ライフサイエンスコーパス: alloimmune

1 -alpha, interferon-gamma, interleukin-6) and alloimmune activation (CD3, interleukin-1 receptor 2, pr

2 rs in this phenomenon include instigation of alloimmune activation associated with tobacco smoke-indu

3 rategy to limit proliferation, inflammation, alloimmune activation, cancer, and vascular proliferativ

4 iated rejection seems to form a continuum of alloimmune activation.

5 s been proposed as a potential treatment for alloimmune and autoimmune disorders, but it is unknown w

6 ombination of nonimmune bronchial injury and alloimmune and autoimmune mechanisms.

7 xpansion, and protect pancreatic islets from alloimmune and autoimmune responses in mice.

8 ion device in protecting these cells against alloimmune and autoimmune responses in mouse models.

9 hat imparts immune privileges by suppressing alloimmune and autoimmune responses through its receptor

10 ic nonobese diabetic recipients against both alloimmune and recurring autoimmune responses.

11 ot impact the timing nor the kinetics of the alloimmune and single antigen-specific memory T cell res

12 erogeneous condition with TRAS-P having both alloimmune and traditional cardiovascular risk factors.

13 the severity of GVHD and the strength of an alloimmune antitumor response could be manipulated by en

14 ns, limitations, perceptions, and utility of alloimmune assays that are currently in use or in develo

15 responsible for several clinically important alloimmune bleeding disorders, including fetal and neona

16 main focus of current research efforts, pure alloimmune causes accounted for only 17.5% of graft fail

17 O; also called TSAd(-/-)) mice, we find that alloimmune CD4(+) Teff responses are fully competent in

18 T cells are central mediators of alloimmune complications and the target of most existing

19 mmune memory responses and increased risk of alloimmune damage to the second allograft.

20 Our alloimmune defense receptor (ADR) selectively recognizes

21 e prevention and treatment of autoimmune and alloimmune disease states.

22 Gestational alloimmune diseases are induced by the placental passage

23 Vaccination for autoimmune and alloimmune diseases has long been an attractive idea.

24 everity of immunopathology in the context of alloimmune diseases such as acute GVHD has been mainly u

25 unologic disorders, including autoimmune and alloimmune diseases.

26 s has been associated with various auto- and alloimmune diseases.

27 oimmunity and in patients with autoimmune or alloimmune disorders has identified a functional group o

28 strategies could prove useful in preventing alloimmune-driven fibrotic lung diseases.

29 AR, distinguishing between different driving alloimmune effector mechanisms.

30 ent for the expansion and differentiation of alloimmune effector T lymphocytes in vivo, and point to

31 RIC) transplantation is largely dependent on alloimmune effects.

32 cts of ATG on the early clinical outcomes of alloimmune events (development of de novo donor specific

33 s were significantly correlated with primary alloimmune events including Banff >=1A T cell-mediated r

34 is the phenotypic expression of gestational alloimmune fetal liver injury.

35 Alloimmune feto-maternal destruction of blood cells is t

36 ctors on immune function and, when known, on alloimmune function, as well as on transplant fate.

37 e groups of renal transplant recipients with alloimmune graft damage.

38 t T cells resulted in delayed development of alloimmune gut and liver injury.

39 MAC-mediated alloimmune injury in congenital alloimmune hepatitis is a novel mechanism of liver injur

40 sts that a single process, namely congenital alloimmune hepatitis, is the principal cause of NH.

41 We established a model of alloimmune, IgG-mediated HTRs in a well-characterized hu

42 The significance of alloimmune immune complex-type deposits in human transpl

43 erglycemia itself does not cause generalized alloimmune impairment.

44 d age of the artery donors vs. the degree of alloimmune-induced changes in vessel morphology.

45 performance of urinary CXCL10 for detecting alloimmune inflammation in renal transplant patients.

46 n the diverse functions of these proteins in alloimmune inflammation.

47 irway microvascular integrity and diminished alloimmune inflammation.

48 tissues; (c) decreases graft infiltration of alloimmune-inflammatory cells; and (d) prolongs allograf

49 hogenesis of transplant arteriosclerosis, an alloimmune initiated vascular stenosis that often result

50 ollowing transplantation are associated with alloimmune injury and allograft failure.

51 In BOS, persistent alloimmune injury and chronic airway inflammation are su

52 which histologic changes were likely due to alloimmune injury and which were due to non-alloimmune i

53 Unopposed alloimmune injury for 10 days was associated with subseq

54 MAC-mediated alloimmune injury in congenital alloimmune hepatitis is

55 icians have few tools to predict the risk of alloimmune injury that would guide immunosuppression man

56 Alloimmune injury to allografts is mediated by pathogeni

57 vorable graft prognosis, likely representing alloimmune injury ultimately resulting in patient morbid

58 standing of the molecular pathophysiology of alloimmune injury.

59 ti-HLA antibodies (DSA) are a major cause of alloimmune injury.

60 ti-HLA antibodies (DSA) are a major cause of alloimmune injury.

61 ronic allograft nephropathy with features of alloimmune injury.

62 nd the degree of airway remodeling following alloimmune injury.

63 alloimmune injury and which were due to non-alloimmune injury.

64 -alpha, interferon-gamma, interleukin-6) and alloimmune (interleukin-1 receptor 2, programmed cell de

65 Alloimmune kinetics in patients on a kidney transplant w

66 HLA or TCR), which can result in unorthodox, alloimmune-like stimulations of T cells.

67 the diagnosis and management of gestational alloimmune liver disease.

68 Alloimmune lung injury, characterized by perivascular ly

69 nist, to determine the effect upon pulmonary alloimmune lung injury.

70 nduced innate immune activation in promoting alloimmune lung injury.

71 ritical to the development of posttransplant alloimmune lung injury.

72 al transplants in mice were used to generate alloimmune-mediated airway lesions.

73 donor-transmitted atherosclerotic lesions on alloimmune-mediated arterial injury in an experimental s

74 t with the majority of clinical studies that alloimmune-mediated intimal injury and vascular remodeli

75 Alloimmune-mediated lung syndromes (allo-LSs) are life-t

76 e of the JCI, Babu and colleagues found that alloimmune-mediated microvascular loss precedes tissue d

77 doptive transfer of CAR Tregs alleviated the alloimmune-mediated skin injury caused by transferring a

78 mismatched donor mouse heart allografts with alloimmune-mediated vasculopathy upregulated expression

79 esults suggest that further investigation of alloimmune monitoring after vaccination is needed.

80 gle nucleotide polymorphisms responsible for alloimmune neonatal thrombocytopenia, and the developmen

81 ection episodes, potentially suggesting that alloimmune phenomena contributed to the chronic injury.

82 e have evaluated other methods of preventing alloimmune platelet refractoriness and demonstrated that

83 of 7) treatment of donor platelets prevented alloimmune platelet refractoriness.

84 responses in vitro and in vivo, in models of alloimmune priming and allotransplantation.

85 modeling, vascular injury, inflammation, and alloimmune processes.

86 better understand and monitor this state of alloimmune quiescence by transcriptional profiling may r

87 The frequency of predicted alloimmune quiescence in stable renal transplant patient

88 scussion of the mechanisms that transform an alloimmune reaction into an autoimmune response.

89 body nephritis is caused by an autoimmune or alloimmune reaction to the NC1 domains of alpha3alpha4al

90 ypes of injury such as ischemia/reperfusion, alloimmune reaction, and inflammation METHODS: The effic

91 did not stimulate significant donor-specific alloimmune reactions.

92 d proinflammatory Th17 effector cells affect alloimmune reactivity and transplant outcome.

93 with augmentation of cellular and/or humoral alloimmune reactivity in >50% of the test subjects.

94 pact of stably immature, donor-derived DC on alloimmune reactivity in rhesus macaques.

95 ed the development of vascular sclerosis and alloimmune reactivity in wild-type C57BL/6 (B6) and Flt3

96 c function for fibroblastic stromal cells in alloimmune reactivity that can be dissociated from their

97 overing donor Tregs to initiate and maintain alloimmune regulation.

98 To explore the role of alloimmune rejection and airway ischemia in the developm

99 metabolic abnormalities during the course of alloimmune rejection in a murine transplant model.

100 MHC II antigens correlated to alloimmune rejection were barely expressed in hUC-MSC sh

101 uting factors include autoimmune recurrence, alloimmune rejection, or immunosuppressant medication to

102 es, including vaccinations, may activate the alloimmune repertoire leading to accelerated allograft i

103 e a significant impact on the potency of the alloimmune repertoire.

104 Overall, 100 (56%) patients developed an alloimmune response (IgM or IgG DSA positive, or both).

105 graft recipients did not exhibit a secondary alloimmune response (P < 0.001).

106 t infiltrate transplanted organs sustain the alloimmune response after T-cell activation has already

107 ave already refined our understanding of the alloimmune response and are pointing to new ways to impr

108 concluded that PKCtheta mice have a defected alloimmune response and are susceptible to tolerance ind

109 DC activation and altered homing during the alloimmune response and could allow early diagnosis and

110 ate the vascular endothelium, amplifying the alloimmune response and increasing microvascular damage.

111 r, the mechanism by which IL-21 orchestrates alloimmune response and interplays with Tregs is still u

112 ver an important role for macrophages in the alloimmune response and may have important clinical impl

113 population from donor grafts may dampen the alloimmune response and prolong graft survival.

114 154 Abs has shown promise in attenuating the alloimmune response and promoting long-term graft surviv

115 d the indirect but not the direct pathway of alloimmune response and were promptly rejected in immune

116 of the FoxP3 Treg chain in the late phase of alloimmune response and, thus, acts as an antitolerogeni

117 M-MDSCs were lower in patients with enhanced alloimmune response as represented by anti-HLA sensitiza

118 It also suppressed alloimmune response as shown by the decreased CD4 IFNgam

119 his report demonstrates that oATP limits the alloimmune response by regulating APC maturation and sup

120 ted rejection, the importance of the humoral alloimmune response has progressively emerged.

121 to their suboptimal inhibition of a chronic alloimmune response has shifted investigative efforts to

122 plenic MSC localization, graft survival, and alloimmune response in mice recipients of kidney allogra

123 We tested this phenomenon during alloimmune response in our previously described model of

124 ovide a more complete picture of the humoral alloimmune response in patients with a history of alloan

125 nsplants suggesting that the strength of the alloimmune response in the latter exceeds the anti-infla

126 l, we investigated the effect of NaCl on the alloimmune response in vitro and in vivo.

127 d the importance of Delta1 in regulating the alloimmune response in vivo.

128 role of tissue expression in regulating this alloimmune response in vivo.

129 Overlooked for decades, the humoral alloimmune response is increasingly recognized as a lead

130 ese hypotheses fail to fully explain how the alloimmune response is initiated after transplantation a

131 e, we have investigated whether the indirect alloimmune response mediates endothelial dysfunction in

132 In an alloimmune response model, transfer of nondiabetic CD4,

133 d by histology and immunohistochemistry, and alloimmune response of proliferative CD8(+) T cells was

134 ead box P3 and efficiently suppress a direct alloimmune response of the original responder lymphocyte

135 unity to observe the adaptive changes in the alloimmune response over time, but such studies have bee

136 However, it is not known what role, if any, alloimmune response plays in inducing autoimmunity.

137 provide insights into the components of the alloimmune response remaining after lymphoablation and m

138 Control of the alloimmune response requires elimination and/or suppress

139 al to the recipient, may trigger an adaptive alloimmune response that impairs the survival of NT-ESC

140 how the immune system reshapes a destructive alloimmune response to a state of tolerance.

141 hemokine pathways involved in generating the alloimmune response to corneal transplants.

142 sed peptide arrays verified a donor-specific alloimmune response to genetically predicted mismatched

143 Redirection of the alloimmune response to the lymph nodes by splenectomy co

144 nti-inflammatory cytokine profile shifts the alloimmune response toward alloantibody production.

145 died for their role in regulating the host's alloimmune response towards the graft, the cytoprotectiv

146 R.Fc and CTLA4-Ig (an inhibitor of the early alloimmune response) leads to robust graft tolerance in

147 only P2X7R is increasingly expressed during alloimmune response, and that P2X1R is augmented in both

148 th AC is associated with a mixed Th1 and Th2 alloimmune response, and the contribution of Th1 cells i

149 mmunity is the principal arm of the cellular alloimmune response, but its development requires help.

150 essed on transplant endothelial cells in the alloimmune response, but the effect of MICA genotype is

151 the alloreactive T cells, including primary alloimmune response, effector/memory response, immunosup

152 lymphatic system plays a crucial role in the alloimmune response, facilitating trafficking of antigen

153 ibodies to vimentin, in conjunction with the alloimmune response, have a pathogenic role in allograft

154 Treg cells, in order to efficiently control alloimmune response, need to be educated first in the ta

155 f the afferent and efferent arms of the host alloimmune response, respectively.

156 aintenance of an effective inhibition of the alloimmune response, whereas reducing drug-related nephr

157 is was induced in the airway wall during the alloimmune response, which was reversed by cyclosporine

158 -6 generation from lung parenchyma during an alloimmune response.

159 ownregulates the immune system, blunting the alloimmune response.

160 uce APC maturation and initiate the adaptive alloimmune response.

161 cative of an active, suboptimally controlled alloimmune response.

162 drug-free tolerant patients, with controlled alloimmune response.

163 rs and directly with a probable influence on alloimmune response.

164 icant role for heart rate in confounding the alloimmune response.

165 ion/allostimulation in the late phase of the alloimmune response.

166 ells in cGVHD recipients was initiated by an alloimmune response.

167 PD-L1 knockout mice, suppressed the in vitro alloimmune response.

168 ting the effector and regulatory arms of the alloimmune response.

169 ion injury and hinders the antigen-dependent alloimmune response.

170 oglobulin mucin protein 1 (TIM-1) during the alloimmune response.

171 3:Pro allele, and defines the unidirectional alloimmune response.

172 e vessel wall may also positively impact the alloimmune response.

173 her than costimulation-poor ECs, initiate an alloimmune response.

174 acts via purinergic receptors to amplify the alloimmune response.

175 tched mouse models were used to evaluate the alloimmune response.

176 pression and thus help determine the risk of alloimmune response.

177 more GVL sensitive, even with a lower-level alloimmune response.

178 tein pathway has an inhibitory effect on the alloimmune response; thereby its inhibition is detriment

179 pes within alpha345NC1 hexamers may initiate alloimmune responses after transplant in X-linked Alport

180 Tregs suppress both autoimmune and alloimmune responses and are particularly effective in p

181 Importantly, the role of crosstalk between alloimmune responses and autoimmune responses in AILD is

182 results identify microRNAs that may regulate alloimmune responses and graft outcomes.

183 inflammatory processes potentially impacting alloimmune responses and graft quality.

184 esions to investigate the impact of PD-L1 on alloimmune responses and histopathological outcome in BO

185 response to infections can modulate ongoing alloimmune responses and modify the fate of transplanted

186 Regulatory T cells (Tregs) actively regulate alloimmune responses and promote transplantation toleran

187 In this model, both decreased T-cell alloimmune responses and the reduction of BO in PD-L1-de

188 role for environmental factors in modulating alloimmune responses and transplant outcomes is only now

189 (Treg) have been implicated in regulation of alloimmune responses and transplant tolerance.

190 It is now recognized that alloimmune responses are responsible for the majority of

191 plays an important role in the inhibition of alloimmune responses as well as in the induction and mai

192 killer (NK) cells play a dichotomous role in alloimmune responses because they are known to promote b

193 d TNF-alpha acted together to promote T cell alloimmune responses both in vitro and in vivo and to im

194 hese cells were highly potent in suppressing alloimmune responses both in vitro and in vivo in an ant

195 athway plays an important role in regulating alloimmune responses but its role in transplantation tol

196 Additionally, both can suppress alloimmune responses by contact-dependent mechanisms by

197 To investigate the dynamics of alloimmune responses directed at HLA antigens, we retros

198 findings demonstrate for the first time that alloimmune responses following lung transplantation are

199 on of the T cell repertoire and induction of alloimmune responses following lymphoablation is poorly

200 onditions to enhance the immunoregulation of alloimmune responses in clinical transplantation.

201 metabolism in the regulation of intra-graft alloimmune responses in humans and provide a set of biom

202 ssor T cells have also been shown to control alloimmune responses in preclinical and clinical models.

203 inflammation is a potential cause of humoral alloimmune responses in renal transplantation, and de no

204 from CD34+ cells or monocytes and stimulate alloimmune responses in transplantation.

205 t, B cells impaired Th1, but not Th2, T cell alloimmune responses in vitro and in vivo, in models of

206 l populations and the source of sCD30 during alloimmune responses in vitro.

207 +)CD25(+) cells exhibited the suppression of alloimmune responses in vivo and in vitro.

208 sly unknown functions of TIM-1 in regulating alloimmune responses in vivo and may provide a novel app

209 plays an important role in the inhibition of alloimmune responses in vivo and suggests a dominant dir

210 nctional significance of this interaction in alloimmune responses in vivo.

211 D-1/PD-L1 interactions, in the regulation of alloimmune responses in vivo.

212 Furthermore, PD-1:PD-L1 pathway can regulate alloimmune responses independent of an intact CD28/CTLA-

213 ole in peripheral tolerance, but its role in alloimmune responses is poorly understood.

214 ther this disruption enhances or hinders the alloimmune responses is unclear.

215 acrophages and their contribution to shaping alloimmune responses is unknown.

216 We hypothesized that persistent alloimmune responses may induce immune activation and co

217 ardiac allograft vasculopathy to clarify the alloimmune responses mediated by intragraft TLOs and whe

218 Alloimmune responses play an important role in progressi

219 s to graft dysfunction and may contribute to alloimmune responses posttransplantation.

220 Elimination of alloimmune responses produces rapid restoration of inner

221 isms by which innate immune signals regulate alloimmune responses remain poorly understood.

222 However, their role in alloimmune responses remains unclear.

223 flora associated with the graft may augment alloimmune responses through TLR4.

224 y disorders and inflammatory stimuli promote alloimmune responses to RBC Ags.

225 therapeutic options that inhibit detrimental alloimmune responses whilst simultaneously promoting all

226 y lymphoid neogenesis is capable of mounting alloimmune responses without SLOs.

227 al role of dendritic cells (DCs) in mounting alloimmune responses, activation of donor DCs by ischemi

228 on donor cardiac tissue regulates recipient alloimmune responses, allograft rejection, and vasculopa

229 te its critical importance for tumor growth, alloimmune responses, and inflammation, the role of lymp

230 eflected in their ability not only to induce alloimmune responses, but also to serve as potential tar

231 blishing that in the absence of Th1-mediated alloimmune responses, CD4 Th17 cells mediate an aggressi

232 Although loss of RIP3 does not eliminate alloimmune responses, chronic graft injury is reduced.

233 Despite proven effectiveness in inhibiting alloimmune responses, clinical use of belatacept in kidn

234 To evaluate the selective depletion of alloimmune responses, donor C57BL/6 splenocytes were coc

235 se results indicate that during late primary alloimmune responses, granzyme C can support CTL-mediate

236 dritic cells (DC), the primary regulators of alloimmune responses, is controlled by chemokines.

237 differences in intrinsic graft function and alloimmune responses, the ability of young and old cells

238 ought to be major effector cells in adaptive alloimmune responses, their respective contribution to a

239 t into the differences between antiviral and alloimmune responses, we performed a case-control study,

240 and rigorous protocols for the monitoring of alloimmune responses.

241 are critical for the local downregulation of alloimmune responses.

242 oduction, which induced NO and downregulated alloimmune responses.

243 egs, and abrogated both cellular and humoral alloimmune responses.

244 tor T cells resistant to Treg suppression of alloimmune responses.

245 raft exposure to danger signals and dampened alloimmune responses.

246 long-lasting therapeutic effects to control alloimmune responses.

247 kade of the CD40/CD154 pathway in preventing alloimmune responses.

248 ulation acts as a negative regulator of host alloimmune responses.

249 a key mechanism in eliciting and sustaining alloimmune responses.

250 of immune responses, including antitumor and alloimmune responses.

251 tic cells, which play a key role in mounting alloimmune responses.

252 on by inhibiting both fibroproliferative and alloimmune responses.

253 d-1/2) plays an important role in regulating alloimmune responses.

254 d events on regulatory circuits which dampen alloimmune responses.

255 nted host-versus-donor and donor-versus-host alloimmune responses.

256 e for their specificity in the regulation of alloimmune responses.

257 latory signals that function to downregulate alloimmune responses.

258 drug toxicities and the emergence of chronic alloimmune responses.

259 esults in a PD-1/CTLA4-dependent decrease in alloimmune responses.

260 ismatches in HLA-DQ and HLA-DP can result in alloimmune responses.

261 ically relevant tool to stratify patients by alloimmune risk and may help guide personalized immunosu

262 stratified into low, intermediate, and high alloimmune risk categories.

263 gh levels and the recipient's individualized alloimmune risk determined by HLA-DR/DQ epitope mismatch

264 Recipients with high HLA alloimmune risk should not target tacrolimus levels <5 n

265 Alloimmune risk stratification in renal transplantation

266 assays in evaluating both memory and primary alloimmune risks.

267 mic B-cell-deficient(muMT) mice, in a purely alloimmune setting (BALB/c into hyperglycemic C57BL/6),

268 leads to robust graft tolerance in a purely alloimmune setting and prolonged islet graft survival in

269 Alloimmune specificity and histocompatibility, driven by

270 cording to statistical properties related to alloimmune status kinetics were unsuccessful, indicating

271 suggests that an individualized strategy for alloimmune status monitoring may be preferable to curren

272 nt differences in the magnitude of change in alloimmune status, especially among patients with a prev

273 ction by regularly monitoring for changes in alloimmune status.

274 this study is to examine the consequences of alloimmune stimulation when allogeneic cells are transpl

275 allograft tolerant recipients would reverse alloimmune suppression mediated by CD4(+) Treg.

276 infection, and malignancy, while holding the alloimmune system in check.

277 ) potential assays to assess the presence of alloimmune T and B cell memory; and (3) progress in the

278 Alloimmune T cell responses induce graft-versus-host dis

279 Alloimmune T cells are central mediators of rejection an

280 m is the most common cause of fetal/neonatal alloimmune thrombocytopenia (F/NAIT) and is thought to b

281 Fetomaternal alloimmune thrombocytopenia (FMAIT) is caused by materna

282 gies can be used to manage fetal or neonatal alloimmune thrombocytopenia (FNAIT) in subsequent pregna

283 ntibodies responsible for fetal and neonatal alloimmune thrombocytopenia (FNAIT) in the white populat

284 Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a condition chara

285 Fetal and neonatal alloimmune thrombocytopenia (FNAIT) is a life-threatenin

286 Fetal/neonatal alloimmune thrombocytopenia (FNAIT) is often caused by m

287 therapeutic antibody for fetal and neonatal alloimmune thrombocytopenia (FNAIT) that would block the

288 PAs) of the fetus mediates fetal or neonatal alloimmune thrombocytopenia (FNAIT).

289 novel approach to the treatment of neonatal alloimmune thrombocytopenia (NAIT) in utero: shielding f

290 HPA 1a)-specific antibodies causing neonatal alloimmune thrombocytopenia (NAIT) possess oligosacchari

291 Transplant-mediated alloimmune thrombocytopenia (TMAT) from donors with immu

292 for the T cell directed response in neonatal alloimmune thrombocytopenia and post-transfusion purpura

293 ding disorders, including fetal and neonatal alloimmune thrombocytopenia and posttransfusion purpura.

294 mann thrombasthenia (GT), 20 associated with alloimmune thrombocytopenia, and 5 associated with aniso

295 Fetomaternal alloimmune thrombocytopenia, caused by the maternal gene

296 anti-HLA antibodies that cause fetomaternal alloimmune thrombocytopenia.

297 s responsible for disorders such as neonatal alloimmune thrombocytopenia.

298 T3 signaling in graft CD4+ T cells links the alloimmune tissue injury of donor graft T cells and the

299 clinical and pathological manifestations of alloimmune tissue injury.

300 ure, both early and late, both nonimmune and alloimmune, to gain better insight into the causes of gr