survival and immune suppression.

36 ce suggests a link between tumor hypoxia and immune suppression.

37 nctional hallmarks of fibrocytes but mediate immune suppression.

38 an enhancement of remyelination rather than immune suppression.

39 cause serious unwanted side effects, such as immune suppression.

40 ific susceptibility factors, such as age and immune suppression.

41 ility of the bacilli to be reactivated after immune suppression.

42 nd immune cells is associated in cancer with immune suppression.

43 the treatment of multiple sclerosis, causes immune suppression.

44 gh levels of inflammatory cells and profound immune suppression.

45 tor T cells are susceptible to Treg-mediated immune suppression.

46 was also necessary for UVB-radiation-induced immune suppression.

47 nd seem to be major actors of sepsis-induced immune suppression.

48 ncreatic neuroendocrine tumors can alleviate immune suppression.

49 ced neurotoxicity and KYN and 3-HAA-mediated immune suppression.

50 of preventing and/or reversing Treg-induced immune suppression.

51 EAE-inflicted mice, without apparent global immune suppression.

52 supports acute HIV infection through innate immune suppression.

53 after T-cell replete transplants given with immune suppression.

54 uring lung cancer by promoting MDSC-mediated immune suppression.

55 obes often have single functions that permit immune suppression.

56 pment without causing lymphoproliferation or immune suppression.

57 hereas CCR2 does not directly participate in immune suppression.

58 have been implicated in fungal virulence and immune suppression.

59 mature T cell subpopulation specialized for immune suppression.

60 erogenic macrophage programming and adaptive immune suppression.

61 y a high degree of inflammation and profound immune suppression.

62 as the first in vivo mediator of hypercapnic immune suppression.

63 by increased IL-6 production and features of immune suppression.

64 fewer cells and reduced risk of nonspecific immune suppression.

65 sing host defense including the induction of immune suppression.

66 orks including pathways involved in acquired immune suppression.

67 nhibitor currently used for reversing tumour immune suppression.

68 men with sirolimus and mycophenolate mofetil immune suppression.

69 the basis of biomarkers of liver disease and immune suppression.

70 recipients often exceed 50%, despite maximal immune suppression.

71 ing of this reflex circuitry blocks post-SCI immune suppression.

72 higher among patients receiving combination immune suppression (54.5 per 1000 p-y) (P > .1 for all).

73 e presence of TM7x, suggesting its potential immune suppression ability.

74 point each for a respiratory rate >/= 30 and immune suppression) accurately identified patients who p

75 ies, arguing for COX activity as a driver of immune suppression across species.

76 Selective immune suppression, adjusted for early recurrence, rathe

77 monocytes and lymphopenia, the hallmarks of immune suppression after extensive ischemia.

78 (IFN-I) are cytokines that can mediate both immune suppression and activation.

79 the regulation of cancer stem cell property, immune suppression and cancer regression.

80 -kidney transplant, which requires life-long immune suppression and carries significant mortality ris

81 mation, postoperative cognitive dysfunction, immune suppression and cell signalling after surgery.

82 occurs in the setting of clinically relevant immune suppression and compared this to the hyperacute G

83 an acute viral disease associated both with immune suppression and development of life-long immunity

84 tryptophan catabolism, which contributes to immune suppression and disease progression.

85 demonstrates the enormity of ways to mediate immune suppression and enforce tissue homeostasis.

86 he tumour microenvironment can contribute to immune suppression and escape of tumours from immunologi

87 t cancer cells that coordinately help enable immune suppression and escape.

88 herapeutic agent for overcoming PDL1-induced immune suppression and facilitating tumor-specific immun

89 oving the outcome for patients with advanced immune suppression and for those with adverse tumor biol

90 ke regulate immune responses associated with immune suppression and healing; however, the relationshi

91 re, we review the ways in which tumors exert immune suppression and highlight the new therapies that

92 ter understanding of the mechanisms of viral immune suppression and host-pathogen interactions.

93 evidence for tumor microenvironment-mediated immune suppression and how radiation can modulate immune

94 d with the etiology of MDD, in line with the immune suppression and immune activation hypothesis of M

95 ring cancer and are associated with adaptive immune suppression and inflammatory metabolite productio

96 ress anti-inflammatory cytokines that induce immune suppression and may promote resistance to T cell

97 implicate TNFR2 in supporting MDSC-mediated immune suppression and metastasis in the liver, suggesti

98 Tumor expression of PD-L1 is correlated with immune suppression and poor prognosis.

99 ll dysfunction may contribute to HIV-related immune suppression and predispose to clinical AIDS event

100 ivery of IL-12 and GM-CSF can overcome tumor immune suppression and promote T cell-dependent eradicat

101 osome accumulation and their contribution to immune suppression and promotion of metastases.

102 coablated microglia and rod cells or applied immune suppression and quantified the kinetics of (i) ro

103 reduce circulating PGE2 levels, attenuating immune suppression and reducing the risk of infection in

104 PAF plays an essential role in UV-induced immune suppression and skin cancer induction.

105 cytic myeloid-derived suppressor cell-driven immune suppression and support that phenformin improves

106 Recent evidence suggests that immune suppression and susceptibility to the malaria par

107 ing that promote macrophage-induced adaptive immune suppression and thereby enable PDA progression.

108 actor receptor 2 (TNFR2) is known to mediate immune suppression and tissue regeneration.

109 interleukin (IL)-6 pathways in postoperative immune suppression and to assess the reversibility of th

110 interactions is an experimental approach to immune suppression and tolerance induction.

111 her regulatory T cells (Tregs) contribute to immune suppression and why both pathways have to be bloc

112 auses a systemic infection leading to fever, immune suppression, and a characteristic maculopapular r

113 sive aspergillosis is often a consequence of immune suppression, and accumulating evidence points to

114 se effects, including excessive weight gain, immune suppression, and bone loss.

115 transplantation is associated with profound immune suppression, and consequent opportunistic infecti

116 al destruction, serum monoclonal gammopathy, immune suppression, and end-organ sequelae.

117 and is required for macrophage polarization, immune suppression, and GBM growth.

118 the local and systemic factors that lead to immune suppression, and immunotherapy approaches to over

119 T-cell defects, immune suppression, and poor antitumor immune responses

120 (TAM) correlates with malignant progression, immune suppression, and poor prognosis.

121 he development of UVB-induced p53 mutations, immune suppression, and skin tumors.

122 fection can be established without antiviral immune suppression, and susceptibility is not donor depe

123 -positive gastric carcinoma does not require immune suppression, and the viral oncoproteins that are

124 a, amyloid, or lymphoma were observed during immune suppression, and there was no association between

125 able tumor-specific antigens, tumor-mediated immune suppression, and toxicity triggered by systemic d

126 ortant to the maintenance of self-tolerance, immune suppression, and tumor immunosurveillance.

127 steroids, which result in local and systemic immune suppression; and IgE-depleting therapies, which c

128 rived from solid tumor cells are involved in immune suppression, angiogenesis, and metastasis, but th

129 Several forms of immune suppression are associated with increased MCC inc

130 Cancer metastasis and immune suppression are critical issues in cancer therapy

131 ctors and mechanisms responsible for causing immune suppression are not completely understood.

132 The mechanisms underlying postinjury immune suppression are not known.

133 ever, the molecular mediators of hypercapnic immune suppression are undefined.

134 s of cancer," altered glucose metabolism and immune suppression, are in fact fundamentally linked.

135 Previous studies have emphasized immune suppression as a key step in bacterial pathogenes

136 a, and, ultimately, PVAN, is associated with immune suppression as well as inflammation and stress fr

137 to combat cancer while reducing the risk of immune suppression associated with JAK3 inhibition was u

138 ays a significant role in the development of immune suppression associated with sepsis.

139 ive incidence of discontinuation of systemic immune suppression at 1, 3, and 5 years after diagnosis

140 ent risk stratification and customization of immune suppression at the onset of BK viremia.

141 of patients with sepsis was consistent with immune suppression at the onset of secondary infection.

142 sustained inflammation in sepsis may lead to immune suppression, because of which the host is unable

143 esents an autologous transplant, it obviates immune suppression before and after transplant, eliminat

144 Ten events occurred during profound immune suppression before day 180 (median DC, 10%; range

145 D4(+)CD25(+) T regulatory cells by enhancing immune suppression, both in in vitro and in vivo.

146 is important to remember that in the face of immune-suppression, both IGRA and TST can be falsely neg

147 al that CCI sepsis patients feature signs of immune suppression but that their T cells exhibit a prim

148 ved suppressor cells, which not only mediate immune suppression, but also promote metastatic dissemin

149 er primarily by attenuation of Treg-mediated immune suppression, but the translatability to human GIT

150 processes may be involved in sepsis-induced immune suppression, but their clinical impact remains po

151 MCs on tumorigenesis was not associated with immune suppression, but with CCL4 (chemokine [C-C motif]

152 engagement counteracts pathogen-induced host immune suppression by activating p38 mitogen-activated p

153 RT1/FOXO3a axis in hepatocytes, resulting in immune suppression by attenuating caspase-3-dependent IL

154 and mouse mesenchymal stem cells can induce immune suppression by attracting and killing autoreactiv

155 The contribution of Tregs to immune suppression by costimulation blockade depends on

156 he development of infection and the level of immune suppression by HIV.

157 In summary, our results reveal how immune suppression by MDSC can be initiated in the tumor

158 L-6 and MDSC expansion, which contributes to immune suppression by modulating cytokine and cellular r

159 tedly, blood-borne MDSC execute far-reaching immune suppression by reducing expression of the L-selec

160 Dendritic cells (DC) are one target for immune suppression by regulatory T cells (Treg), because

161 Immune suppression by regulatory T cells and regulatory

162 This typically requires immune suppression by steroids, thiopurines, methotrexat

163 Immune suppression by T(reg) cells must be overcome to m

164 to enhance graft survival demonstrated that immune suppression can augment OEC contact-mediated prot

165 Preimmunized but not naive mice resisted immune suppression caused by an unrelated tumor burden,

166 ratory pathogens at least in part because of immune suppression caused by the condition for which the

167 eriods of time after clinical recovery, with immune suppression, chronic inflammation, and persistenc

168 This previously undescribed mechanism of immune suppression during chronic infection provides a v

169 cing a transcriptional program that promotes immune suppression during inflammation and tumour growth

170 une cell infiltration, thymic apoptosis, and immune suppression during polymicrobial sepsis were unaf

171 id organ malignancies, organ transplant, and immune suppression for nonmalignant conditions.

172 Lower and time-limited doses of immune suppression for patients predicted to have low-ri

173 a growing evidence base supports the use of immune suppression for the treatment of skin and lung fi

174 Measles infection leads to immune suppression for weeks to months.

175 ell paralysis as a major cause of protracted immune suppression from sepsis.

176 NP RNase in arenavirus replication and host immune suppression have not been characterized systemati

177 f the NP RNase in viral replication and host immune suppression have not been well characterized.

178 .g., above thoracic level 5) causes systemic immune suppression; however, the underlying mechanisms a

179 he host and tumour compartment contribute to immune suppression in a non-redundant fashion, suggestin

180 They cause immune suppression in a rodent model at serum concentrat

181 n macrophage polarization states can control immune suppression in cancer and other disorders.

182 erived suppressor cells (MDSC) contribute to immune suppression in cancer, but the mechanisms through

183 ered myeloid cells play an important role in immune suppression in cancer, in angiogenesis, and in tu

184 at the cross-roads of immune stimulation and immune suppression in cancer.

185 of cytokines can coexist with marked innate immune suppression in children with critical influenza.

186 but also promotion of acute inflammation or immune suppression in chronic inflammation and cancer.

187 nfiltrating PD-1(+)B7-H1(+) DCs in mediating immune suppression in ovarian cancer.

188 ely to account for sepsis and the associated immune suppression in patients with severe infection.

189 f the surrounding environment facilitate the immune suppression in patients, and immunotherapy can co

190 We used these mice to study immune suppression in PDA.

191 Reversal of postinjury immune suppression in SCI mice can be achieved by pharma

192 ter-inflammation with major implications for immune suppression in sepsis.

193 esults in both uncontrolled inflammation and immune suppression in septic patients.

194 ide (DC1-MUC1) can circumvent tumor-mediated immune suppression in the host, activate multiple immune

195 The need for additional immune suppression in the intestine reflects commensal m

196 Generalized immune suppression in the tumor draining lymph nodes has

197 ppressor cell infiltration, angiogenesis and immune suppression in the tumor microenvironment, all of

198 IL-12 promotes a rapid reversal of immune suppression in the tumor microenvironment.

199 mulates the TBK1-NFkappaB pathway and innate immune suppression in the tumor microenvironment.

200 responses, whether or not it plays a role in immune suppression in this case is unclear.

201 nvironment provides an opportunity to reduce immune suppression in tumor host.

202 erived suppressor cells (MDSC) contribute to immune suppression in tumor-bearing individuals and are

203 enzyme CSN5 leads to PD-L1 stabilization and immune suppression in tumors.

204 Treg and conventional T cell development and immune suppression in vivo using a transgenic mouse expr

205 d regMPhi induce a profound antigen-specific immune suppression in vivo.

206 antitumor benefits, mainly owing to multiple immune suppressions in established tumor lesions.

207 Age-related immune suppression increases susceptibility to infectiou

208 However, Breg cell mediated immune suppression, independent of IL-10, also occurs.

209 In fact, mechanisms other than immune suppression involve biologic effects mediated by

210 ltrating T cells is a widely cited theory of immune suppression involving B7-H1 in ovarian cancer.

211 UV radiation-induced systemic immune suppression is a major risk factor for skin cance

212 ppresses the immune response, and UV-induced immune suppression is a major risk factor for skin cance

213 n patients, the occurrence of sepsis-induced immune suppression is associated with delayed mortality,

214 Severe, early innate immune suppression is highly associated with both S. aur

215 This immune suppression is most profound during GVHD after bo

216 To test the hypothesis that this immune suppression is partially mediated by malaria-spec

217 mechanisms by which malignancies can induce immune suppression is through the production of cytokine

218 nd simultaneously reducing the tumor-induced immune suppression is well-tolerated and shows signs of

219 olimus is presently the most frequently used immune suppression (IS) regimen in islet transplantation

220 Sepsis is considered to induce immune suppression, leading to increased susceptibility

221 Subsequent immune suppression leads to viral reactivation from late

222 0 and cell-surface receptors associated with immune-suppression limit antigen presentation and T-cell

223 ere, we provide evidence that a part of this immune suppression may be attributable to dysfunction of

224 rther impairs normal skin barrier functions (immune suppression, mechanical stress), we studied the p

225 uman-pathogenic arenaviruses share an innate immune suppression mechanism that is based on viral Z pr

226 rinsic defects and instead highlights active immune suppression mediated by abundant CD71(+) cells in

227 eceptor) complex, we show that disruption of immune suppression mediated by CD8(+) Treg cells results

228 main (TIGIT), which results in resistance to immune suppression mediated by myeloid-derived suppresso

229 To further overcome the immune suppression mediated by programmed death-ligand 1

230 to determine the mechanism or mechanisms of immune suppression mediated by the nanovesicles.

231 ics and epigenetics, tumor microenvironment, immune suppression, metastasis, therapeutic resistance,

232 Despite VPA-mediated immune suppression, mice were not at significantly incre

233 ompared with patients with no known systemic immune suppression (n=430; 74% MCC-specific survival at

234 rve injury is due to an active, constitutive immune suppression of dorsal horn pain activity.

235 (IL-10)-dependent, antigen-specific systemic immune suppression of pathogenic antibody formation (imm

236 we characterized the viral growth and innate immune suppression of recombinant RNase-defective mutant

237 rom Lin(-) progenitor cells and reversed the immune suppression on T-cell proliferation and function

238 ignals that control whether PDL-1 stimulates immune suppression or activation is important as immune

239 esponses and thus drive general and systemic immune suppression or activation.

240 or function ex vivo and no evidence of overt immune suppression, our estimates are at the lower end o

241 Though innate responses are critical for immune suppression, our understanding of early innate im

242 M1]), chemoattraction (CCL20, CCL5, CXCL10), immune suppression (PD-L1, NFKB1B, TNFAIP3, CGB), apopto

243 mality is the key to predict the response to immune suppression, plasma infusion, and complement-inhi

244 ; osteomyelitis (hazard ratio 1.5; 0.7-3.1); immune suppression; prior sacral infections, and duratio

245 ational tolerance in the absence of complete immune suppression provides strong clinical implications

246 l successes include the definition of modern immune suppression, reductions in conditioning intensity

247 sms of HPV16 entry into LC and HPV16-induced immune suppression remain undefined.

248 ne, a tryptophan-related metabolite, induces immune suppression remains poorly understood.

249 L-6 in the clinical setting of postoperative immune suppression remains unclear.

250 se features, together with potential lack of immune suppression, render these unnatural glycopeptides

251 nses through the inhibition of tumor-derived immune suppression represents a promising strategy in th

252 ns into the mechanisms underlying UV-induced immune suppression reshaped our understanding of basic i

253 Effective control of this immune suppression-resistant T-cell activation represent

254 ing diminished chronic immune activation and immune suppression, restored lymphoid tissue architectur

255 Strategies to reverse this exposure-induced immune suppression should be examined to aid in the deve

256 of T cell-depleted transplants, receiving no immune suppression, showed diminished NK cell degranulat

257 chanisms for maintaining stability-including immune suppression, spatial structuring, and feeding of

258 of TLR7/8 agonists to reverse mMDSC-mediated immune suppression suggests that they might be useful ad

259 P RNase function is essential for the innate immune suppression that allows the establishment of a pr

260 a fundamentally new mechanism of MC-mediated immune suppression that broadly impacts multiple arms of

261 ll a major complication during the period of immune suppression that follows the procedure.

262 espite advancements in islet procurement and immune suppression that have increased islet transplant

263 we identify iNOS as a potential mediator of immune suppression that might be actionable using pharma

264 ed to re-evaluate current thoughts about the immune suppression that might occur during a persistent

265 ark of severe Lassa fever is the generalized immune suppression, the mechanism of which is poorly und

266 stem cell phenotype, invasion, angiogenesis, immune suppression, the premetastatic niche, intravasati

267 nor livers and complications associated with immune suppression, there is an urgent need for new ther

268 nes and promote localized MDSC expansion and immune suppression, thereby promoting tumor progression.

269 osomes (TEX) are harbingers of tumor-induced immune suppression: they carry immunosuppressive molecul

270 We report a novel mechanism for immune suppression through adenosine generation by B cel

271 e-stage HCC, demonstrating progressive local immune suppression through inefficient T cell infiltrati

272 cific preventive measures aimed at reversing immune suppression through targeting the altered redox s

273 provide evidence for pathogen-mediated host immune suppression through the destruction of a host tra

274 ryptophan metabolism pathway, which promotes immune suppression through the enzyme indoleamine 2,3-di

275 ient mice, the balance appears to shift from immune suppression to inflammation, and results in more

276 dosing while maintaining a similar level of immune suppression to more frequently and i.v. administe

277 ngevity, repeated re-infection and selective immune suppression to prevent protective Th2 responses.

278 amino acid catalytic activity may reinforce immune suppression to promote tumorigenesis and persiste

279 In the absence of local immune suppression, transferred cytotoxic T cells more e

280 gs), a key mediator in regulating anti-tumor immune suppression, tumor immune escape, metastasis and

281 nder cells were susceptible to Treg-mediated immune suppression up to 24 h after stimulation.

282 nonmyeloablative American Systemic Sclerosis Immune Suppression versus Transplant, and Autologous Ste

283 ectal distension) elicits AD and exacerbates immune suppression via a mechanism that involves aberran

284 ry role for Dkk1 in regulating tumor-induced immune suppression via targeting beta-catenin in MDSCs.

285 By competing risk regression analysis, immune suppression was a stage-independent predictor of

286 ment, maximal respiratory rate, and baseline immune suppression were independent predictors of progre

287 mast cells were dispensable for UVB-induced immune suppression, whereas basophil-derived AREG was es

288 he inflammatory response may accelerate host immune suppression, whereas use of traditional antibioti

289 re also autologous to eliminate the need for immune suppression, which can have severe side effects a

290 ls (LC), the APC of the epithelium, inducing immune suppression, which is mediated by the HPV16 L2 mi

291 mented tryptophan catabolism associated with immune suppression, which was highly represented in RCC

292 Therefore, combined antiangiogenesis and immune suppression will be more effective in maintaining

293 d almost one-third of those required further immune suppression with anti-TNFalpha therapy.

294 In this study, we demonstrate that immune suppression with cyclosporin after SCT limits T-h

295 , and administration of IL-15/IL-15Ralpha or immune suppression with rapamycin could restore NK-cell

296 The multiparous brain exhibited features of immune suppression, with dampened baseline microglial ac

297 s an important regulator of inflammation and immune suppression within the tumor microenvironment.

298 osis, antiretroviral treatment, or degree of immune suppression would implicate HIV infection-related

299 mphangiogenesis is associated with increased immune suppression, yet lymphatic vessels are required f

300 s (MDSC) play a major role in cancer-related immune suppression, yet the nature of this suppression r