ライフサイエンスコーパス: antigen-specific

1 Treg cell suppression was shown to be antigen specific.

2 mmunosuppression induced by these T cells is antigen specific.

3 ical trials are either polyclonal, donor- or antigen-specific.

4 n is evident during antigen-specific and non-antigen-specific activations.

5 ngeneic tumor immunotherapy models including antigen-specific adoptive T-cell transfer, agonistic ant

6 he skin, in the presence of IL-33, developed antigen-specific airway inflammation when later challeng

7 This disease-modifying effect is both antigen-specific and antigen-driven.

8 2/PGE2-induced suppression is evident during antigen-specific and non-antigen-specific activations.

9 The T cell lines were antigen-specific and showed no nonspecific alloreactivit

10 We quantified antigen-specific antibodies after infection and found si

11 Immunoprecipitation with HBV core antigen-specific antibodies after removal of the HBV sur

12 use of surface plasmon resonance to quantify antigen-specific antibodies and evaluate their apparent

13 itial disease resulting from proximal tubule antigen-specific antibodies and immune complex formation

14 Moreover, antigen-specific antibodies raised against sheaths prese

15 oral immunity is generated and maintained by antigen-specific antibodies that counter infectious path

16 HBV DNA were quantified by PCR reaction, and antigen-specific antibodies were detected by immunocytoc

17 l center B cells, and plasma cells secreting antigen-specific antibodies, as well as macrophages, upo

18 munization, B-cells generate a repertoire of antigen-specific antibodies.

19 s') that induce the selective degradation of antigen-specific antibodies.

20 ovel cytometric bead array for assessment of antigen-specific antibody concentration in plasma to eva

21 Antigen-specific antibody concentration measured 1 month

22 ighly accelerated plasma cell generation and antigen-specific antibody production.

23 me of immunization delays the development of antigen-specific antibody responses but does not permane

24 Clinical studies indicate that antigen-specific antibody responses can be maintained fo

25 ful vaccine must generate desired long-term, antigen-specific antibody responses devoid of polyreacti

26 ed vaccines induced robust innate responses, antigen-specific antibody responses of a greater magnitu

27 especially the generation of class-switched, antigen-specific antibody responses.

28 triple adjuvant combination showed increased antigen-specific antibody titer with an overall balanced

29 Vaccination induces robust antigen-specific antibody, plasmablasts, and CD4(+) T ce

30 B cells resulted in a dramatic reduction of antigen-specific antibody-secreting cells, whereas delet

31 inflammasome contributes to the induction of antigen-specific antitumour immunity and pathogenesis of

32 By simultaneously analyzing antigen-specific ASCs and ABCs in human blood after vacc

33 This stimulation induces antigen-specific B cell proliferation, differentiation o

34 creen and magnetically enrich the responding antigen-specific B cells before fusion and validation, t

35 Antigen-specific B cells bifurcate into antibody-secreti

36 ent of reagents to identify and characterize antigen-specific B cells has been challenging.

37 NV-1 infections to analyze the phenotypes of antigen-specific B cells that reflected their exposure o

38 Importantly, very high numbers of antigen-specific B cells were detected in local genital

39 wo weeks and analysed by CN54gp140 ELISA and antigen-specific B cells were measured by flow cytometry

40 e and transcriptional program of a subset of antigen-specific B cells, which we have called 'activate

41 required for the generation of high-affinity antigen-specific B cells.

42 These data show that antigen-specific B lymphocytes and T lymphocytes are act

43 Antigen-specific B-cell development and affinity maturat

44 t about 30% of CLL patients have stereotyped antigen-specific B-cell receptors (BCRs) with a high lev

45 Malaria antigen-specific B5 T cell receptor (TCR) transgenic (Tg

46 ble to modify T cells to secrete solid tumor antigen-specific BITEs, enabling T cells to redirect res

47 rotubule-based motor increases activation of antigen-specific CD4 T cells by infected cells and impro

48 In addition, antigen-specific CD4 T cells deficient in MCPIP1 were tr

49 et to date, TB vaccine candidates that boost antigen-specific CD4 T cells have conferred little or no

50 immunity induced by IKEPLUS is dependent on antigen-specific CD4(+) T cell memory, we hypothesized t

51 chanisms underlying long-term persistence of antigen-specific CD4(+) T cells are not well-defined.

52 e able to present the antigens to autologous antigen-specific CD4(+) T cells in a major histocompatib

53 al IFN-gamma ELISpot with an assay to detect antigen-specific CD4(+) T cells that does not rely on te

54 emerged as a powerful tool for interrogating antigen-specific CD4(+) T cells without relying on effec

55 rophages and dendritic cells to activate Mtb antigen-specific CD4(+) T cells.

56 a from co-cultures of DCs and autologous Mtb antigen-specific CD4(+) T cells.

57 secreted inflammatory cytokines and induced antigen-specific CD4(+) T-cell activation.

58 esxH-deficient strain induced fivefold more antigen-specific CD4(+) T-cell proliferation in the medi

59 Antigen-specific CD4+ T cells have long been regarded as

60 ers are an essential tool for characterizing antigen-specific CD4+ T cells.

61 The antigen-specific CD4CD25 T cells that control rejection

62 lsion promoted most robust, functional HSV-2 antigen-specific CD8 T cell responses and high titers of

63 unization, the frequency and cytotoxicity of antigen-specific CD8 T cells in DRAGA mice was significa

64 ation, increasing their capacity to activate antigen-specific CD8 T cells in renal draining lymph nod

65 ggesting that local virus replication drives antigen-specific CD8 T cells into the breast.

66 onstrate that the PD-1 epigenetic program in antigen-specific CD8 T cells is fixed during the priming

67 though evidence for the importance of HSV-2 antigen-specific CD8 T cells is mounting in animal model

68 values predicted that human LC activation of antigen-specific CD8 T cells would be differentially reg

69 ue to determine the frequency and potency of antigen-specific CD8 T cells.

70 protein 4) immunotherapy generated a potent antigen-specific CD8 T-cell response, enhancing expansio

71 x elicits 10 times more frequent peripheral antigen-specific CD8(+) cytotoxic T lymphocytes with imm

72 els of Chagas disease have demonstrated that antigen-specific CD8(+) gamma interferon (IFN-gamma)-pos

73 gen 1 (TSA1), induced significant numbers of antigen-specific CD8(+) IFN-gamma-positive cells followi

74 cDC depletion abrogated antigen-specific CD8(+) T cell proliferative expansion,

75 e-treated dendritic cells (DCs) to stimulate antigen-specific CD8(+) T cell responses.

76 Both antigen-specific CD8(+) T cells and profibrotic cytokine

77 to a synergistic increase in total and tumor antigen-specific CD8(+) T cells expressing both IFN-gamm

78 deficiency does not affect the generation of antigen-specific CD8(+) T cells following IAV infection;

79 rgo release was the generation of long-lived antigen-specific CD8(+) T cells that accumulate in mucos

80 nt manner, and generates a pool of activated antigen-specific CD8(+) T cells with cytotoxic potential

81 y increased the number of effector-phenotype antigen-specific CD8(+) T cells within the tumor.

82 approaches and transcriptional profiling of antigen-specific CD8(+) T cells, we reveal a common prog

83 d qualitative effects on effector and memory antigen-specific CD8(+) T cells.

84 total number of B cells, CD4(+) T cells, and antigen-specific CD8(+) T cells.

85 o evolve in the presence of autologous tumor antigen-specific CD8(+) T cells.

86 immunity and specifically the activation of antigen-specific CD8(+) T cells.

87 3 and 4-1BB can identify dysfunctional tumor antigen-specific CD8(+) TIL.

88 When examining antigen-specific CD8+ T cell function, all the LRAs exce

89 phenotype and proliferative ability of tumor antigen-specific CD8+ T cells was assessed in the presen

90 s- presented soluble prototypical protein to antigen-specific CD8+ T cells.

91 After influenza challenge, antigen-specific cells underwent several divisions in dr

92 e induced significantly higher proportion of antigen specific central memory CD8(+) cells, and both a

93 critically dependent on the balance between antigen-specific central memory T (Tcm) and effector mem

94 lter the tumor microenvironment allowing for antigen-specific clearance tumor cells.

95 nd effects of antigen exposure on individual antigen-specific clones, the cellular subset structure p

96 have utility as HIV-1 immunogens or in other antigen-specific contexts, such as with B-cell probes.

97 PC nanogel significantly enhanced antigen-specific cross-presentation and cytotoxic T lymp

98 II candidate T-cell epitopes with potential antigen-specific cross-reactivity between influenza and

99 a bolus of enhanced IL-21-primed polyclonal antigen-specific CTL combined with CTLA4 blockade might

100 Thus, a fully functional, ongoing, antigen-specific CTL response may influence bystander CD

101 udy reveals a positive feedback loop between antigen-specific CTLs and APC to amplify adaptive immuni

102 t exposure of tumours to IFN-gamma-producing antigen-specific CTLs in vivo results in copy-number alt

103 er CD8(+) T cells, but the contribution from antigen-specific CTLs is not well understood.

104 Perforin from antigen-specific CTLs is required for NLRP3 inflammasome

105 Conclusion We demonstrate that combining antigen-specific CTLs with CTLA-4 blockade is safe and p

106 egulated kinase (ERK) antigen, the action of antigen-specific cytotoxic T cell (CTL) in vivo results

107 h TCR-engineered HSPCs produced T cells with antigen-specific cytotoxicity and near-complete lack of

108 al and inhibited HCV RNA replication through antigen-specific cytotoxicity.

109 Achromobacter species possess a Vi antigen-specific depolymerase enzyme missing in S enteri

110 tigen receptors (CARs) for the generation of antigen-specific effector T cells suggests that a simila

111 antified, and phenotype and functionality of antigen-specific effector T cells were analyzed with flo

112 Alternatively, antigen-specific effector/memory TH17 cells, generated i

113 Our findings suggest that antigen-specific ELISAs, particularly the OPS-ELISA, may

114 The cVLPs induced antigen specific endpoint titers and avidity indices of

115 ifunctional switches that consist of a tumor antigen-specific Fab molecule engrafted with a peptide n

116 e first evidence that NK cells respond in an antigen-specific fashion came from experiments revealing

117 iently eradicated subcutaneous myeloma in an antigen-specific fashion.

118 feline Ig sequences, a technique to express antigen-specific felinized monoclonal antibodies, and th

119 B cells but not on DCs in the generation of antigen-specific follicular helper T cells, antigen-spec

120 oreover, murine fetal DCs effectively primed antigen-specific forkhead box P3(+) regulatory T cells a

121 MAC, and disruption of this complex restored antigen-specific functional responses in these cells.

122 ced serum and vaginal wash antibodies and an antigen-specific gamma interferon-dominated Th1-biased T

123 antigen-specific follicular helper T cells, antigen-specific GC B cells, and high-affinity class-swi

124 ion, including the difficulty of quantifying antigen-specific GC Tfh cells and the difficulty of trac

125 We define the half-lives of antigen-specific germinal centers (23.3 days), IgE(+) an

126 orm, it is theoretically possible to produce antigen-specific highly neutralizing therapeutic polyclo

127 velopment and function of human CD4 T cells, antigen-specific human CD8 T cells, and immunoglobulin c

128 that mTOR signals play an essential role in antigen-specific humoral immune responses by differentia

129 inal centre formation, and the inhibition of antigen-specific hypersensitivity reactions.

130 asma cells producing somatically mutated gut antigen-specific IgA antibodies but have also been sugge

131 independent antigen, a substantial number of antigen-specific IgA-secreting cells was found in the li

132 the airway epithelium; and the production of antigen-specific IgE and IgG1 in serum.

133 une responses associated with development of antigen-specific IgE antibodies can contribute to pathol

134 ssically elicited by antigen crosslinking of antigen-specific IgE bound to the high-affinity IgE rece

135 , plasma histamine levels, basophil numbers, antigen-specific IgE, cytokine levels, and IL-4, INF-gam

136 Recently, tumor antigen-specific IgEs were reported to restrict cancer c

137 revealed that all animals exhibited mucosal antigen-specific IgG and IgA with the IgA responses 30-f

138 itors 1 and 2 led to effective inhibition of antigen-specific IgG and IgM formation after immunizatio

139 selection-Tcrbeta repertoire is impaired and antigen-specific IgG antibody responses following immuni

140 that the microbiota is critical for inducing antigen-specific IgG production after intranasal immuniz

141 d germ-free (GF) mice had reduced amounts of antigen-specific IgG, smaller recall-stimulated cytokine

142 ion of Tnfrsf14, diminishes plasma levels of antigen-specific IgG1 and IgE antibodies, airway hyperre

143 /34 influenza virus induced higher levels of antigen-specific IgG2c isotype dominant antibodies in CD

144 There was significant correlation between antigen-specific IgGs for longevity but not for magnitud

145 onic hepatitis with 10-fold lower titers and antigen-specific IgGs, (anti-HBs, anti-HBc), consistent

146 activation in FALCs, resulting in local and antigen-specific IgM production.

147 ed differentiation of the naive T cells into antigen-specific IL-22-secreting cells.

148 Importantly, antigen-specific IL-6Ralpha(+)IL-7R(+) CD4(+) T cells em

149 s reveal that circulating and skin-resident, antigen-specific, IL-22-secreting T cells are detectable

150 PCA is a therapeutic modality for selective, antigen-specific immune modulation with significant tran

151 , how T-cells feedback to APCs to sustain an antigen-specific immune response is not completely clear

152 RIP-GP in C57BL/6) was used to evaluate the antigen-specific immune response.

153 reatment, which was sufficient to trigger an antigen-specific immune response.

154 We have elicited local genital antigen-specific immune responses after topical applicat

155 ation heightens the intensity and breadth of antigen-specific immune responses in young and aged mice

156 CD8(+) T cells mediate antigen-specific immune responses that can induce reject

157 he immune system and evaluated the resulting antigen-specific immune responses.

158 ntigens provides an attractive way to induce antigen-specific immune tolerance.

159 The generation of effective levels of antigen-specific immunity at the mucosal sites of pathog

160 application as an approach to initiate local antigen-specific immunity, enhance previously existing s

161 e skin early after antigen challenge retards antigen-specific immunity.

162 Antigen-specific immunoglobulin (Ig) G targeting Duffy b

163 en peptides currently being investigated for antigen specific immunotherapy (ASI) of type 1 diabetes.

164 Antigen specific immunotherapy mediated via the sustaine

165 Successful antigen-specific immunotherapy (ASIT) would allow for im

166 on and/or lymphocyte depletion prior to oral antigen-specific immunotherapy will likely be required t

167 bactericidal antibody (SBA) titers against 3 antigen-specific indicator strains, which are not necess

168 Here we show that antigen-specific, induced IgM plasma cells also persist

169 DCs is accompanied by reduced generation of antigen-specific, inducible FoxP3(+) regulatory T cells

170 anner became potent stimulators of localized antigen-specific inflammatory responses in the skin.

171 Adaptive cellular immunity is initiated by antigen-specific interactions between T lymphocytes and

172 suggesting peripheral innate activation (non-antigen-specific) is not required for immune priming.

173 NP-adjuvanted vaccines induced antigen-specific, long-lived plasma cells (LLPCs), which

174 GA-KAg via intranasal route showed increased antigen specific lymphocyte proliferation and enhanced t

175 ction of bringing together antigens and rare antigen-specific lymphocytes to foster induction of adap

176 In principle, unlabelled, highly tumour antigen specific mAb conjugates are, in a first step, ad

177 s (B cells, CD4(+) and CD8(+) T cells) in an antigen-specific manner.

178 st can suppress TH2-mediated responses in an antigen-specific manner.

179 es, where they suppress CD4(+) T cells in an antigen-specific manner.

180 hesis of OVA-specific IgG2a antibodies in an antigen-specific manner.

181 that anergy was selectively induced in fetal antigen-specific maternal CD4(+) T cells during pregnanc

182 of presenting vaccine antigen to autologous antigen-specific memory CD4(+) T cells ex vivo.

183 or the kinetics of the alloimmune and single antigen-specific memory T cell responses in the absence

184 suggesting CD161 is a marker for long-lived antigen-specific memory T cells.

185 ikely dominant T-cell epitopes, establishing antigen-specific memory T-cell lines for identifying CD8

186 mediated gene therapy effectively terminates antigen-specific memory T-cell responses and this can al

187 Techniques to obtain large quantities of antigen-specific monoclonal antibodies (mAbs) were first

188 After purification, antigen-specific mouse memory B cells are first single-c

189 clone the variable antibody region of single antigen-specific mouse memory B cells for antibody produ

190 and delivery method elicited high levels of antigen-specific mucosal IgA and large numbers of local

191 Increased antigen-specific mucosal immune responses were induced i

192 Whole-genome bisulfite sequencing of antigen-specific murine CD8 T cells at the effector and

193 nses in vivo via a Foxp3-dependent effect on antigen-specific naive CD4(+) T cell precursors.

194 . falciparum-infected erythrocytes activated antigen-specific naive CD4(+) T cells to proliferate and

195 he enhancer and super-enhancer landscapes in antigen-specific naive, differentiated effector, and cen

196 on neutrophils required the presence of the antigen-specific or activated T cells whereas exposure t

197 Furthermore, an activated, antigen-specific PD1(+)ICOS(+) cTfh subset clonally expa

198 itis, suggesting that disease is mediated by antigen-specific peripherally activated CD4(+) T cells t

199 Increased frequency of antigen-specific plasma cells and long-lived bone marrow

200 cine-induced immune response revealed strong antigen-specific polyfunctional CD4(+) and CD8(+) T cell

201 IL-10 production by a chronically stimulated antigen-specific population of differentiated Th1 cells.

202 ltiple sclerosis (MS), is suggested to be an antigen-specific process, yet which cells provide this s

203 ocyte-activation gene 3 (LAG3)(+) TR1 cells, antigen-specific proliferative responses, and cytokine p

204 findings were validated using two distinct, antigen-specific rcSso7d variants, which were isolated f

205 stem leverage a highly diverse repertoire of antigen-specific receptors to protect the human body fro

206 ytotoxicity and cytokine production but lack antigen-specific receptors, and they are important regul

207 ce the TH2 cytokines IL-5 and IL-13 but lack antigen-specific receptors.

208 Antigen-specific recognition by T cells is via the T cel

209 les triggers the generation and expansion of antigen-specific regulatory CD4(+) T cell type 1 (TR1)-l

210 Antigen-specific regulatory T (Treg)-cell induction was

211 T cell subsets in the gut as well as loss of antigen-specific regulatory T cell induction in the mese

212 We previously generated engineered antigen-specific regulatory T cells (Tregs), created by

213 in (RAP) in nanoparticles is known to induce antigen-specific regulatory T cells (Tregs), we adapted

214 ggering the differentiation and expansion of antigen-specific regulatory T cells in vivo.

215 gy of antigen-specific T cells; induction of antigen-specific regulatory T cells; or immune deviation

216 A blood polyfunctional, Mtb DosR latency antigen specific, regulatory, central memory response is

217 e practical strategies to improve the shared antigen-specific response to breast cancer.

218 polyfunctionality was related to the size of antigen-specific response.

219 by Baruj Benacerraf to explain differential antigen-specific responses in animal models, have become

220 ignaling pathway may contribute to decreased antigen-specific responses in vivo.

221 ced T cell proliferation, effector function, antigen-specific responses, and long-term T cell memory.

222 ing and transporting antigen and influencing antigen-specific responses.

223 A damage response pathway also occurred upon antigen-specific restimulation in TCR-transduced TIL1383

224 , we found that chronic immunization induced antigen-specific serological responses with diverse SHM-

225 Vaccine antigen-specific serum antibody responses were detected

226 ass antibodies emerged in a Chinese donor by antigen-specific single B cell sorting, structural and f

227 cytokine production following polyclonal and antigen-specific stimulation.

228 Their antigen-specific suppressor function could be preserved

229 PorB is capable of mounting an antigen specific T cell response by efficiently stimulat

230 ent did not affect the proliferation of auto-antigen specific T cells or their production of cytokine

231 vated T cell (NFAT) family are essential for antigen-specific T cell activation and differentiation.

232 did not produce ET-1 even when stimulated by antigen-specific T cell activation.

233 cytomegalovirus (CMV) infection, paralleling antigen-specific T cell differentiation.

234 gen peptide via MN was effective at reducing antigen-specific T cell proliferation in the pancreatic

235 c viral infections in which a hyporesponsive antigen-specific T cell repertoire prevents clearance of

236 d significantly higher levels of Th1 and Th2 antigen-specific T cell responses and increased IgG1 and

237 Strong and long-lasting antigen-specific T cell responses are critical for thera

238 ealed an essential role for CD103(+) cDCs in antigen-specific T cell responses during subclinical vir

239 cell function and downmodulation of filarial antigen-specific T cell responses.

240 antigen is presented during viral infection, antigen-specific T cells access the retina and autoimmun

241 o deep cervical lymph nodes where they prime antigen-specific T cells and exacerbate experimental aut

242 In model antigen systems, we found that antigen-specific T cells become enriched within scaffold

243 Antigen-specific T cells can control cancer, as revealed

244 Antigen-specific T cells exerted dynamic translational c

245 One limitation is the elimination of self-antigen-specific T cells from the immune repertoire.

246 ers are able to detect two- to fivefold more antigen-specific T cells in both human and murine CD4(+)

247 n synthesis, but translational regulation in antigen-specific T cells in vivo has not been well defin

248 ted that enumeration and characterization of antigen-specific T cells provide essential information a

249 -cell receptors (TCRs) isolated from minor H antigen-specific T cells represent an untapped resource

250 Both viral and nonviral tumor antigen-specific T cells resided predominantly in the pr

251 hich were transferred with effector neo-self-antigen-specific T cells to assess whether an autoimmune

252 During infection, antigen-specific T cells undergo tightly regulated devel

253 Immune checkpoint therapies target tumor antigen-specific T cells, but less is known about their

254 ditions results in a short-term expansion of antigen-specific T cells, whereas under inflammatory con

255 ptive immunity by facilitating activation of antigen-specific T cells.

256 challenging due to the small pool of tumour antigen-specific T cells.

257 ction, isolation, and phenotypic analysis of antigen-specific T cells.

258 of infection and autoreactive antibodies or antigen-specific T cells.

259 igrate to lymph nodes and present antigen to antigen-specific T cells.

260 in the development of chronically activated antigen-specific T cells.

261 consequence of either deletion or anergy of antigen-specific T cells; induction of antigen-specific

262 ucing type I interferons (IFNs) and enhances antigen-specific T helper 1 (Th1) responses in a type I

263 xtremely rapid clonal proliferation of rare, antigen-specific T lymphocytes to form effector cells.

264 termed "unconventional." These cells express antigen-specific T or B cell receptors, but behave with

265 though adoptive transfer of autologous tumor antigen-specific T-cell immunotherapy can produce remark

266 nti-VEGF and anti-PD-L1 combination improves antigen-specific T-cell migration.

267 he resulting change in the balance within an antigen-specific T-cell population further correlates wi

268 nd 6 of 22 patients without ocular symptoms, antigen-specific T-cell responses against retina-specifi

269 Antigen-specific T-cell responses were maintained, but t

270 T20-deficient mice failed to mount effective antigen-specific T-cell responses, and their T cells fai

271 d mice with rLmIII/a30 induced the strongest antigen-specific T-cell responses, including splenic and

272 m, may have a significant role in regulating antigen-specific T-cell responses.

273 The findings point toward a future when antigen-specific T-cell therapies will play a central ro

274 human lung tumor slices and autologous tumor antigen-specific T-lymphocyte clones to provide evidence

275 ar, at low Rapa MP doses, vaccines increased antigen-specific TCM, resulting in enhanced T cell expan

276 In response to viral infection, the antigen-specific TCR repertoire is progressively diversi

277 ized, and the extent of the Valpha2-bearing, antigen-specific TCR repertoire was characterized by hig

278 y that segregates self-derived and exogenous antigen-specific TCRs according to the monomeric interac

279 humoral immunity, yet the impact of aging on antigen specific TFH responses remains unclear.

280 alis infection is associated with diminished antigen-specific Th1- and Th17-associated responses and

281 Although frequencies of antigen-specific TH2 cells in peripheral blood determine

282 rmore, differentiation of naive T cells into antigen-specific TH22 cells is dependent on aryl hydroca

283 -1)45 represents an important step toward an antigen-specific therapy for anti-MAG neuropathy.

284 diabetes and has implications for the use of antigen-specific therapy in tolerance induction.

285 Thymic dendritic cells (DC) delete self-antigen-specific thymocytes, and drive development of Fo

286 agnosis, these kits rely on the detection of antigens specific to malarial parasites.

287 ely influence disease incidence or result in antigen-specific tolerance assessed by IL-10 measurement

288 of dendritic cells (DCs) in the induction of antigen-specific tolerance mediated by extrathymic regul

289 ritic cells (DCs) initiate immunity and also antigen-specific tolerance mediated by extrathymic regul

290 rophylactically or therapeutically to induce antigen-specific tolerance might overcome these obstacle

291 ified red blood cells as a means of inducing antigen-specific tolerance.

292 ic acid-modified antigens instruct DCs in an antigen-specific tolerogenic programming, enhancing Treg

293 Whether oral immunotherapy (OIT) leads to antigen-specific TR1 cell induction has not been establi

294 These intestinal antigen-specific Tr1 cells have the ability to migrate t

295 ) cells is still debated.In vitro studies of antigen specific Treg has been difficult as they die in

296 for activation of tTreg produce more potent antigen-specific Treg that only suppress specific donor

297 sly described model of GVHD protection using antigen specific Tregs.

298 the stage for using this approach for making antigen-specific Tregs for therapy of multiple diseases.

299 ared with polyclonal Tregs, disease-relevant antigen-specific Tregs may have numerous advantages, suc

300 imensional phenotypic profiling reveals that antigen-specific, tumour-infiltrating T cells are highly