ライフサイエンスコーパス: alloantigen

1 rance is induced in addition to tolerance to alloantigen.

2 es induced by classical indirectly presented alloantigen.

3 d defective responses to viral infection and alloantigen.

4 ly manipulating the T cells, which recognize alloantigen.

5 y CD4 T cells specific for a second "helper" alloantigen.

6 concomitant conventional T-cell response to alloantigen.

7 by memory responses to the accessory helper alloantigen.

8 entionally, by Th cell recognition of target alloantigen.

9 he Tregs that are induced by AC injection of alloantigen.

10 ssive effects of MSCs on T-cell responses to alloantigen.

11 apidly underwent cell death upon exposure to alloantigen.

12 h T cells from mice rendered unresponsive to alloantigen.

13 mechanism of early action in the absence of alloantigen.

14 (LTx), when there is continuous exposure to alloantigen.

15 in duration and strength according to target alloantigen.

16 crease IFNgamma production after exposure to alloantigens.

17 duced tolerogenic effects selective to islet alloantigens.

18 roduced locally and activated by trophoblast alloantigens.

19 gs showed specific unresponsiveness to donor alloantigens.

20 rance and immunity to pathogens, cancer, and alloantigens.

21 nce of T-cell subsets and responses to donor alloantigens.

22 in turn regulate in vivo T cell responses to alloantigens.

23 eas in GVHD, all host cells directly present alloantigens.

24 T-cell tolerance upon reexposure to the same alloantigens.

25 ific proliferative responses to donor airway alloantigens.

26 induction of both T and B cell tolerance to alloantigens.

27 (IL-13) cytokines when challenged with donor alloantigens.

28 for induction of specific tolerance to donor alloantigens.

29 eans of tolerizing peripheral CD4 T cells to alloantigens.

30 tudy drugs, and none have been sensitized to alloantigens.

31 uce humoral unresponsiveness to transplanted alloantigens.

32 d polyclonal CD8+ T cells raised to viral or alloantigens.

33 d recognize epitopes encoded by that gene as alloantigens.

34 meras, suggesting central tolerance to donor alloantigens.

35 primed by antigen-presenting cell presenting alloantigens.

36 educed ability to proliferate in response to alloantigens.

37 subsets defined by expression of plasma cell alloantigen 1 (PC1), also known as ectonucleotide pyroph

38 , MMc magnitude was enough to cause membrane alloantigen acquisition (mAAQ; "cross-dressing") of host

39 colysis was required for optimal function of alloantigen-activated T cells and induction of GVHD, as

40 DZNep caused selective apoptosis in alloantigen-activated T cells mediating host tissue inju

41 ory effect on the production of GNLY by drug/alloantigen-activated T cells.

42 known about T cell metabolism in response to alloantigens after hematopoietic cell transplantation (H

43 odulating responses against autoantigens and alloantigens after kidney transplant.

44 be harmful when they target an autoantigen, alloantigen, allergen, or biotherapeutic.

45 human primate regulatory T cells (Treg) with alloantigen (alloAg) specificity would allow their testi

46 on the RBC surface at different levels, most alloantigens also represent completely different structu

47 GVHD is initiated by alloantigens, although both alloantigens and tumor-speci

48 e preserved by stimulation by specific donor alloantigen and cytokines from activated lymphocytes.

49 sm and limiting Tem expansion in response to alloantigen and homeostatic proliferation.

50 Thus, alpha345NC1 hexamers are the culprit alloantigen and primary target of all alloantibodies med

51 itic cells (DCs), of both intact MHC class I alloantigen and processed alloantigen would deliver link

52 ive pathway for the acquisition of recipient alloantigen and that once acquired, this cross-dressed M

53 cells play a cardinal feature in response to alloantigens and are able to generate effector/memory T

54 They prevent immune responses to auto- and alloantigens and are thus under close scrutiny as cellul

55 lls in response to TCR activators, including alloantigens and autoantigens.

56 at inhibited the T effector cell response to alloantigens and converted T conventional cells into CD4

57 physiochemical polymorphisms of HLA class II alloantigens and correlated these with humoral alloimmun

58 ough CD62L(-) T cells are able to respond to alloantigens and deplete host radioresistant immune cell

59 CD B cells act as APCs and present alloantigens and microbial Ags to T cells.

60 whether B-cell tolerance to A/B-incompatible alloantigens and pig xenoantigens could be achieved in i

61 is initiated by alloantigens, although both alloantigens and tumor-specific antigens (TSAs) initiate

62 xpressed by immune cells during priming with alloantigen, and the net sum of costimulatory and coinhi

63 ing effect in preventing T cell responses to alloantigens, and produced long-term cardiac allograft s

64 rived Treg cells with specific receptors for alloantigen are activated by either IL-2 or IL-4 but rap

65 Humoral immune responses to alloantigens are a growing clinical problem in transplan

66 tional tissue transplants insofar as not all alloantigens are revealed during tolerance induction.

67 earing other low-frequency platelet-specific alloantigens, are relatively rare in the population and

68 ty over time and were eventually tolerant to alloantigens as a result of prolonged antigen exposure,

69 Alloreactive T cells target their inducing alloantigens as well as third-party alloantigens but gen

70 ents showed lower proliferative responses to alloantigen, as well as to polyclonal stimulation, than

71 nd limitations of negative vaccination using alloantigen-bearing "tolerogenic" DCs.

72 ly reacted against autologous tumor, but not alloantigen-bearing recipient cells with increased secre

73 tive B cells retained their ability to sense alloantigen because they continued to drive T cell matur

74 ause of insufficient priming to male partner alloantigens before conception.

75 ent tolerance required exact matching of all alloantigens between the adoptively transferred allogene

76 f C57BL/6 (B6) DCs presented acquired H-2(d) alloantigen both as processed allopeptide and as unproce

77 tive development of Th17 immune responses to alloantigen both in vitro and in vivo occurred, resultin

78 through naive Th cell recognition of target alloantigen but, crucially, blockade was ineffective whe

79 em not only through prior sensitization with alloantigens but also through previous exposure to envir

80 inducing alloantigens as well as third-party alloantigens but generally fail to target self-antigens.

81 epresentation of conformationally intact MHC alloantigen by recipient APC can induce cytotoxic alloim

82 /= 3 d, whereas indirect presentation of MHC alloantigen by recipient APCs led to activation of T cel

83 entation of intact and processed MHC class I alloantigen by recipient dendritic cells (DCs) (the "sem

84 nti-OX40 attenuates CD8+ T-cell responses to alloantigen by reducing the pool of effector T cells, su

85 tory T cells to suppress T cell responses to alloantigen by supporting, rather than diminishing, regu

86 arising from developmental corecognition of alloantigens by activating and inhibitory receptors with

87 e presentation of drug-modified donor DC MHC alloantigens by recipient APCs and activation of recipie

88 tection of antibodies against human platelet alloantigens by using gene-edited stem cell-derived targ

89 expression after LPS stimulation or in vivo alloantigen challenge.

90 innate and adaptive immunity in response to alloantigens, challenged the conventional view, develope

91 strates circulating human B cells binding an alloantigen (DBY-2) and that these DBY-2-specific B cell

92 tently strong, the response against class II alloantigen decayed within 2 weeks.

93 polyclonal T cell proliferative responses to alloantigen, defined peptide antigens, and viral infecti

94 ocompatibility complex-disparate third-party alloantigens, demonstrating functional donor-specific T-

95 may influence alloantibody formation is RBC alloantigen density.

96 icient recipients were hyporesponsive toward alloantigen, despite increased numbers of CD8(+) effecto

97 ess how indirect responses against different alloantigens differ in their strength and longevity, and

98 n that effector memory T cells not primed to alloantigen do not cause GVHD yet transfer functional T

99 e superior to wild-type Tregs in suppressing alloantigen-driven expansion of T cells in vitro and in

100 in the absence of exogenous pathogens is the alloantigen-driven parent-into F1 model of acute graft-v

101 Foxp3 in iTregs followed homeostatic and/or alloantigen-driven proliferation and was unrelated to GV

102 rejection and report that unlike exposure to alloantigens during transplantation, platelet transfusio

103 ssociated with accelerated T cell death upon alloantigen encounter, suggesting these proteins might p

104 tical to the maintenance of tolerance toward alloantigens encountered during postnatal life pointing

105 X40L interactions at the time of exposure to alloantigen enhanced the ability of regulatory T cells t

106 RBC alloantigens exist at different densities on the RBC sur

107 tants of polyclonally activated B cells from alloantigen exposed (n = 13) or nonexposed (n = 10) indi

108 mmune response in patients with a history of alloantigen exposure.

109 Direct presentation of alloantigen expressed on donor leukocytes is recognized

110 ferent species; IPD-human platelet antigens, alloantigens expressed only on platelets and IPD-ESTDAB,

111 ility complex of different species; IPD-HPA, alloantigens expressed only on platelets; and IPD-ESTDAB

112 We found that alloantigen expression by the host APCs is necessary and

113 pact of differences in Ag density from other alloantigen features that may also influence RBC alloimm

114 Donor T cells that respond to host alloantigens following allogeneic bone marrow transplant

115 eactive CD8 T cells and as processed peptide alloantigen for recognition by indirect-pathway CD4 T ce

116 Human platelet alloantigens (HPAs) reside on functionally important pla

117 hin the mLNs is driven by profound levels of alloantigen, IL-12, and IL-6 promoted by Toll-like recep

118 t HLA type are strong predictors of class II alloantigen immunogenicity and alloantibody response bef

119 lammatory cytokine production in response to alloantigen in mice.

120 N) were removed and rechallenged with BALB/c alloantigen in vitro with subsequent assay of interferon

121 could facilitate iTreg-mediated tolerance to alloantigens in humans.

122 some amino acids that are known polymorphic alloantigens in humans.

123 r, the impact of developmentally encountered alloantigens in shaping the phenotype and function of iN

124 nied by impaired responsiveness toward donor alloantigens in vitro after IL-2 cplx treatment was stop

125 lls proliferated and expanded in response to alloantigens in vivo, their ability to produce interleuk

126 ane microdomains containing the acquired MHC alloantigens included CD86, but completely excluded PD-L

127 immunologic risk because of sensitization to alloantigens, including those who have exhibited early o

128 ocytes, enhanced CD8(+) cytotoxicity against alloantigen, increased alloantibody production, and a de

129 an be provided by CD4 T cells that recognize alloantigen "indirectly," as self-restricted allopeptide

130 Donor Stat1 deficiency resulted in reduced alloantigen-induced activation and expansion of donor T

131 Col(V) plus CsA was associated with alloantigen-induced expression of IL-10 in mediastinal l

132 e provided CsA sustained release, decreasing alloantigen-induced immune responses in the draining lym

133 revented rejection pathology, down-regulated alloantigen-induced production of IFN-gamma and IL-17A,

134 In vitro, pioglitazone inhibited both alloantigen-induced proliferation and superantigen-induc

135 significantly inhibits both homeostatic and alloantigen-induced proliferation of Treg, and promotes

136 t low ratios (<1:320), potent suppressors of alloantigen-induced proliferation without significant su

137 unity, this study investigated their role in alloantigen-induced T cell activation and asked whether

138 as in murine allogeneic skin transplant and alloantigen-induced T cell expansion in draining lymph n

139 TRAIL-R costimulation efficiently inhibited alloantigen-induced T cell proliferation and CD3/28-indu

140 hole limpet hemocyanin-induced Ab responses, alloantigen-induced T cell proliferation, "heart-to-ear"

141 Additionally, pirfenidone effects on alloantigen-induced T-cell proliferation in vivo were as

142 A to granzyme B mRNA (P<0.01) were higher in alloantigen-induced Tregs (alloTregs) compared with nTre

143 ection after LTx, rather than persistence of alloantigen, induces the accumulation of dysfunctional C

144 use they measure events downstream of T cell-alloantigen interactions.

145 mulation of naive donor T cells by recipient alloantigen is central to the pathogenesis of graft-vers

146 terruption of the process by which recipient alloantigen is presented to donor T cells to generate gr

147 Uniquely, alloantigen is recognised by two pathways: as intact ant

148 on (alloSCT), there is no specific pathogen, alloantigen is ubiquitous, and signals that induce APC m

149 D has no physiological equivalent in nature; alloantigen is ubiquitous, persists indefinitely, and ca

150 that a possible way in which B cells present alloantigens is via acquisition of MHC-peptide complexes

151 Here, we review our current understanding of alloantigen, its presentation by various antigen-present

152 n and cytotoxic degranulation in response to alloantigen late after LTx.

153 on of hematopoietic cells carrying the fetal alloantigen leads to enhanced demise of semiallogeneic f

154 omosome 1 harboring an alternative CD45/Ly-5 alloantigen (Ly-5.1).

155 sponses against previously encountered graft alloantigen may be the dominant mechanism for providing

156 to suggest that harmful immune responses to alloantigens may be abrogated as well.

157 fied CD8(+) T(CM) not specifically primed to alloantigens mediate GVHD in the MHC-mismatched C57BL/6

158 In this article, we show that the alloantigen-mediated activation of naive and memory CD4(

159 producing IFN-gamma and IL-17 in response to alloantigens (MLR), anti-CD3, and the glycolipid alpha-g

160 sponse with no evidence for sensitization to alloantigens nor acceleration of rejection of allogeneic

161 n, direct-pathway CD8 T cells that recognize alloantigen on donor cells require CD4 help for activati

162 (GVHD), naive donor CD4(+) T cells recognize alloantigens on host antigen-presenting cells and differ

163 Ks expressing intact homozygous glycoprotein alloantigens on the cell surface that carry the appropri

164 f TCR-transgenic CD4 T cells that recognized alloantigen only as conformationally intact protein (dir

165 transferred into C57BL/6 mice that received alloantigen or cardiac allografts.

166 hy donors immunized against foreign rhesus D alloantigen or vaccinia virus.

167 rated T-cell responses to donor C57BL/6 (B6) alloantigens or stimulate cytotoxic T lymphocyte (CTL) r

168 Exogenous C3a enhanced IL-17 production from alloantigen- or autoantigen (type V collagen)-reactive l

169 ies of T cells responding to autoantigen and alloantigen peptide-MHC tetramers in TCRalpha(+/-) mice.

170 The memory T cells immunized to alloantigens persisted even after myeloablative (1000 cG

171 e maternal immune system is exposed to fetal alloantigens, possibly explaining the relationship betwe

172 However, in alloantigen-presensitized mice, NK cells are dispensable

173 Despite the high level of recipient-derived alloantigen present on the surface of donor DCs, donor T

174 orward cascade of donor DC-mediated indirect alloantigen presentation and cytokine secretion within t

175 nic T-cell population that promotes indirect alloantigen presentation and pathological damage within

176 Tc17 differentiation is dependent on alloantigen presentation by host dendritic cells (DCs) t

177 This results in donor DC expansion and alloantigen presentation in the colon and subsequent mig

178 Critically, alloantigen presentation in the mLNs imprints gut-homing

179 The recognition that alloantigen presentation is also critical to the develop

180 , we demonstrate that GVHD markedly enhances alloantigen presentation within the mesenteric lymph nod

181 In addition, GM-CSF promoted indirect alloantigen presentation, resulting in the accumulation

182 nd up-regulated CD80, CD86, and IL-12 during alloantigen presentation, whereas CD11b(+) APCs expresse

183 amplifies expansion of donor APCs and their alloantigen presentation.

184 stence of a foreign virus, the large mass of alloantigen presented by an allograft in chronic residen

185 ated only in response to processed recipient alloantigen presented via the indirect pathway and not i

186 ions had reduced HVEM expression and greater alloantigen-presenting capacity than wild-type lymphoma

187 LN and colocalize in exclusive regions with alloantigen-presenting cells, a process required for Tre

188 N that were permissive for colocalization of alloantigen-presenting cells, alloreactive T cells, and

189 ministration at the time of DST matures host alloantigen-presenting dendritic cells, prevents the est

190 Importantly, alloantigen-primed and CD4(+) T cell-helped macrophages

191 ed only by CD4 T cells that recognize target alloantigen, processed and presented by the allospecific

192 ments, maternal T cells specific for a fetal alloantigen proliferate after fetal intervention, escape

193 ice: T cells recognizing intact acquired MHC alloantigens proliferated, whereas those responding to a

194 er type 2 (Th2) cytokine, IL-4, and specific alloantigen promote allograft tolerance.

195 This represented class I alloantigen provides a conformational epitope for direct

196 Alloantigen-reactive 4-1BB(+)CD40L(-) nTreg were charact

197 4-1BB and absence of CD40L expression, human alloantigen-reactive Foxp3(+) nTreg can be directly isol

198 d box P3, and strategies to expand or induce alloantigen-reactive Treg in vivo and in vitro.

199 0L(-) nTreg maintain the nTreg phenotype and alloantigen-reactivity after in vitro expansion.

200 GVL effect is due to largely unopposed Tcon alloantigen recognition in bone marrow.

201 Chemokine receptor signaling and alloantigen recognition were required for trafficking of

202 However, although distinct alloantigens reside on the RBC surface at different leve

203 n had more remarkable effect in reducing the alloantigen response with prolonged graft survival.

204 t coordinate tissue damage in autoimmune and alloantigen responses.

205 nd spleen T-cell population, and splenocytes alloantigen responsiveness of graft recipients.

206 ed T-cell responses when present only during alloantigen restimulation.

207 e found that previous sensitization to donor alloantigens resulted in the development of antidonor al

208 cific Tregs suppressed responses to specific alloantigen selectively and were approximately 100-fold

209 Regulatory T cells (Tregs) control alloantigen-sensitized inflammation of GVHD, sustain GVT

210 oups of recipients: nonsensitized wild type, alloantigen-sensitized wild-type and CCR5(-/-) mice that

211 he prenatal interaction between NK cells and alloantigens shapes the developing NK cell repertoire to

212 uces Ab responses to multiple tissue-derived alloantigens simultaneously.

213 Suppression by alloTregs was alloantigen specific and was observed at the level of re

214 e therapy (P=0.0003), and the protection was alloantigen specific.

215 suggesting that this cytokine production was alloantigen specific.

216 quency, growth requirements, and function of alloantigen-specific (allospecific) Tregs from human blo

217 ed a new acute GVHD model mediated by clonal alloantigen-specific 4C CD4(+) Tconv.

218 fferentiate naive, high abundant CD4+ T into alloantigen-specific and allograft protective Foxp3+Treg

219 differentiate the polyclonal CD4+ cells into alloantigen-specific and allograft protective Tregs.

220 granule exocytosis, that is, cytotoxicity of alloantigen-specific and polyclonal CD8(+) CTL in vitro.

221 rejecting recipients lacked alloantibody and alloantigen-specific CD4 T-cell responses.

222 Alloantigen-specific CD4(+) T cells transferred at time

223 the proliferation of adoptively transferred alloantigen-specific CD4(+) T cells, demonstrating that

224 egulation of fetomaternal tolerance using an alloantigen-specific CD4(+) TCR transgenic mouse model s

225 n part promotes their survival.Whether these alloantigen-specific CD4CD25FOXP3 regulatory T (Treg) ce

226 tudy, we show that functionally suppressive, alloantigen-specific CD8(+) Foxp3(+) T cells can be indu

227 ion (CD4(+)CD25(bright)CD127(-) T cells) was alloantigen-specific expanded using HLA-mismatched immat

228 y to generate potent, functional, and stable alloantigen-specific human Tregs markedly enhances their

229 AR) and its application in the generation of alloantigen-specific human Tregs.

230 put forward a successful strategy to induce alloantigen-specific hyporesponsiveness towards stem cel

231 augment their production of IL-12 and expand alloantigen-specific IFN-gamma(+) T cells.

232 Using an alloantigen-specific Ig transgenic system, we demonstrat

233 and the cortical ridge that correlated with alloantigen-specific immunity or immune tolerance.

234 became hyporesponsive to restimulation in an alloantigen-specific manner and contained higher percent

235 very low Treg-to-T effector cell ratio in an alloantigen-specific manner.

236 Thus, innate myeloid cells acquire alloantigen-specific memory that can be targeted to impr

237 s to our knowledge the first report using an alloantigen-specific model that establishes a link betwe

238 of exogenous IL-15, for expansion of stable alloantigen-specific nTregs with superior suppressive fu

239 ed for their capacity to generate functional alloantigen-specific nTregs.

240 lls, this phenotype favors the generation of alloantigen-specific regulatory CD4(+) or CD8(+) T cells

241 CD4 T-cell alloantigen-specific responses and donor-specific alloan

242 antigen-presenting cells (APCs) in inducing alloantigen-specific responses.

243 e from transplant tolerant hosts to transfer alloantigen-specific suppression to lymphopenic recipien

244 Treg-specific demethylated region and showed alloantigen-specific suppressive properties superior to

245 Phenotype and homing of alloantigen-specific T cells or their perforin/granzyme-

246 ogic GVHD, whereas antitumor cytotoxicity of alloantigen-specific T cells was maintained.

247 ly Notch-regulated molecular events occur in alloantigen-specific T cells.

248 leukemias were completely eradicated by the alloantigen-specific T cells.

249 88-dependent fashion and drove expansion of alloantigen-specific T lymphocytes.

250 This led to the finding that alloantigen-specific T suppressor cells express IL-2 rec

251 reover, treatment with TAK-779 (a) decreased alloantigen-specific T-lymphocyte proliferation and numb

252 iltration into the graft, (b) attenuation of alloantigen-specific T-lymphocyte proliferative response

253 ereafter, local IL-6 secretion induces donor alloantigen-specific Th17 cells to preferentially expand

254 in grafted, rapamycin-treated mice disrupts alloantigen-specific tolerance induction.

255 pecific splenocyte transfusion (DST) induces alloantigen-specific tolerance.

256 n target of rapamycin (Rapa) synergizes with alloantigen-specific Treg (AAsTreg) to permit long-term,

257 ied by expansion of Foxp3(+) Tregs, enhanced alloantigen-specific Treg function, and modulation of tr

258 Current methods to generate alloantigen-specific Tregs rely on expansion with alloge

259 lograft may play a role in the generation of alloantigen-specific Tregs, but this role remains undefi

260 a similar approach could be used to generate alloantigen-specific Tregs.

261 egulatory T cells, including those that were alloantigen-specific, which served an increasingly criti

262 Moreover, graft protection was alloantigen-specific.

263 The alloantigen specificity demonstrated by B cell-expanded

264 nTregs, however, are sparse and lack alloantigen specificity, and these properties pose chall

265 ssion of IDO suppressed the proliferation of alloantigen-stimulated splenocytes.

266 We conclude that graft alloantigen stimulates the de novo generation of aTregs,

267 eta/T-cell receptor (TCR)/CD28 activation or alloantigen stimulation in vitro compared with wild-type

268 regulated in miR-146a(-/-) T cells following alloantigen stimulation.

269 3 mAb in combination with anti-CD28 mAb, and alloantigen stimulation.

270 se non-HLA antigens are classified as either alloantigens, such as the major histocompatibility compl

271 d not depend on T cell specificity for donor alloantigens suggesting an important role for posttransp

272 The HPA-1a/HPA-1b alloantigen system, also known as the Pl(A1)/Pl(A2) poly

273 ransplantation and may be the main source of alloantigen that drives CD8(+) cytotoxic T cell response

274 Patr-AL is an alloantigen that participates in negative and positive s

275 e show that in mice primed to an MHC class I alloantigen, the accelerated graft rejection T memory re

276 ubsets that function as potential sources of alloantigens, the cross talk of innate lymphoid cells wi

277 tologous T lymphocytes, activated in vivo by alloantigens, the survival and growth of primary CFSE-la

278 t ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor

279 esenting cells (APCs) to efficiently present alloantigen to donor T cells while releasing cytokines (

280 ence has accumulated that targeting of donor alloantigen to quiescent dendritic cells (DC) in situ or

281 ze major histocompatibility complex class II alloantigens to suppress skin transplant rejection.

282 with a history of pretransplant exposure to alloantigens, to predict subsequent humoral events and t

283 ntrast, DZNep did not affect the survival of alloantigen-unresponsive T cells in vivo and naive T cel

284 despite acquiring similar amounts of H-2(d) alloantigen upon coculture, MHC class II-deficient B6 DC

285 ce it in the context of the known functional alloantigen variation of these genes.

286 eloped when T cell memory against the helper alloantigen was first generated.

287 hereas the indirect response against class I alloantigen was longlasting and persistently strong, the

288 When alloantigen was presented directly, the precursor freque

289 When alloantigen was presented indirectly, the frequency of s

290 ytotoxicity of CD8(+) T cells in response to alloantigens was also diminished under these conditions,

291 To control for donor CD4 recognition of alloantigen, we used H-2(d) identical DBA/2 and B10.D2 d

292 receptor-transgenic) after stimulation with alloantigen were assessed in vitro by the incorporation

293 cy, pTreg cells specific to a model paternal alloantigen were generated in a CNS1-dependent manner an

294 ansgenic TEa CD4 cells that recognized donor alloantigen were transferred into C57BL/6 mice that rece

295 d-type hypersensitivity responses to C57BL/6 alloantigens were evaluated by a conventional ear swelli

296 alloantibody responses (P<0.001); only 6% of alloantigens with 0 to 2 mismatched AA-induced alloantib

297 orescence intensity 37) compared with 82% of alloantigens with more than or equal to 20 mismatched AA

298 during pregnancies sired by males expressing alloantigens with overlapping NIMA specificity, thereby

299 intact MHC class I alloantigen and processed alloantigen would deliver linked help, but has not been

300 d that T-regulatory cells specific for donor alloantigens would protect a renal transplant during par