ライフサイエンスコーパス: alloreactive

1 CRalpha, and we hypothesized they are highly alloreactive.

2 ese findings dovetail with recent studies of alloreactive and autoimmune TCRs and suggest that the bi

3 Thus, the requirements for tolerizing alloreactive and autoreactive NOD CD4 cells are distinct

4 egs) control the activation and expansion of alloreactive and autoreactive T cell clones.

5 ional mechanism for activating and expanding alloreactive and autoreactive T cells.

6 Here, we demonstrate that alloreactive and nonalloreactive TCR differ specifically

7 Instead, macrophages become alloreactive and readily recognize and reject allogeneic

8 Alloreactive antibodies were solely found in dexDC-treat

9 was used to monitor glucose, C-peptide, and alloreactive antibodies.

10 led that, despite fundamental differences in alloreactive B cell fates in sensitized versus naive rec

11 plant immunology has been on controlling the alloreactive B cell population, long-term transplant pat

12 Collectively, these data suggest that alloreactive B cell responses in this model of tolerance

13 on of T cell help as well as the deletion of alloreactive B cells in the periphery.

14 for the identification of comparable memory alloreactive B cells in transplant recipients.

15 ing tools to monitor donor-specific B cells, alloreactive B cells were shown to increase in accordanc

16 steps that are involved in the generation of alloreactive B cells, with a specific emphasis on how kn

17 high sensitivity or specificity but not for alloreactive B-cells, especially among recipients predis

18 rease in the activation and proliferation of alloreactive CD4 and CD8 T cells after transplantation a

19 a 3-cell tolerance model involving directly alloreactive CD4 cells, donor antigen-expressing bone ma

20 Alloreactive CD4 T cell-mediated MVEC death involves TNF

21 In vitro, alloreactive CD4 T cells were competent to lyse donor ma

22 Alloreactive CD4 T cells were isolated from peripheral b

23 s and culminates in the deletion of directly alloreactive CD4 T cells.

24 visualization of the fate of TCR-transgenic alloreactive CD4(+) and CD8(+) T cells after encounterin

25 reveal parallel roles for Notch signaling in alloreactive CD4(+) and CD8(+) T cells that differ from

26 e studied the effects of Notch inhibition in alloreactive CD4(+) and CD8(+) T cells using mouse model

27 rolling proliferation and differentiation of alloreactive CD4(+) conventional T cells in draining lym

28 We detected significant numbers of alloreactive CD4(+) donor T cells expressing IL-17, IL-1

29 However, Notch-deprived alloreactive CD4(+) T cells retained significant cytotox

30 Anti-CD20 Ab had a major effect on alloreactive CD4(+) T cells, increasing the expansion of

31 T cells increased IFN-gamma production from alloreactive CD4(+) T cells, whereas blockade of dendrit

32 g of Treg, which diminished proliferation of alloreactive CD4(+) T cells.

33 immunotherapy is limited by the increase in alloreactive CD4(+) T lymphocytes.

34 Alloreactive CD4CD45RA/CD45RO T cells generated in 9-day

35 ioresistant immune cells in GVHD recipients, alloreactive CD62L(-) T cells lost the reactivity over t

36 /PD-L1 pathway is needed to rapidly tolerize alloreactive CD8 cells in a model that requires CD4 cell

37 nating in deletional tolerance of peripheral alloreactive CD8 cells.

38 multaneously present it as intact protein to alloreactive CD8 T cells and as processed peptide alloan

39 the magnitude, diversity, and specificity of alloreactive CD8 T cells in patients who developed GVL r

40 h B cells expressing Patr-AL produced potent alloreactive CD8 T cells with specificity for Patr-AL an

41 Alloreactive CD8 T effector (Teff) activation and T memo

42 treated with costimulation blockade deleted alloreactive CD8 T-cells and exhibited prolonged islet a

43 Although B cells were important for optimal alloreactive CD8 Teff/Tmem function in the sensitization

44 se recipients, the rejection was mediated by alloreactive CD8(+) T cells presumably primed in the bon

45 ulting in reduced frequencies of circulating alloreactive CD8(+) T cells.

46 ated that CD27low NK cells directly regulate alloreactive CD8+ Tcell responses under costimulatory bl

47 ot inhibit nTreg-mediated suppression of Th1 alloreactive cells but increased IL-17 production by eff

48 WT recipients of these alloreactive cells developed anti-dsDNA autoantibodies s

49 LR revealed increased dual TCR T cells among alloreactive cells.

50 ble to drive proliferation of autologous and alloreactive conventional T cells, as seen with B cells

51 The alloreactive CTL precursor (CTLp) frequency was determin

52 that irradiated allografts did not elicit an alloreactive delayed-type hypersensitivity response in g

53 However, perforin-deficient alloreactive DLI induced significantly less apoptosis of

54 Alloreactive DNMAML T cells exhibited decreased Ras/MAPK

55 arenchymal cells controls the second wave of alloreactive donor CD8(+) T cell expansion and the assoc

56 aft-versus-host disease (GVHD), triggered by alloreactive donor cells, has remained a major complicat

57 Alloreactive donor cytolytic T lymphocytes play a critic

58 Efforts to limit GVHD mediated by alloreactive donor T cells after allogeneic bone marrow

59 Alloreactive donor T cells against host minor histocompa

60 ighlight CNS sensitivity to damage caused by alloreactive donor T cells and represent the first chara

61 Alloreactive donor T cells are critical for causing GVHD

62 Alloreactive donor T cells are the driving force in the

63 Alloreactive donor T cells attack leukemia cells, mediat

64 Alloreactive donor T cells can damage thymic epithelium,

65 by extensive activation and proliferation of alloreactive donor T cells causing significant morbidity

66 PD-1H coinhibitory receptor potently arrests alloreactive donor T cells from activation and expansion

67 s-host disease (GVHD), which is initiated by alloreactive donor T cells that recognize mismatched maj

68 ggest that infusion of sufficient numbers of alloreactive donor T cells will induce GVHD in the absen

69 y antigen-presenting cells (APCs) that prime alloreactive donor T cells.

70 sease (GVHD) is initiated by APCs that prime alloreactive donor T cells.

71 )FOXP3(+)) through the in vivo conversion of alloreactive donor T effectors (Teffs; CD4(+)CD25(-)FOXP

72 ectively protects against GVHD by modulating alloreactive donor T-cell responses, and that CXCR3 sign

73 energetics profile analysis of proliferating alloreactive donor T-cells demonstrated increased aerobi

74 oreover, under IL-4 neutralizing conditions, alloreactive double-deficient T cells upregulated Eomeso

75 A significant fraction of alloreactive Drak2-/- T cells underwent apoptosis follow

76 ves the rapid rejection of the NE-CBU, whose alloreactive effect might also contribute to graft-versu

77 an allograft via the differential control of alloreactive effector and regulatory T cell survival.

78 Alloreactive effector CD4(+) T cells toward 1 or more mi

79 hylation leads to selective apoptosis of the alloreactive effector cells.

80 Here, we demonstrate that alloreactive effector T cells (Teff) use fatty acids (FA

81 e preserving GVL by peripheral conversion of alloreactive effector T cells into FOXP3(+) Tregs and ep

82 vivo administration of Dll4 Ab reduced donor-alloreactive effector T cells producing IFN-gamma and IL

83 Alloreactive effector T cells that expanded in the absen

84 ability of the resulting T cells to suppress alloreactive effector T-cell proliferation was assessed.

85 on, type I differentiation, and expansion of alloreactive effectors.

86 CD19-specific (CD19-CAR) T cells possessing alloreactive endogenous T-cell receptors.

87 essing clonal anti-H2K T cell receptor (TCR) alloreactive for MHC I, graft survival was significantly

88 the most potent at inducing high numbers of alloreactive Foxp3(+) cells.

89 per T-cell increases, elevated antiviral and alloreactive functional responses, and significantly gre

90 both T-bet and RORgammat differentiated into alloreactive GATA-3-expressing Th2 cells, which promptly

91 geneic immunity, with complete prevention of alloreactive H-Y Ab development in male patients with fe

92 between CBUs in dUCBT, we hypothesized that alloreactive HLA class II-specific CD4(+) T cells from t

93 Consequently, alloreactive HLA-A2-specific cytotoxic T cells failed to

94 beta-cells in the absence or presence of an alloreactive human immune system.

95 mechanisms associated with their actions on alloreactive human T cells are not fully understood.

96 as associated with an increased frequency of alloreactive IFN-gamma-, IL-4-, and IL-6-producing splen

97 was accompanied by increased frequencies of alloreactive IFN-gamma-, IL-6-, and IL-17-producing sple

98 ted a standard operating procedure (SOP) for alloreactive IFNgamma ELISPOT assays in several research

99 e requires elimination and/or suppression of alloreactive immune cells.

100 VHD without altering the load or function of alloreactive immune cells.

101 lerogenic cytokine that efficiently inhibits alloreactive immune responses and mediates transplant to

102 f the potential importance of fetal-specific alloreactive immune responses within disorders of pregna

103 h CD8+ and CD4+ Tregs and markedly inhibited alloreactive immune responses.

104 survival by inhibiting the proliferation of alloreactive interferon-gamma+CD8+ T cells.

105 C5aR signaling on induction and stability of alloreactive iTreg.

106 cell transplantation in which donor-derived (alloreactive) KIR2DS1(+) NK cells, upon CCR7 acquisition

107 proinflammatory cytokines, and expansion of alloreactive luc-transgenic T cells.

108 cally, a transient reversal in the anergy of alloreactive lymphocytes is seen in parallel with the gl

109 s dependent on the frequency and function of alloreactive lymphocytes, making the identification and

110 timulatory blockade conditions by regulating alloreactive memory CD8+ T-cell responses.

111 et-/- recipients showed strikingly increased alloreactive memory CD8+ Tcell responses, as indicated b

112 Alloreactive memory helper T cells can induce potent all

113 blockade regimen suppressed proliferation of alloreactive memory T cells and attenuated their cytokin

114 Recent evidence suggests that alloreactive memory T cells are generated by the process

115 stant rejection and specifically the role of alloreactive memory T cells in mediating this resistance

116 The presence of alloreactive memory T cells is a major barrier for induc

117 e efficacy of the regimen, since preexisting alloreactive memory T cells might be stimulated by the t

118 Alloreactive memory T cells prevent costimulatory blocka

119 cell responses and long-term persistence of alloreactive memory T cells specific for the tumor, ofte

120 was able to suppress cytokine production by alloreactive memory T cells that was resistant to belata

121 To compare the fates of alloreactive naive (T(N)) or memory (T(M)) T cells, we d

122 terfere with immunoregulation established by alloreactive natural CD4(+)Foxp3(+) Tregs.

123 Alloreactive natural killer (NK) cells are an important

124 Alloreactive natural killer (NK) cells can be recruited

125 V-1 transmission and that this may be due to alloreactive NK cell killing of the HIV-1-infected partn

126 In conclusion, KIR2DS2 identifies potent alloreactive NK cells against GBM that are mediated by c

127 will inform strategies to develop functional alloreactive NK cells for therapeutic use.

128 egulated inflammatory cytokine production by alloreactive NK cells in response to infectious challeng

129 , rapid killing of donor lymphocytes by host alloreactive NK cells is essential.

130 d hematopoietic stem cell transplants induce alloreactive NK cells, which prevent leukemia relapse.

131 These findings suggest that alloreactive passenger B cells/plasma cells within the k

132 role for interactions of CTLA-4 expressed by alloreactive peripheral CD4 T cells with CD80/86 on reci

133 It is also effective in depleting both alloreactive plasma cells in acute Ab-mediated transplan

134 It results from alloreactive processes induced by minor MHC incompatibil

135 In addition, hPB-MSCs suppressed alloreactive proliferation as well as the production of

136 d that this antitumor effect was mediated by alloreactive rather than EBV-specific T cells.

137 Quantitative assessment of the alloreactive repertoire demonstrated a nearly 50% reduct

138 e that within the functionally heterogeneous alloreactive repertoire, there is the potential for high

139 strain has significantly impacted the immune alloreactive response in the GVHD model by causing alter

140 d mononuclear cells (PBMC) and the resultant alloreactive response studied.

141 ensors, effectors, suppressors of the immune alloreactive response, and the resultant tissue damage f

142 of suppression utilised by Tregs to control alloreactive responses are ongoing.

143 yclophosphamide (pt-Cy) effectively prevents alloreactive responses from unmanipulated grafts, but it

144 eptors such as CCR5 plays a critical role in alloreactive responses, and previous data suggest that C

145 respectively, which allowed us to study the alloreactive role of each subset in an experimental tran

146 Although simple alloreactive rules have been established for inhibitory

147 ts; however, although TR cells proved highly alloreactive, SE cells showed a favorable safety profile

148 Importantly, also putatively alloreactive single KIR(+) NK cells were eliminated by P

149 l tolerance was caused by clonal deletion of alloreactive specificities from the primary B cell reper

150 d developing approaches to track and analyze alloreactive T and B cells in mice and humans and provid

151 s, making the identification and analysis of alloreactive T and B cells in transplant recipients crit

152 models, which implicates clonal deletion of alloreactive T and B cells, induction of cell-intrinsic

153 a proinflammatory gene program that enhances alloreactive T cell activation and development of cardia

154 gated by the presence of anti-K(d) mAbs, and alloreactive T cell activation as well as acute rejectio

155 Current therapies to prevent alloreactive T cell activation largely cause generalized

156 PD-1 signaling inhibits alloreactive T cell activation, and can promote induced

157 ss damage inflicted exclusively by DSAs when alloreactive T cell and B cell responses coincide.

158 long-term graft survival was associated with alloreactive T cell anergy.

159 opoietic cells is involved in the control of alloreactive T cell apoptosis and expansion.

160 oreover, PDL1 blockade inhibited Ag-specific alloreactive T cell apoptosis and induced apoptosis of T

161 The repertoire of alloreactive T cell clones is distinct for every donor-r

162 in vivo proliferation but preserved overall alloreactive T cell expansion while enhancing accumulati

163 toire demonstrated a nearly 50% reduction in alloreactive T cell frequency among T cells incapable of

164 ed a low-fat diet, correlating with enhanced alloreactive T cell function.

165 We directly demonstrated expansion of the alloreactive T cell repertoire at the single cell level

166 The size and diversity of the HLA-alloreactive T cell repertoire has thus far precluded th

167 associated with a lack of a proinflammatory alloreactive T cell response and an activation/expansion

168 The factors that drive the alloreactive T cell response are not completely understo

169 ation of donor DCs efficiently initiates the alloreactive T cell response that causes acute rejection

170 reof we demonstrated that the attenuation of alloreactive T cell responses after G-CSF mobilization r

171 By separating these seemingly similar alloreactive T cell responses based on the context of in

172 Accordingly, these mice restricted alloreactive T cell responses during graft-versus-host r

173 cure hematological malignancies by inducing alloreactive T cell responses targeting minor histocompa

174 Mismatched HLA-DP is targeted by direct alloreactive T cell responses with important implication

175 h its phenotype and suppression of antidonor alloreactive T cell responses.

176 D4(+) Tregs and potently suppressed in vitro alloreactive T cell responses.

177 Previously, we found that alloreactive T cell targeting of GVL-sensitive bcr-abl-i

178 s among T(N) and T(M), and to track fates of alloreactive T cells after transplantation.

179 pient lymphoid tissues and directly activate alloreactive T cells against donor MHC molecules.

180 -gamma-deficient donor T cells, or depleting alloreactive T cells all compromised intratumoral IFN-ga

181 for the potentially different frequencies of alloreactive T cells among T(N) and T(M), and to track f

182 mice, enhanced the ability of APCs to prime alloreactive T cells and accelerated graft rejection, su

183 unded by effector mechanisms of uncontrolled alloreactive T cells and anti-HLA antibodies.

184 Alloreactive T cells and anti-human leukocyte antigen an

185 Integrin-mediated adhesion between alloreactive T cells and antigen-presenting cells is ess

186 sentation of donor MHC molecules to directly alloreactive T cells and delayed graft rejection in mice

187 In cGVHD, alloreactive T cells and germinal center (GC) B cells of

188 ction of PD-1H as a coinhibitory receptor on alloreactive T cells and its function in the regulation

189 -mediated suppression and thymic deletion of alloreactive T cells and may represent general condition

190 neic BM transplantation tolerizes peripheral alloreactive T cells and permits establishment of mixed

191 vation of DN T cells specifically suppressed alloreactive T cells and prevented the development of gr

192 cells are thought to control the priming of alloreactive T cells and the induction of acute GVHD aft

193 isms of tGVHD and interactions between donor alloreactive T cells and thymic tissues remain poorly de

194 is PD-1(Hi)ROS(Hi) phenotype was specific to alloreactive T cells and was not observed in syngeneic T

195 Alloreactive T cells are crucial for graft-versus-host d

196 We show in this study that alloreactive T cells are initially primed within lung al

197 it has been difficult to selectively delete alloreactive T cells because the majority of protocols e

198 t singularly dependent on depletion of donor alloreactive T cells but also requires rapidly recoverin

199 de of FA oxidation decreased the survival of alloreactive T cells but did not influence the survival

200 indicate that PD-1 facilitates apoptosis in alloreactive T cells by increasing ROS in a process depe

201 ithymocyte globulin facilitates apoptosis of alloreactive T cells by means of caspase-3 activation, w

202 Thus in GVHD, alloreactive T cells can be activated when pathways crit

203 Selective depletion of the alloreactive T cells causing graft-versus-host disease (

204 We found that both murine and human alloreactive T cells concomitantly upregulated PD-1 expr

205 emory T cells provide help for activation of alloreactive T cells despite the costimulatory blockade.

206 We demonstrate that alloreactive T cells expressing CD28-costimulated CD19 C

207 rvous system (CNS) can be a direct target of alloreactive T cells following allo-HSCT in mice.

208 Heterologous memory alloreactive T cells generated by infections prior to tr

209 ctions, as effector, regulatory, memory, and alloreactive T cells have distinct metabolic needs in im

210 ole in the transplant setting by maintaining alloreactive T cells in a hyporesponsive state, but has

211 eic antigens and activate both CD4+ and CD8+ alloreactive T cells in an MHC-restricted fashion.

212 PD-1H may be a target for the modulation of alloreactive T cells in GVHD and transplantation.

213 igated the impact of donor NK cells on donor alloreactive T cells in GVHD induction.

214 ys can provide a new window into the fate of alloreactive T cells in human transplant recipients.

215 rkedly increased accumulation of DLI-derived alloreactive T cells in parenchymal GVHD target tissues.

216 tch inhibition decreased the accumulation of alloreactive T cells in the intestine, a key GVHD target

217 Spi6(-/-) nTregs and impaired suppression of alloreactive T cells in vitro.

218 Alloreactive T cells increased FA transport, elevated le

219 D, novel strategies that selectively deplete alloreactive T cells or modulate the balance of effector

220 ifferential susceptibility of proliferating, alloreactive T cells over nonproliferating, nonalloreact

221 In addition, alloreactive T cells primed in the absence of Notch sign

222 Furthermore, to mediate tGVHD, donor alloreactive T cells required trafficking molecules, inc

223 splant studies indicate that GVHD-initiating alloreactive T cells reside primarily in naive and centr

224 rdiac allograft vasculopathy lesions contain alloreactive T cells that secrete interferon-gamma, a va

225 fts associated with impaired localization of alloreactive T cells to heart grafts.

226 Attempts to manipulate alloreactive T cells to spare normal cells while killing

227 al and fluorescent microscopy, we found that alloreactive T cells traffic distinctly into the toleran

228 inflamed endothelium, is important for donor alloreactive T cells trafficking into GVHD target organs

229 Donor alloreactive T cells used the cognate proteins FasL and

230 whether PTCy works singularly by eliminating alloreactive T cells via DNA alkylation or also by resto

231 In vivo expansion of alloreactive T cells was diminished while displaying a T

232 Lymphoid neogenesis containing alloreactive T cells was observed in the lungs, which re

233 in which we were able to selectively deplete alloreactive T cells with an indirect specificity by tar

234 and IFNgamma production, by naive and memory alloreactive T cells, and observed an increased frequenc

235 he degree of antigen specificity mediated by alloreactive T cells, and their ability to discriminate

236 ocalization of alloantigen-presenting cells, alloreactive T cells, and Tregs.

237 Therefore, direct priming of alloreactive T cells, as well as rejection and regulator

238 se inhibitors can block all Notch signals in alloreactive T cells, but lead to severe on-target intes

239 PT-Cy selectively eliminates proliferating alloreactive T cells, but whether and how it affects nat

240 d decreased IFN-gamma and IL-4 production by alloreactive T cells, especially when combined with depl

241 2 ablation retained antileukemia activity in alloreactive T cells, leading to improved overall surviv

242 in T-cell allografts attenuates expansion of alloreactive T cells, leading to lower GVHD.

243 Thus, although TAC inhibits all alloreactive T cells, SRL promotes the differentiation a

244 t murine TRAIL+ T cells induced apoptosis of alloreactive T cells, thereby reducing GVHD in a DR5-dep

245 although Th17 cells differentiate from naive alloreactive T cells, these cells do not arise from natu

246 show here that even minimal numbers of donor alloreactive T cells, which caused mild nonlethal system

247 MEK inhibitors would preferentially inhibit alloreactive T cells, while sparing more differentiated

248 an endothelial cells to recruit and activate alloreactive T cells.

249 ction via direct cytotoxicity and priming of alloreactive T cells.

250 -mediated suppression and thymic deletion of alloreactive T cells.

251 VL) effect that is mediated by donor-derived alloreactive T cells.

252 genic profile and inhibited proliferation of alloreactive T cells.

253 se herbs for their ability to suppress human alloreactive T cells.

254 questration of IL-2 produced by conventional alloreactive T cells.

255 but decreased the functional activity of the alloreactive T cells.

256 ng in vivo prevented miR-214 upregulation in alloreactive T cells.

257 ate the CD40-CD154-independent activation of alloreactive T cells.

258 molecules on host APCs and the generation of alloreactive T cells.

259 tokines, consequently enhancing responses of alloreactive T cells.

260 ing the CD40-CD154-independent activation of alloreactive T cells.

261 enting cells (APCs) and decreased priming of alloreactive T cells.

262 llenges, and recent advances in the study of alloreactive T cells.

263 e of Notch ligands during in vivo priming of alloreactive T cells.

264 e activated and triggered full activation of alloreactive T cells.

265 ceiving heart allografts have suppression of alloreactive T effector cells and delayed acute rejectio

266 AAT treatment reduced the expansion of alloreactive T effector cells but enhanced the recovery

267 Alloreactive T lymphocytes are the primary mediators of

268 e amelioration of GA primarily by inhibiting alloreactive T-cell accumulation and consequent IFN-gamm

269 that disrupts essential signals required for alloreactive T-cell activation.

270 Alloreactive T-cell apoptosis may explain reduced immuno

271 and incubated with either indirect or direct alloreactive T-cell clones.

272 , LFA-1 blockade inhibits initial endogenous alloreactive T-cell expansion and induces more regulatio

273 anti-human leukocyte antigen antibodies, and alloreactive T-cell immunity (interferon-gamma ELISPOT)

274 ay CD4 T cells are likely to be the dominant alloreactive T-cell population late after transplantatio

275 esulted in decreased T-cell infiltration and alloreactive T-cell priming as well as improved function

276 S did not directly interfere with vigorously alloreactive T-cell proliferation in vivo and in vitro.

277 how no effect on moDC maturation/activation, alloreactive T-cell proliferation, Treg expansion, or al

278 se of CsA to the culture medium, suppressing alloreactive T-cell proliferation.

279 re directly demonstrated by expansion of the alloreactive T-cell repertoire through the addition of p

280 ctor composition of both ones protective and alloreactive T-cell repertoire.

281 o T cells, thus causing the equivalent of an alloreactive T-cell response.

282 T cells may underlie its ability to inhibit alloreactive T-cell responses after transplantation.

283 erum levels of HS, leading to a reduction in alloreactive T-cell responses and GVHD severity.

284 nor-derived DCs, which otherwise would prime alloreactive T-cell responses.

285 ing the negative role of B7-H4 in regulating alloreactive T-cell responses.

286 enhancement of dendritic cell maturation and alloreactive T-cell responses.

287 ystem that could be used to monitor indirect alloreactive T-cells.

288 asing interest in the monitoring of indirect alloreactive T-cells.

289 When these "alloreactive" T cells were removed from the MHC(B) reper

290 d cytotoxic T lymphocyte-mediated killing of alloreactive target cells.

291 gulating the differentiation and function of alloreactive Tc cells in vitro was explored by stimulati

292 Here, we show how an alloreactive TCR achieves peptide and MHC specificity.

293 s help explain the paradox of specificity in alloreactive TCRs and have implications for their use in

294 in unclear, the existence of highly specific alloreactive TCRs has led to their use as immunotherapeu

295 indicating that additional pathways restrain alloreactive TEM TS1 TN also caused more severe GVHD wit

296 1c-specific Rictor(-/-) mice, we confirm the alloreactive Th1 and Th17 cell-polarizing ability of end

297 n WT, in vivo cytotoxic activity analysis of alloreactive Tmem recall response has revealed decreased

298 erent affinity for MHC, most T cells are not alloreactive to a given MHC.

299 s educated on these mutant MHC molecules are alloreactive to each other and to WT cells, and vice ver

300 e B cells preferentially induce expansion of alloreactive Treg cells, we report herein that human Tre