ライフサイエンスコーパス: immunosuppression

1 to patients remains limited due to lifelong immunosuppression.

2 utaneous SCC and other SCC in the setting of immunosuppression.

3 islets in the presence or in the absence of immunosuppression.

4 that the risk could be reduced by a tailored immunosuppression.

5 its effective treatment are associated with immunosuppression.

6 age, era, immunological status, and initial immunosuppression.

7 be an effective treatment for sepsis-induced immunosuppression.

8 s modulator, stimulates PKC, thereby causing immunosuppression.

9 logic or solid malignancies and nonmalignant immunosuppression.

10 mpared to patients treated with conventional immunosuppression.

11 ention of long-term toxicity associated with immunosuppression.

12 e due to their potential for minimization of immunosuppression.

13 cular complications and visual outcomes with immunosuppression.

14 transplant recipient care and management of immunosuppression.

15 l of islet allografts without requirement of immunosuppression.

16 rectly regulate immune responses, leading to immunosuppression.

17 sed (n = 71), or cyclosporine-based (n = 73) immunosuppression.

18 transplant recipients treated with TAC based immunosuppression.

19 ction and the requirement for high levels of immunosuppression.

20 ation 7 to 11 weeks post-HTx or standard CNI immunosuppression.

21 of life and longevity because of drug-based immunosuppression.

22 subsets is important for understanding tumor immunosuppression.

23 t of naive wild-type mice with IL-33 induces immunosuppression.

24 logy of PTLD in the modern era of transplant immunosuppression.

25 jection without the side effects of systemic immunosuppression.

26 0 islet equivalents/mouse) in the absence of immunosuppression.

27 ecreased risk of relapse after discontinuing immunosuppression.

28 ansforming growth factor beta 1 that mediate immunosuppression.

29 as a major function in the induction of this immunosuppression.

30 tional risk for colon cancer associated with immunosuppression.

31 tively, independent of era, age, and initial immunosuppression.

32 contributes to apoptotic Treg-cell-mediated immunosuppression.

33 ncrease the risk of herpes zoster by causing immunosuppression.

34 or systemic corticosteroids supplemented by immunosuppression.

35 defects collectively known as sepsis-induced immunosuppression.

36 All patients received systemic immunosuppression.

37 for the abrogation of tumor microenvironment immunosuppression.

38 in clinically relevant sites without chronic immunosuppression.

39 Burden of OH might be improved with immunosuppression.

40 al dissemination via IDO1-mediated localized immunosuppression.

41 important confounding factors, particularly immunosuppression.

42 viating the need for additional prophylactic immunosuppression.

43 oral steroids and 13.8% required second-line immunosuppression.

44 w designs for clinical trials for transplant immunosuppression.

45 t, elevated inflammatory markers, or greater immunosuppression.

46 ncy of patients to relapse without long-term immunosuppression.

47 ve also been associated with B cell-mediated immunosuppression.

48 inical potential in overcoming tumor-induced immunosuppression.

49 and improved motor assessments with minimal immunosuppression.

50 o exhibit features typically associated with immunosuppression.

51 n a low dose of donor BM cells and transient immunosuppression.

52 oup of 10 patients treated with conventional immunosuppression.

53 at allow their survival and function without immunosuppression.

54 ejection early despite an unaltered baseline immunosuppression.

55 eatment are treated with corticosteroids and immunosuppression.

56 nd should not necessarily rule out EVR-based immunosuppression.

57 l-derived beta cell transplantation) without immunosuppression.

58 ed removal of the allograft and cessation of immunosuppression.

59 aracterized by regulatory T (Treg) cells and immunosuppression.

60 s mimicking chronic viral infection, induced immunosuppression.

61 rine continued to receive cyclosporine-based immunosuppression.

62 egulatory T cells (Treg cells) as drivers of immunosuppression.

63 olely with antibody removal and conventional immunosuppression.

64 I) has become a real threat with devastating immunosuppression.

65 ost-derived PD-L1 can play critical roles in immunosuppression.

66 strategies for islet transplantation without immunosuppression.

67 as a major impediment to achieving effective immunosuppression.

68 biocompatibility without the need for broad immunosuppression.

69 x (209 [41%] vs 47 [63%], adjusted p=0.011), immunosuppression (30 [6%] vs 11 [15%], adjusted p=0.011

70 ctions in both proteinuria (80%) and overall immunosuppression (64%).

71 tologic malignancies (106), and nonmalignant immunosuppression (77).

72 of BKVAN relies on pre-emptive adaptation of immunosuppression according to viral load monitoring.

73 Here we show that the immunosuppression activity of PD-L1 is stringently modul

74 Immunosuppression after liver transplantation (LT) is pr

75 CTs), for conversion from CNI to mTORi-based immunosuppression after liver transplantation.

76 etic-neuroendocrine adrenal reflex mediating immunosuppression after SCI, implying that therapeutic n

77 erapy targeting detrimental inflammation and immunosuppression after SS/SS to improve currently obser

78 Immunosuppression after transplantation consisted of tac

79 patients due to drug-drug interactions with immunosuppression agents.

80 e in the levels of inhibition of UVB-induced immunosuppression amongst mice that were treated topical

81 e alive at 10 years due to the toxicities of immunosuppression and alloimmunity.

82 s, this suggests that ABOi with conventional immunosuppression and antibody removal, without rituxima

83 3 pathway in TME can be exploited to reverse immunosuppression and augment therapeutic benefits beyon

84 tory T cell-derived TGF-beta1 contributes to immunosuppression and can be inhibited with anti-GARP Ab

85 that this state of persisting inflammation, immunosuppression and catabolism contributes to many of

86 The underlying cause of inflammation-immunosuppression and catabolism syndrome is currently u

87 critical illness and persistent inflammation-immunosuppression and catabolism syndrome may require a

88 ess often exhibit "a persistent inflammation-immunosuppression and catabolism syndrome," and it is pr

89 milar characteristics, implying that ongoing immunosuppression and chronic virus exposure do not comp

90 graft rejection that complement contemporary immunosuppression and could lead to improved outcomes fo

91 ique and versatile approach to help overcome immunosuppression and enhance T-cell responses to tumor

92 nologically desirable strategy for reversing immunosuppression and enhancing antitumor immunity.

93 (ld-IL-2) inducing immunoregulation without immunosuppression and established its protective effect

94 The patient was able to discontinue immunosuppression and exogenous immunoglobulin support,

95 gic signaling pathway in transplantation and immunosuppression and explores possible future applicati

96 Nonmalignant immunosuppression and hematologic malignancies were inde

97 The immunosuppression and immune dysregulation that follows

98 ute spinal cord injury (SCI) causes systemic immunosuppression and life-threatening infections, thoug

99 jection mandates the use of prolonged global immunosuppression and limits the life span of transplant

100 , duration of follow-up, and use of systemic immunosuppression and ocular procedures in treatment.

101 t eGFR will require sustained improvement in immunosuppression and other aspects of post-transplant c

102 nical, nonhuman primate model of HIV-induced immunosuppression and Pneumocystis coinfection.

103 melanoma growth by impairing aTreg-mediated immunosuppression and potentiated the effects of anti-PD

104 nism accounting for the role of IFN-alpha in immunosuppression and predicts that type I IFN modulatio

105 To reduce calcineurin inhibitor immunosuppression and preserve kidney function, we have

106 eractions will contribute to overcome cancer immunosuppression and reinforce antimicrobial immunity,

107 With proper immunosuppression and repeat procedure in case of failur

108 e focus on the role of regulatory T cells in immunosuppression and show that regulatory T-cell prolif

109 nic properties that contribute to persistent immunosuppression and susceptibility to secondary infect

110 GADD45beta for reprogramming TAM to overcome immunosuppression and T-cell exclusion from the TME.Sign

111 tabolic lability resulting from the need for immunosuppression and the shortage of donor organs.

112 TV), which might mirror the overall level of immunosuppression and thus help determine the risk of al

113 hanisms and determine whether PLN-associated immunosuppression and tumor growth can be reversed using

114 were more likely to be treated with systemic immunosuppression and were followed for longer at our cl

115 nfection with MRCPEC is associated with sex, immunosuppression, and previous antibiotic exposure, whi

116 the later phases of sepsis in mice, promote immunosuppression, and reduce survival.

117 Chronic immune activation, immunosuppression, and T cell exhaustion are hallmarks o

118 felong transplant acceptance without ongoing immunosuppression, and with preservation of protective i

119 se receptor (CD206/MRC1) contribute to tumor immunosuppression, angiogenesis, metastasis, and relapse

120 Further trials of immunosuppression, antiviral, and immunomodulating thera

121 l sequelae, and the potential late effect of immunosuppression are still needed to support broader im

122 for many cancers and prolonged survival with immunosuppression, ART exposure, and ageing.

123 Treatment with PLN increased immunosuppression as evidenced by increased expression o

124 t our understanding of morbillivirus-related immunosuppression as well as the application of measles

125 Our study uncovers a critical mechanism of immunosuppression associated with blood-stage malaria th

126 Sepsis-induced immunosuppression associates with a defect in the capaci

127 ients and 30% of MUD patients never required immunosuppression beyond PTCy.

128 suppressor cells (MDSCs) induce detrimental immunosuppression, but little is known about the role of

129 apsulation may allow transplantation without immunosuppression, but thus far islets in large microcap

130 Immunosuppression by human Tregs can be inhibited by ant

131 a blocking antibody against beta8 inhibited immunosuppression by human Tregs in a model of xenogenei

132 tosis via downregulation of BIM and achieves immunosuppression by MAPK/NF-kB-dependent activation of

133 a non-classical monocyte-mediated M2-skewed immunosuppression by the Asian-lineage ZIKV infection.

134 when used properly, oral corticosteroids and immunosuppression can be given safely for up to 7 years

135 Both immune dysfunction and therapy-related immunosuppression can inhibit cancer-related immune surv

136 der PHIVY were at increased risk of viremia, immunosuppression, CDC-B events, CDC-C events, and morta

137 ormed with antibody removal and conventional immunosuppression continues to provide excellent patient

138 Induction immunosuppression decreases the risk for acute rejection

139 patients who were taking tacrolimus required immunosuppression dose adjustments during HCV treatment.

140 nal thickness, number and dosage of systemic immunosuppression drugs, vitreous haze score, and presen

141 Immune disorders are common; immunosuppression during active disease causes susceptib

142 results illustrate how extrinsic pathways of immunosuppression elaborated by melanoma cells dominate

143 with aplastic anemia that was refractory to immunosuppression, eltrombopag, a synthetic thrombopoiet

144 Among HIV-infected patients with advanced immunosuppression, enhanced antimicrobial prophylaxis co

145 patients to consider treatment with systemic immunosuppression even in the absence of diagnosis confi

146 e levels for over 370 days in the absence of immunosuppression (excluding the first 5 days after tran

147 tes an attractive pharmacological target for immunosuppression, fibroproliferative disorders, atheros

148 Treatment with anti-CCR2 antibody alleviates immunosuppression following activation of the STING path

149 A systemic immunosuppression follows UV irradiation of the skin of

150 Nonalkylating-agent immunosuppression for >3 years with control of the infla

151 Despite the ongoing presence of full immunosuppression for a functioning kidney allograft, th

152 ro studies indicated different mechanisms of immunosuppression for biTregs and cTregs.

153 ellent 5-year outcomes after minimization of immunosuppression for BK viremia and after no interventi

154 allograft pancreatectomy while on continued immunosuppression for functional kidney allografts.

155 e median durations of systemic pharmacologic immunosuppression for the BuCy MRD, BuFlu MRD, BuCy MUD,

156 nide implant vs systemic corticosteroids and immunosuppression for treatment of severe noninfectious

157 transfer, thereby avoiding potential overall immunosuppression from non-specific Tregs.

158 The KS was successfully treated by switching immunosuppression from tacrolimus to sirolimus.

159 ause of travel or relocation, occupation, or immunosuppression; fungal pathogens appearing in geograp

160 ups: continued supportive care or additional immunosuppression (GFR>/=60 ml/min per 1.73 m(2): 6-mont

161 With advances in immunosuppression, graft and patient outcomes after kidn

162 sis also showed that infants with non-severe immunosuppression had stronger selection in CTL-restrict

163 immune-competent status (patients with HIV, immunosuppression, haematological malignancies, and prev

164 Nonalkylating-agent immunosuppression has a low rate of sustained, drug-free

165 ence of mechanisms counterbalancing neonatal immunosuppression has not been investigated.

166 al has significantly improved as advances in immunosuppression have occurred, long-term patient and g

167 vances in medical treatments that also cause immunosuppression have produced an ever-growing cohort o

168 , the squirrel monkeys developed more-severe immunosuppression, higher viral load, and a broader rang

169 clinical trials exist so far, after reducing immunosuppression (if possible): ganciclovir dose escala

170 had documented responsiveness to intensified immunosuppression (IIS), 1155 had kidney biopsy results,

171 1-RPS19 interaction decreases RPS19-mediated immunosuppression, impairs tumor growth, and delays the

172 mplicated in breast carcinogenesis and tumor immunosuppression in advanced disease, but its involveme

173 activation by high-affinity ligands mediates immunosuppression in association with increased regulato

174 eg imbalance is associated with inflammatory immunosuppression in cancer.

175 deficient in ST2 (IL-33R) develop attenuated immunosuppression in cases that survive sepsis, whereas

176 bsets in DLBCL, as well as new mechanisms of immunosuppression in DLBCL.

177 ls, the mechanisms underlying SAg-associated immunosuppression in humans are ill-defined.

178 propose a novel mechanism of SAg-associated immunosuppression in humans.

179 The role of immunosuppression in IgA nephropathy (IgAN) is controver

180 Following immunosuppression in kidney transplant patients, BK poly

181 okiol has the ability to inhibit UVB-induced immunosuppression in preclinical model and, thus, has po

182 Cellular signaling events leading to immunosuppression in sepsis are not well defined.

183 isorders that will probably mandate systemic immunosuppression in severe AD cases.

184 events or chronic negative impacts, such as immunosuppression in the face of an infection, are also

185 rgistic p53-dependent processes: reversal of immunosuppression in the TME and induction of tumor immu

186 ted thymic atrophy, which is associated with immunosuppression in the tumor microenvironment, compare

187 sis and is a proven drug target for inducing immunosuppression in therapy of human disease as well as

188 Currently trials of immunosuppression in transplantation are in decline beca

189 little is known about factors that initiate immunosuppression in tumors and act at the interface bet

190 otic exposure, gastric acid suppression, and immunosuppression increase risk for progression to infec

191 memory B-cell compartment contributes to the immunosuppression induced by sepsis.

192 appropriate risk stratification, risk-based immunosuppression intensity, and prospective DSA surveil

193 graft function, early hospital readmission, immunosuppression intolerance, and mortality.

194 iet-induced obese mice significantly reduced immunosuppression, intratumor vascularization, and local

195 Under certain conditions, such as immunosuppression, invasion of the epithelia occurs.

196 Immune tolerance to avoid chronic immunosuppression is a critical goal in the field, recen

197 ccepted that impaired immune function due to immunosuppression is a primary cause of EBV+ PTLD.

198 al to overcome tumor microenvironment-driven immunosuppression is being explored.

199 or cells escape from immune attack and favor immunosuppression is essential for the improvement of im

200 the novel theme in neonatal immunology that immunosuppression is essential to dampen robust immune r

201 ant tolerance to eliminate the dependency on immunosuppression is ideal, but remains challenging.

202 Immunosuppression is recommended for patients with cardi

203 One key mechanism involved in DC-mediated immunosuppression is the expression of tryptophan-metabo

204 novo donor-specific antibodies, therapeutic immunosuppression is the most obvious parameter in which

205 Lowering immunosuppression is the only established approach to pr

206 on with azithromycin, 13 in association with immunosuppression (IS) reduction.

207 erience with pediatric PTLD nonresponsive to immunosuppression (IS) withdrawal, managed after stratif

208 gain and the most to lose from discontinuing immunosuppression (IS).

209 It is unclear whether immunosuppression leads to younger ages at cancer diagno

210 ions with EBR/GZR and monitor for changes in immunosuppression levels to ensure safety with its use i

211 Providers monitored immunosuppression levels; both patients who were taking

212 mbined with alemtuzmab induction with triple immunosuppression maintenance does not result in prolong

213 in small cohorts of children and can enhance immunosuppression management, but await validation and c

214 Thus, oral corticosteroids and immunosuppression may be a preferred initial therapy for

215 icating either T-cell exhaustion or systemic immunosuppression may be markers of selection for respon

216 ilemma, immunotherapy targeting NPC-specific immunosuppression may bring new hope.

217 for further elucidation of the mechanism of immunosuppression mediated by the retroviral envelope gl

218 y CD8(+) T cells are considered a barrier to immunosuppression-mediated acceptance of most tissues an

219 sera taken at predetermined intervals during immunosuppression minimization before and at clinically

220 tories of the same profile during supervised immunosuppression minimization diagnosed rejection up to

221 Trial designs for new transplant immunosuppression must be intelligently restructured to

222 lminth infections, exacerbated by coincident immunosuppression, must be considered.

223 The long-term decision for immunosuppression needs to be carefully individualized.

224 omen's blood led to an exacerbated M2-skewed immunosuppression of non-classical monocytes in conjunct

225 It has long been speculated that Varroa via immunosuppression of the bees, activate a covert infecti

226 therapy to initial viral load, the effect of immunosuppression on outcomes, and the need to continue

227 hese strategies is the introduction of early immunosuppression or combination therapy with biological

228 a new opportunity to treat diabetes without immunosuppression or immunoprotective encapsulation or w

229 ic memory T cell responses in the absence of immunosuppression or in the presence of MMF/FK-506 combi

230 ogical tolerance, because the high levels of immunosuppression otherwise required would likely have u

231 However, changes in immunosuppression practice had a positive effect on aver

232 Chronic immunosuppression promotes nonmelanocytic squamous cell

233 Subjects undergoing immunosuppression reduction for BK viremia had 10-year o

234 ecipients, with CD20(+) PTLD unresponsive to immunosuppression reduction, were treated with four week

235 The modern immunosuppression regimen has greatly improved short-ter

236 posttransplant compared with a standard TAC immunosuppression regimen.

237 Modern immunosuppression regimens effectively control acute rej

238 tacrolimus is the basis of most maintenance immunosuppression regimens for kidney transplantation, c

239 Current immunosuppression regimens in organ transplantation prim

240 BV) causes endemic Burkitt lymphoma (BL) and immunosuppression-related lymphomas.

241 Ribavirin monotherapy and a minimization of immunosuppression represent the treatment of choice, wit

242 epithelial receptor nectin-4, while causing immunosuppression, resulted in only a mild and transient

243 polyclonal IgGs in the absence of additional immunosuppression results in a vigorous response against

244 Systemic intravenous administration without immunosuppression results in significant and sustained l

245 ural invasion (RR, 2.95; 95% CI, 2.31-3.75), immunosuppression (RR, 1.59; 95% CI, 1.07-2.37), and loc

246 antly anti-inflammatory response may lead to immunosuppression, secondary infection, and late deaths.

247 <7.5 mg/day) are ineffective, implying that immunosuppression should be part of the initial regimen.

248 ultivariate analysis including age, sex, and immunosuppression showed that, relative to MCC patients

249 ogenic roles in tumor neovascularization and immunosuppression.Significance: This study highlights th

250 before implant, and subjects under standard immunosuppression (SIS) without rejection and with acute

251 Complications associated with immunosuppression, specifically nephrotoxicity and infec

252 ell nevus syndrome, geographical region, and immunosuppression status.

253 ould determine whether sex- and age-specific immunosuppression strategies are warranted for kidney gr

254 tal modifier of tumor neovascularization and immunosuppression, strengthening emerging evidence of th

255 microenvironment are major drivers of T-cell immunosuppression, strongly supporting the concept of ta

256 lysis, we separately analyzed data from each immunosuppression subgroup and the corresponding patient

257 r growth through macrophage polarization and immunosuppression that can be targeted and inactivated t

258 ratified by center report of nonadherence to immunosuppression that compromised recovery.

259 nction may help avoid a state of generalized immunosuppression that could otherwise result from repea

260 otherapy, broad exposure to antibiotics, and immunosuppression), the incidence of opportunistic funga

261 The type of immunosuppression, the route of infection, the timing of

262 ng developed to replace our current clinical immunosuppression therapies.

263 Immunosuppression therapy after lung transplantation fai

264 tes to reprogram TAM and curb tumor-mediated immunosuppression, thereby empowering mAb efficacy.

265 bling individualized risk stratification and immunosuppression through the identification of variants

266 nor) was performed 4 months post-BMT without immunosuppression to assess for robust donor-specific to

267 icosteroid response, but required additional immunosuppression to overcome steroid dependency.

268 isk and help guide the type and intensity of immunosuppression to prevent antibody-mediated graft inj

269 and 7 weeks after the discontinuation of all immunosuppression to test immune response.

270 -term safety and effectiveness of minimizing immunosuppression to treat BK viremia.

271 Immunosuppression treatment with antithymyocyte globulin

272 dent of immunologic stability, etiology, and immunosuppression type.

273 In patients requiring further immunosuppression, typically only 1 to 2 agents were req

274 nal failure (dialysis or nondialysis), prior immunosuppression use, and markers of inflammation (C-re

275 plants of the genus Magnolia, on UVB-induced immunosuppression using contact hypersensitivity (CHS) a

276 to adenosine via CD39 and CD73, and mediate immunosuppression via the adenosine and A2A pathways.

277 The resulting cellular immunosuppression was characterized by a reduced nodulat

278 thin 2 months posttransplant, and no de novo immunosuppression was given.

279 Standard induction immunosuppression was with interleukin-2 receptor antago

280 bilities of being alive and off all systemic immunosuppression were 61%, 53%, 53%, and 51% and 3-year

281 epleting antibodies, and delayed revision of immunosuppression were associated with an increased risk

282 matic autoimmunity or clinically significant immunosuppression were randomly assigned 1:1 to receive

283 b-induced depletion and belatacept/sirolimus immunosuppression were studied longitudinally for marker

284 Tailored immunosuppression when transplanting an old kidney may b

285 raft was accepted more than 294 days without immunosuppression, whereas non-Treg cell BMT recipients

286 inase C isoforms, failed to provide adequate immunosuppression, whereas the Janus kinase 3 inhibitor

287 Ultraviolet (UV) radiation exposure induces immunosuppression, which contributes to the development

288 can be accompanied or followed by a state of immunosuppression, which in turn jeopardizes the host's

289 spanic whites (aIRR = 2.09); after induction immunosuppression with alemtuzumab (aIRR = 3.12), monocl

290 allenges, such as organ shortages, necessary immunosuppression with associated complications, and chr

291 Immunosuppression with cyclophosphamide stabilised lucif

292 stemic therapy with oral corticosteroids and immunosuppression with regional corticosteroid treatment

293 All patients were discharged on maintenance immunosuppression with tacrolimus and mycophenolate mofe

294 ties of clinical trials for renal transplant immunosuppression with the current unmet needs and to pr

295 nts enrolled in the Immune Tolerance Network immunosuppression withdrawal (ITN030ST) and Clinical Tri

296 designed to select transplant recipients for immunosuppression withdrawal have met with limited succe

297 e previously showed full donor chimerism and immunosuppression withdrawal in highly mismatched allogr

298 e trajectory of ACR diagnostic miRNAs during immunosuppression withdrawal were also evaluated in sera

299 loped rejection during trials of intentional immunosuppression withdrawal.

300 iruses selectively lyse tumor cells, disrupt immunosuppression within the tumor, and reactivate antit