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 We hypothesised an alloimmune aetiology for the disorder on the basis of it

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 ts highlight an important difference between alloimmune and conventional immune responses.

11 ation, as well as the ability to prevent the alloimmune and recurrent autoimmune response following i

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

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

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

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

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

17 finding suggests that the initial priming of alloimmune CD4 T cell responses occurs within draining l

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 e prevention and treatment of autoimmune and alloimmune disease states.

21 Gestational alloimmune diseases are induced by the placental passage

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

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

24 unologic disorders, including autoimmune and alloimmune diseases.

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

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

27 AR, distinguishing between different driving alloimmune effector mechanisms.

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

29 RIC) transplantation is largely dependent on alloimmune effects.

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

31 Alloimmune feto-maternal destruction of blood cells is t

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

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

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

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

36 d the bone marrow in arriving at a state of "alloimmune homeostasis" in humans.

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

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

39 erglycemia itself does not cause generalized alloimmune impairment.

40 Using an in vitro alloimmune incompatibility model, sCR1 inhibited complem

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

42 of inflammatory chemoattractant molecules on alloimmune induction.

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

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

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

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

47 Unopposed alloimmune injury for 10 days was associated with subseq

48 MAC-mediated alloimmune injury in congenital alloimmune hepatitis is

49 val of alloimmunity if the initial period of alloimmune injury is sufficient.

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

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

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

53 ronic allograft nephropathy with features of alloimmune injury.

54 nd the degree of airway remodeling following alloimmune injury.

55 standing of the molecular pathophysiology of alloimmune injury.

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

57 Alloimmune lung injury, characterized by perivascular ly

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

59 nduced innate immune activation in promoting alloimmune lung injury.

60 ritical to the development of posttransplant alloimmune lung injury.

61 These results further support an alloimmune mechanism for recurrent neonatal haemochromat

62 hematopoietic stem cell transplantation, and alloimmune mechanisms mediating host-versus-graft and gr

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

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

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

66 r, CD28/CD154 blockade completely blocks the alloimmune-mediated islet rejection.

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

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

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

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

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

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

73 rent methods of leukoreduction in preventing alloimmune platelet refractoriness was evaluated in a ca

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

75 e this hypothesis, we examined the impact of alloimmune pressure on PNH and normal cells in the clini

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

77 A central proposition is that MHC-driven alloimmune processes play a necessary role in CAV, as sh

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

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

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

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

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

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

84 did not stimulate significant donor-specific alloimmune reactions.

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

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

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

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

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

90 ibodies, suggesting that the augmentation of alloimmune reactivity was most likely due to a nonspecif

91 overing donor Tregs to initiate and maintain alloimmune regulation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 154 Abs has shown promise in attenuating the alloimmune response and promoting long-term graft surviv

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

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

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

111 C) not only constitute a major target of the alloimmune response but also produce substantial amounts

112 ion, it is essential for down-regulating the alloimmune response by inducing the apoptosis of host im

113 The alloimmune response can be divided into specific junctur

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

115 sion of C3 is an unexpected regulator of the alloimmune response in mouse kidney transplantation.

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

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

118 allografts and to evaluate the nature of the alloimmune response in the setting of T-cell depletion.

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

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

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

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

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

124 tokines in influencing the progression of an alloimmune response leading ultimately to either allogra

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

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

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

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

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

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

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

132 ivation; however, its role in regulating the alloimmune response remains unexplored.

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

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

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

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

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

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

139 2-presented peptides of WT1, a dominant anti-alloimmune response usually obscures detection of peptid

140 ice was observed irrespective of whether the alloimmune response was CD4 or CD8 T cell-mediated and c

141 he important role of foreign peptides in the alloimmune response was recently recognized.

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

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

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

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

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

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

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

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

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

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

152 allograft support an important role for the alloimmune response, there is considerable evidence impl

153 To prevent the alloimmune response, we used blockade of CD28:B7 and CD4

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

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

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

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

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

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

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

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

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

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

164 3:Pro allele, and defines the unidirectional alloimmune response.

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

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

167 nsplantation is a persistent T cell-mediated alloimmune response.

168 donor epithelium-bound C3 can upregulate the alloimmune response.

169 rejection even in the face of an established alloimmune response.

170 e immunity to the initiation of the adaptive alloimmune response.

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

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

173 -6 generation from lung parenchyma during an alloimmune response.

174 ownregulates the immune system, blunting the alloimmune response.

175 uce APC maturation and initiate the adaptive alloimmune response.

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

177 rs and directly with a probable influence on 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 c and temporal characteristics of CD4 T cell alloimmune responses and demonstrates that CD4 T cell pr

183 iabetes, showing that even in the absence of alloimmune responses and given an adaptation period, the

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

185 inflammatory processes potentially impacting alloimmune responses and graft quality.

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

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

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

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

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

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

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

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

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

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

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

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

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

199 propensity to activate CD4- or CD8-dependent alloimmune responses can be distinguished.

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

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

202 dTGF-beta1 Rh MDDC) significantly suppressed alloimmune responses in [ H]thymidine uptake mixed leuko

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

204 timulation pathway has been shown to mediate alloimmune responses in normal recipients, little is kno

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

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

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

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

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

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

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

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

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

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

215 ctions of the ICOS-B7h pathway in regulating alloimmune responses in vivo.

216 gen-presenting cells are required to trigger alloimmune responses in vivo.

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

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

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

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

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

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

223 Alloimmune responses play an important role in progressi

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

225 Elimination of alloimmune responses produces rapid restoration of inner

226 nisms underlying physiological regulation of alloimmune responses remain poorly defined.

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

228 However, their role in alloimmune responses remains unclear.

229 n regular heterosexual partners could elicit alloimmune responses that might be associated with inhib

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

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

232 Significant alloimmune responses were also seen in corresponding mal

233 , whereas hepatocyte-initiated CD4-dependent alloimmune responses were not.

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

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

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

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

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

239 including brain death, ischemia-reperfusion, alloimmune responses, and viral infections.

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

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

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

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

244 t that CD134-CD134L is a critical pathway in alloimmune responses, especially recall/primed responses

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

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

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

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

249 raft exposure to danger signals and dampened alloimmune responses.

250 long-lasting therapeutic effects to control alloimmune responses.

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

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

253 of immune responses, including antitumor and alloimmune responses.

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

255 on by inhibiting both fibroproliferative and alloimmune responses.

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

257 d events on regulatory circuits which dampen alloimmune responses.

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

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

260 latory signals that function to downregulate alloimmune responses.

261 tory T (Treg) cells are potent modulators of alloimmune responses.

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

263 inhibit aggressive T(H)1-mediated auto- and alloimmune responses.

264 ggesting that CD30 may be important in human alloimmune responses.

265 quired for full activation of T cells during alloimmune responses.

266 drug toxicities and the emergence of chronic alloimmune responses.

267 and rigorous protocols for the monitoring of alloimmune responses.

268 oduction, which induced NO and downregulated alloimmune responses.

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

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

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

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

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

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

275 Alloimmune specificity and histocompatibility, driven by

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

277 n, the grafts initially exposed to 7 days of alloimmune stimulus had few abnormalities.

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

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

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

281 Alloimmune T cells are central mediators of rejection an

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

283 Fetomaternal alloimmune thrombocytopenia (FMAIT) is caused by materna

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

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

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

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

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

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

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

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

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

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

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

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

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

297 Fetomaternal alloimmune thrombocytopenia, caused by the maternal gene

298 anti-HLA antibodies that cause fetomaternal alloimmune thrombocytopenia.

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

300 clinical and pathological manifestations of alloimmune tissue injury.