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 ecial emphasis on therapeutic resistance and immune suppression.

4 of hyperinflammation, as well as protracted immune suppression.

5 reas device in diabetic primates without any immune suppression.

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

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

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

9 obes often have single functions that permit immune suppression.

10 have been implicated in fungal virulence and immune suppression.

11 mature T cell subpopulation specialized for immune suppression.

12 erogenic macrophage programming and adaptive immune suppression.

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

14 tion in the TME and can reverse ADO-mediated immune suppression.

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

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

17 fewer cells and reduced risk of nonspecific immune suppression.

18 sing host defense including the induction of immune suppression.

19 orks including pathways involved in acquired immune suppression.

20 nhibitor currently used for reversing tumour immune suppression.

21 men with sirolimus and mycophenolate mofetil immune suppression.

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

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

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

25 atic autonomic hyperreflexia and post-injury immune suppression.

26 flammation subsides, thus avoiding excessive immune suppression.

27 nisms and those not directly associated with immune suppression.

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

29 has a prominent role in activating systemic immune suppression.

30 ammation, while inducing several pathways of immune suppression.

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

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

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

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

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

36 s MDSC expansion is accompanied by sustained immune suppression.

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

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

39 immune responses without requiring systemic immune suppression.

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

41 totic death in contributing to cytopenia and immune suppression.

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

43 ings suggest involvement in tumor-associated immune suppression.

44 lication while maintaining allograft-sparing immune suppression.

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

46 a benefit of diminishing iatrogenic systemic immune suppression.

47 tastatic dissemination, and the induction of immune suppression.

48 incidence of MCC among persons with systemic immune suppression.

49 idence has shown that hypoxia promotes local immune suppression.

50 acrophages (TAMs) playing a critical role in immune suppression.

51 tent host, a concept defined as compensatory immune suppression.

52 hogen interaction, to acute inflammation, to immune suppression.

53 herapeutic cells typically requires systemic immune suppression.

54 ssion of GILZ, thereby maintaining effective immune suppression.

55 cells, and thus its essential function is in immune suppression.

56 tumor growth, survival, drug resistance, and immune suppression.

57 uses B cell malignancies under conditions of immune suppression.

58 Pregnancy is accompanied by immune suppression.

59 has been associated with drug resistance and immune suppression.

60 (IVDA), diabetes, indwelling catheters, and immune suppression.

61 d against the viral capsid, prompting use of immune suppression.

62 nsidering whether to treat with prophylactic immune suppression.

63 s or platelets also promote tumor growth via immune suppression.

64 es virus infects immune cells, causing acute immune suppression.

65 ions for solid organ transplantation without immune suppression.

66 NF-kappaB pathway genes as the regulators of immune suppression.

67 hereas CCR2 does not directly participate in immune suppression.

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

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

70 characterised by systemic viral replication, immune suppression, abnormal inflammatory responses, maj

71 ntigenicity, intratumoral heterogeneity, and immune suppression across cancers.

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

73 Selective immune suppression, adjusted for early recurrence, rathe

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

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

76 erge as the major mechanism of tumor-induced immune suppression and as an underestimated barrier to s

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

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

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

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

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

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

83 t pro-metastatic effects of surgery, prevent immune suppression and enhance immunostimulatory respons

84 tivation of beta2-ARs could help to overcome immune suppression and enhance the efficacy of immunothe

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

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

87 ly associated with systemic inflammation and immune suppression and have been associated with a poor

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

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

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

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

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

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

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

95 thus coordinating metastasis initiation with immune suppression and neoangiogenesis.

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

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

98 tumorigenic capability via myeloid-mediated immune suppression and provides proof of concept for tar

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

100 hibiting VISTA- and PD-L1-signaling relieved immune suppression and reduced br-met burden.

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

102 microglia (TAMs), which are key mediators of immune suppression and resistance to immunotherapy.

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

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

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

106 ients who had ACLF at enrollment, those with immune suppression and the highest KP activity, both at

107 to the conjugated antigen, avoiding systemic immune suppression and the risk of increased susceptibil

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

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

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

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

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

113 The gene networks of EMT, angiogenesis, immune-suppression and T cell exhaustion are closely cor

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

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

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

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

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

119 o sepsis, acute inflammation, sepsis-related immune suppression, and sepsis-related organ failure.

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

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

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

123 T(R)(eg) cells contribute to compensatory immune suppression, and therapies targeting the immunosu

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

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

126 require very long incubation times or severe immune suppression, and tumor penetrance is low.

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 Cancer metastasis and immune suppression are critical issues in cancer therapy

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

131 Pathogenic inflammation and immune suppression are the cardinal features that underl

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

133 Among various mechanisms responsible for immune suppression, arginase-1 (ARG1)-carrying small ext

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

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

136 equires combinatorial strategies to overcome immune suppression associated with the tumor microenviro

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

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

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

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

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

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

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

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

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

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

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

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

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

150 g milieu are significantly more resistant to immune suppression by CD8+ T cells compared to control T

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

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

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

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

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

156 Immune suppression by regulatory T cells and regulatory

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

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

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

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

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

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

163 pre-conception viraemia, and pre-conception immune suppression could identify women in this populati

164 uced grade 2 to 3 infections, improvement in immune suppression discontinuation and patient-reported

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

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

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

168 se to swollen/fixed conidia, suggesting that immune suppression enhances detrimental inflammation, wh

169 ified metastasis-correlated gene networks of immune-suppression, epithelial-mesenchymal transition (E

170 experiments of treated bees to show that the immune-suppression exerted by Clothianidin is associated

171 ll-known ocular complications of HIV-related immune suppression, few studies have examined the preval

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

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

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

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

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

177 ndscape shaped by oncogenic drivers promotes immune suppression from the earliest stages of tumor inc

178 PD-L1 induced immune suppression has increasingly gained attention in

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

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

181 nces in surgical procedures, technology, and immune suppression have transformed organ transplantatio

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

183 s elucidated novel mechanisms of UVR-induced immune suppression, implicated in melanoma immune evasio

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

185 utocrine and paracrine signals that maintain immune suppression in aggressive melanomas.

186 stently, Ccr2-/- cancer cells did not induce immune suppression in Batf3-/- mice lacking CD103+ DCs.

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

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

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

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

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

192 Thus, signaling by CXCR4 causes immune suppression in human pancreatic ductal adenocarci

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

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

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

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

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

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

199 induced upregulation of PD-L1 contributes to immune suppression in the skin microenvironment, which m

200 PD-L1 as a critical component of UV-induced immune suppression in the skin, which facilitates immuno

201 2 thus plays a multifaceted role in inducing immune suppression in the tumor microenvironment, throug

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

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

204 end, small molecules that can either reduce immune suppression in the tumor milieu or enhance activa

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

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

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

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

209 ts were sufficient to reverse VISTA-mediated immune suppression in vivo.

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

211 trated their role in promoting angiogenesis, immune suppression, invasion, migration, drug resistance

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

213 Immune suppression is a crucial component of immunoregul

214 cancers and most other cancers suggest that immune suppression is a key mechanism contributing to an

215 Tumor-driven immune suppression is a major barrier to successful immu

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

217 l and proliferation as well as contribute to immune suppression is an active area of research.

218 -CD73 feedforward circuit and A(2A)-mediated immune suppression is crucial for improving therapeutic

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

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

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

222 The 'net state of immune suppression' is a conceptual framework of all fac

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

224 0 and cell-surface receptors associated with immune-suppression limit antigen presentation and T-cell

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

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

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

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

231 displayed mechanisms of resistance including immune suppression, mutational escape, and/or tumor evol

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

233 ne therapeutic approach targeting human TAMs immune suppression of NK- and T-cell antitumor activitie

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

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

236 1007560) now suggests that influenza-induced immune suppression of Staphylococcus aureus is mediated

237 selection can be used to prevent unintended immune suppression of TLR7.

238 ults imply that there may not be significant immune suppression of untreated benign and malignant col

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

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

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

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

243 , by increased Gli-driven Treg cell-mediated immune suppression, paving the way for a potential new t

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

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

246 nt tissue cysts that can be reactivated upon immune suppression, potentially damaging key organ syste

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

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

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

250 NAs provide a versatile platform for a local immune suppression regimen that can be applied to alloge

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

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

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

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

255 h in turn regulates metabolic reprogramming, immune suppression, resistance to apoptosis, angiogenesi

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

257 shed that chronic viral infections can cause immune suppression, resulting in increased susceptibilit

258 Immune tolerance and active immune suppression results in unchecked cancer growth an

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

260 rts a role of sexual conflict in post-mating immune suppression, suggesting divergence of male genoty

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

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

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

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

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

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 systemic inflammation and/or marked systemic immune suppression. There is unlikely to be a "one size

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

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

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

272 establishment of pathogenic inflammation and immune suppression through elevated expression of inflam

273 a beta-galactoside-binding lectin, promotes immune suppression through T-cell inhibition, and progra

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

275 e balance between inflammatory responses and immune suppression, tipping the scale between brain prot

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

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

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

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

280 Targeting immune suppression using checkpoint inhibition has resul

281 vascular endothelial growth factor-mediated immune suppression via angiogenesis inhibition may augme

282 lassaemia patients is a significant cause of immune suppression via HO-1 induction and may underlie t

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

284 Distinct from pharmacologic immune suppression, we have developed what we believe is

285 Pre-conception viraemia and immune suppression were also strong risk factors for pos

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

287 ipants, "apprehension," "side effects," and "immune suppression" were most salient.

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

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

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

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

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

293 astic knockout of TLR9 similarly resulted in immune suppression with a significant reduction in tumor

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

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

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

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

298 TGF-beta is also central to immune suppression within the tumor microenvironment, an

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

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