ライフサイエンスコーパス: alloantigen

1 es induced by classical indirectly presented alloantigen.

2 d defective responses to viral infection and alloantigen.

3 ly manipulating the T cells, which recognize alloantigen.

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

5 h T cells from mice rendered unresponsive to 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 tor 6, are also resistant to tolerization to alloantigen.

12 mechanism of early action in the absence of alloantigen.

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

14 in duration and strength according to target alloantigen.

15 apidly underwent cell death upon exposure to alloantigen.

16 rance is induced in addition to tolerance to alloantigen.

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 m induces robust systemic tolerance to donor alloantigens.

35 meras, suggesting central tolerance to donor alloantigens.

36 primed by antigen-presenting cell presenting alloantigens.

37 educed ability to proliferate in response to alloantigens.

38 crease IFNgamma production after exposure to alloantigens.

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

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

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

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

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

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

45 vival could be enhanced by administration of alloantigen (Ag)-pulsed immature dendritic cells (DC) af

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

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

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

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

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

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

52 14 and IL-2 transcript levels increase after alloantigen and mitogen stimulation and are suppressed b

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

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

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

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

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

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

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

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

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

62 hout compromising global immune responses to alloantigens and nominal antigens.

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

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

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

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

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

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

69 trate that circulating exosomes transporting alloantigens are captured by splenic DCs of different li

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

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

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

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

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

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

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

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

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

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

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

81 regs in suppressing T cell responses against alloantigens, but also revealed some novel immunobiologi

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

83 /= 3 d, whereas indirect presentation of MHC alloantigen by recipient APCs led to activation of T cel

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

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

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

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

88 sentation to T cells and to be recognized as alloantigens by other T cells.

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

90 expression after LPS stimulation or in vivo alloantigen challenge.

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

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

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

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

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

96 may influence alloantibody formation is RBC alloantigen density.

97 of the adaptive immune system recognize MHC alloantigen-derived peptide on self-MHC molecules, has e

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

99 eived a transplant of low doses of NIMA-like alloantigens develop vigorous memory cytotoxic responses

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

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

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

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

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

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

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

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

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

109 RBC alloantigens exist at different densities on the RBC sur

110 Direct presentation of alloantigen expressed on donor leukocytes is recognized

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

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

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

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

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

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

117 ial within the first 48 hours of exposure to alloantigen for the establishment of tolerance and mixed

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

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

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

121 lammatory cytokine production in response to alloantigen in mice.

122 T cells stimulated in vitro with mitogen and alloantigen in the presence or absence of immunosuppress

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

124 responses to anti-CD3 monoclonal antibody or alloantigens in a major histocompatibility complex nonsp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 anti-CD28-PV1-IgG3 exhibited suppression of alloantigen-initiated proximal TCR signaling events, inc

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

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

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

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

150 The alloantigen is restricted by I-A and appears to be widel

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

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

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

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

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

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

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

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

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

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

161 allograft survival by reducing activation of alloantigen-mediated key signaling events in T cells tha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 between the direct and indirect pathways of alloantigen presentation and suggests that MHC transfer

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

178 These data suggest that although alloantigen presentation in secondary lymphoid organs is

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

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

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

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

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

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

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

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

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

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

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

190 n vitro, and mixed lymphocyte reaction using alloantigen-primed Mac-1(-/-) macrophages resulted in si

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 e pathways involved in T-cell activation and alloantigen recognition, effector cells and pathways med

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

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

205 t coordinate tissue damage in autoimmune and alloantigen responses.

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

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

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

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

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

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

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

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

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

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

216 suggesting that this cytokine production was alloantigen specific.

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

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 The strategy of induction of alloantigen-specific hyporesponsiveness ("alloanergizati

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 antagonize tolerogenic regimens by enhancing alloantigen-specific immune responses independently of t

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

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

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

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

248 ombined CXCR3 and CCR5 blockade also reduced alloantigen-specific T lymphocyte proliferation.

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 Moreover, graft protection was alloantigen-specific.

262 The alloantigen specificity demonstrated by B cell-expanded

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

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

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

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

267 1(-/-) T cells proliferated vigorously under alloantigen stimulation, and also that the antigen-prese

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

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

270 of IL-10 in response to both polyclonal and alloantigen stimuli.

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

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

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

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

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

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

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

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

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

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

281 anism by which passenger leukocytes transfer alloantigens to recipient's APCs and amplify generation

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

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

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

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

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

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

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

289 When alloantigen was presented directly, the precursor freque

290 When alloantigen was presented indirectly, the frequency of s

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

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

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

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

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