ライフサイエンスコーパス: tumor rejection

1 e to a tumor Ag, resulting in the failure of tumor rejection.

2 in the connectivity between autoimmunity and tumor rejection.

3 sponses to specific mutations and to lead to tumor rejection.

4 some instances, was sufficient to result in tumor rejection.

5 -presentation in responses to viruses and in tumor rejection.

6 ynergized with vaccination to achieve potent tumor rejection.

7 tumor Ags or use FasL to mediate intraocular tumor rejection.

8 essive cell types, which ultimately leads to tumor rejection.

9 encoding LIGHT, a cytokine known to promote tumor rejection.

10 olecule OX40 and OX40 ligand (OX40L) enhance tumor rejection.

11 regs and Teffs that directly correlated with tumor rejection.

12 liferation of transferred T cells as well as tumor rejection.

13 pact of systemic immune responses that drive tumor rejection.

14 temic tumor immunity resulting in indigenous tumor rejection.

15 le to expand in vivo and to provide help for tumor rejection.

16 nderstanding the dynamics of immune-mediated tumor rejection.

17 type 1 helper T cell responses important for tumor rejection.

18 otifs (CpG ODN) in enhancing MVAp53-mediated tumor rejection.

19 anisms of anti-CTLA-4- and anti-PD-1-induced tumor rejection.

20 romal cells may contribute to the failure of tumor rejection.

21 th prevention of autoimmunity and failure of tumor rejection.

22 restricted NKT-cells, and antibodies mediate tumor rejection.

23 immunogenic and triggers CD8 T cell-mediated tumor rejection.

24 ve tumor antigen-specific T cells leading to tumor rejection.

25 oxicity is additionally required for optimal tumor rejection.

26 ermine the particular mechanisms involved in tumor rejection.

27 12 (IL-12) induced CD8+ T-cell responses and tumor rejection.

28 Both CD4+ and CD8+ T cells were required for tumor rejection.

29 T(reg) by Ab therapy leads to more efficient tumor rejection.

30 at B7-CD28 and B7-CTLA4 interactions promote tumor rejection.

31 1BB-specific Abs can lead to T cell-mediated tumor rejection.

32 CD4(+) T cells are required for SDF-mediated tumor rejection.

33 y correlate with the occasional instances of tumor rejection.

34 ngth of vaccine-induced immune responses and tumor rejection.

35 resulted in enhanced T-cell infiltration and tumor rejection.

36 ctivity was not sufficient to induce in vivo tumor rejection.

37 pies for autoimmunity, graft acceptance, and tumor rejection.

38 the roles of these activities in subsequent tumor rejection.

39 ducing, Th1/Tc1 phenotype may be optimal for tumor rejection.

40 xpressing mM-CSF (T9/mM-CSF) resulted in 80% tumor rejection.

41 N elicits prolonged survival times and brain tumor rejection.

42 hages in vivo, did not diminish CD8-mediated tumor rejection.

43 th anti-B7-2 monoclonal antibody resulted in tumor rejection.

44 FN-gamma play a role in immunoregulation and tumor rejection.

45 a biologic response modifier that stimulated tumor rejection.

46 nner, but complete deletion of MTS decreased tumor rejection.

47 ed NF-kappaB activity, which is required for tumor rejection.

48 MB results in potent CD4(+) T cell-mediated tumor rejection.

49 receptor gene may play an important role in tumor rejection.

50 beta to subcutaneous sites protected against tumor rejection.

51 ted peptides expressed by tumors, leading to tumor rejection.

52 ease and that CD8+ T cells are necessary for tumor rejection.

53 oxic T lymphocytes (CTL) and thereby mediate tumor rejection.

54 ty, for Con A stimulation of T cells, and in tumor rejection.

55 ormal self-antigens can serve as targets for tumor rejection.

56 NKG2D ligand, causes NK cell activation and tumor rejection.

57 responses to tumor-associated Ags to induce tumor rejection.

58 aR) deletion and compromised T-cell-mediated tumor rejection.

59 ity that can limit immune escape and promote tumor rejection.

60 -polarized CD8(+) T cell response to bolster tumor rejection.

61 ression of free L chain secretion reinstated tumor rejection.

62 lls and can overcome some of the barriers to tumor rejection.

63 omatic DNA mutations in cancer cells lead to tumor rejection.

64 tissue to induce CTL dysfunction and prevent tumor rejection.

65 , and spontaneous as well as therapy-induced tumor rejection.

66 at together facilitate immune cell-dependent tumor rejection.

67 g that both T cell subsets are necessary for tumor rejection.

68 nevertheless generally impotent in eliciting tumor rejection.

69 with immune checkpoint inhibitors to promote tumor rejection.

70 acquired CD8 T cell- or IFN-gamma-dependent tumor rejection.

71 genous type I IFN during lymphocyte-mediated tumor rejection.

72 significantly diminished, thereby impairing tumor rejection.

73 nd M1 macrophages were involved in mediating tumor rejection.

74 y an important role in immune regulation and tumor rejection.

75 n and play a role in immune surveillance and tumor rejection.

76 ponse, kinetics, and correlates that predict tumor rejection.

77 ells that are involved in immune defense and tumor rejection.

78 ller cells has no effect on vaccine-mediated tumor rejection (100% of mice were tumor free).

79 both CD4 and CD8 T cells and as a result of tumor rejection, a long-term tumor-specific immunity was

80 on of established tumors and can augment the tumor rejection achieved through therapeutic vaccination

81 oducibly converted lymphoma Ig into a potent tumor rejection Ag in mice.

82 ed the crystallographic structure of a major tumor rejection Ag, gp100(209-217), in complex with the

83 the unrelated JBRH melanoma, indicating that tumor rejection Ags are tumor-specific rather than share

84 Molecular identification of tumor rejection Ags has helped define several classes of

85 stimulation on CD8 T cells and the nature of tumor rejection Ags have yet to be determined.

86 CTL were directed toward molecularly defined tumor rejection Ags.

87 TLA-4 antibodies for their ability to induce tumor rejection and autoimmunity.

88 ive, syngeneic protein and could induce both tumor rejection and autoimmunity.

89 NK cells are essential for both tumor rejection and CTL development in the combination t

90 ecreted T(H)1 cytokine IFN-gamma and induced tumor rejection and growth suppression after a lethal ch

91 otential to facilitate immune cell-dependent tumor rejection and have distinct advantages over cell-b

92 IL-21 is in clinical use to promote tumor rejection and is an emerging target for neutraliza

93 lls are neither necessary nor sufficient for tumor rejection and raise interesting questions regardin

94 lls appeared to act at the effector phase of tumor rejection and responded to B16-derived Ags in vitr

95 The combination therapy also induced tumor rejection and skin depigmentation in B cell-defici

96 ct ICOS-L expression by tumor cells enhanced tumor rejection and survival when administered along wit

97 identifies a critical role basophils play in tumor rejection and that this role can be exploited for

98 a variety of immune responses sufficient for tumor rejection and the suppression of metastatic tumor

99 lobulin were greater in mice undergoing TUBO tumor rejection and thyroglobulin injection than in thos

100 istant to suppression and is associated with tumor rejection and unimpaired cytotoxicity.

101 te lymphocytes that play an integral role in tumor rejection and viral clearance.

102 found that high NF-kappaB activity leads to tumor rejection and/or growth suppression in mice.

103 ion of a sufficient immune response to cause tumor rejection, and approaches to overcome evasion of i

104 ded help for cytotoxic T lymphocyte-mediated tumor rejection, and developed T cell memory.

105 ve mice resulted in leukocytic infiltration, tumor rejection, and induction of RP3-specific T cells.

106 such as insulin-dependent diabetes mellitus, tumor rejection, and infectious diseases where NKT cells

107 tiators of transplant rejection, spontaneous tumor rejection, and some forms of autoimmunity.

108 stage-specific embryonic antigen 4 (SSEA-4), tumor rejection antigen 1-60 (TRA 1-60), and tumor rejec

109 tumor rejection antigen 1-60 (TRA 1-60), and tumor rejection antigen 1-81 (TRA 1-81) (traditional mar

110 attractive candidate for a broadly expressed tumor rejection antigen because telomerase is silent in

111 mutated tumor antigen to be identified, is a tumor rejection antigen for J558 plasmacytoma in mice wi

112 Thus, P1A is not a necessary tumor rejection antigen for the J558 tumor cells.

113 -associated fibroblasts, could function as a tumor rejection antigen in a broad range of cancers.

114 mor line serves as an immunization-dependent tumor rejection antigen in normal syngeneic mice.

115 ransgenic CD8+ T cells against the unmutated tumor rejection antigen P1A to analyze whether this mAb

116 Therefore, even though P1A can be a tumor rejection antigen, the effector function of P1A-sp

117 e shows that it is highly similar to gp96, a tumor rejection antigen-1, and contains an endoplasmic r

118 tify the human IL-13Ralpha2 chain as a novel tumor rejection antigen.

119 oncofetal antigen can serve as an effective tumor rejection antigen.

120 trated that this epitope represents a potent tumor rejection antigen.

121 n of tumor-associated antigens (TAAs) and/or tumor rejection antigens (TRAs).

122 The onconeural antigens appear to serve as tumor rejection antigens in the paraneoplastic neurologi

123 ulates that peptide mimetics of glycosylated tumor rejection antigens might be further developed for

124 and their possible coexistence as potential tumor rejection antigens on associated tumors.

125 libraries can therefore be used to identify tumor rejection antigens that can cooperate to induce an

126 of Tms requires designing vaccines based on tumor rejection antigens, which are often not available

127 munotherapy depends on the identification of tumor-rejection antigens (Ags).

128 ity to neu, and possibly to similar putative tumor-rejection antigens, may lead to more potent in viv

129 accines will require identifying appropriate tumor-rejection antigens; optimizing the interactions of

130 pleiotropic effects on human T cell-mediated tumor rejection are lacking.

131 The specific T cells that mediate tumor rejection are unknown.

132 CD8+ T cells, which are necessary for tumor rejection, are activated rather than suppressed du

133 n CD8(+) T cells to facilitate IL-10-induced tumor rejection as well as in situ expansion and prolife

134 Peli1 ablation profoundly promotes tumor rejection, associated with increased tumor-infiltr

135 ous activities of CD1d-restricted T cells in tumor rejection, autoimmune disease, and microbial infec

136 that CD8+ T cells used TNF-alpha to mediate tumor rejection, because Ad5E1 tumor cells were highly s

137 been surprisingly poor at inducing complete tumor rejection, both in experimental models and in the

138 al or reduction of immunosuppression-permits tumor rejection but risks allograft rejection.

139 ng antibodies such as ipilumimab can promote tumor rejection, but the full scope of their most suitab

140 ent immune privilege and mediate intraocular tumor rejection by a TNF-alpha-dependent manner while le

141 ted by MHC class I molecules are targets for tumor rejection by CD8+ CTLs.

142 efore be an important effector mechanism for tumor rejection by CD8+ T cells.

143 nction is essential for MHC class I-mediated tumor rejection by CTLs.

144 es by MHC class I molecules is important for tumor rejection by CTLs.

145 In an HER2-dependent tumor model, tumor rejection by HER2-specific CAR-Ts was associated w

146 0) exerts profound effects both in mediating tumor rejection by Hsp70-based vaccines and in autoimmun

147 zed, but not naive, T cells is essential for tumor rejection by IL-12 and Cy+IL-12.

148 ncogene induces cytolytic susceptibility and tumor rejection by interactions with cellular proteins o

149 mice, was effective in preventing B7-2+ P815 tumor rejection by mice in which the B7-1 gene was disru

150 ich was ineffective in preventing B7-2+ P815 tumor rejection by normal wild-type mice, was effective

151 ess, these Treg abrogate CD8 T cell-mediated tumor rejection by specifically suppressing the cytotoxi

152 der to understand the mechanism(s) governing tumor rejection by the immune system in response to TA-s

153 ation of the tumor significantly potentiated tumor rejection by these carcinoembryonic Ag-specific CT

154 It has been previously documented that Ad5E1 tumor rejection can occur in the absence of CD8+ T cells

155 CD8+ T cells specific for tumor Ags promote tumor rejection, CD8+ T cells specific for unrelated Ags

156 CB T cells mediated enhanced tumor rejection compared with equal numbers of PB T cell

157 Tumor rejection correlated with changes in the lymphocyt

158 Because tumor rejection correlates with expression of class II w

159 h anti-4-1BB mAb exhibited markedly enhanced tumor rejection, delayed tumor progression, and prolonge

160 death protein-1 antibodies promoted complete tumor rejection, demonstrating the relevance of CD25 as

161 Tumor rejection depended on host-derived CD8(+) T cells

162 tween the effects of T reg cell depletion on tumor rejection dependent on whether depletion occurs be

163 imilar in the absence of CD4(+) T cells, and tumor rejection did not depend upon CD40-CD40L interacti

164 Interestingly, tumor rejection did not involve natural killer cells but

165 pression of TLR9, we unexpectedly found that tumor rejection did not require host expression of TLR9.

166 dy demonstrates that CD4(+) T cell-dependent tumor rejection does not occur in IFN-gamma-deficient mi

167 on between measurable systemic responses and tumor rejection during CD25-directed T reg cell depletio

168 inversion of the ratio and correlation with tumor rejection during Gvax/anti-CTLA4 immunotherapy.

169 After s.c. tumor rejection, enhanced antitumor immunity is achieved

170 1(+) CD3(-) cells were responsible for acute tumor rejection, establishing the relationship of NK1.1(

171 mor-infiltrating lymphocytes that accomplish tumor rejection exhibit enhanced effector functions in b

172 umor-rejector mice could mediate intraocular tumor rejection following adoptive transfer to SCID mice

173 ut not CD8+, T cells play a critical role in tumor rejection following vaccination with irradiated gl

174 , which increases CTL activity that mediates tumor rejection; however, this does not occur in the eye

175 h a combination of these two antigens caused tumor rejection in 100% of the immunized mice.

176 The tumor rejection in 3H1-pulsed DC-treated mice was associ

177 orly immunogenic tumors, leading to complete tumor rejection in a high proportion of mice.

178 dy the impact of CD4+ T cell polarization on tumor rejection in a model mimicking human disease, we g

179 -mediated cytotoxicity and was necessary for tumor rejection in a multiple myeloma model.

180 depletion proves permissive for spontaneous tumor rejection in a murine model of established intracr

181 ments translated into a greater frequency of tumor rejection in a PAP-expressing solid tumor model.

182 bination adjuvant with HPV E7 protein caused tumor rejection in all tumor-bearing mice.

183 CpG ODN with MVAp53 resulted in tumor rejection in BALB/c mice bearing poorly immunogeni

184 therapy achieved effective local and distant tumor rejection in colorectal cancer models.

185 independent of IFN-gamma, as demonstrated by tumor rejection in IFN-gamma knockout mice.

186 ow that administration of DTA-1 induces >85% tumor rejection in mice challenged with B16 melanoma.

187 ated T cell activation in vitro and mediated tumor rejection in mice.

188 Recombinant soluble MULT1 stimulated tumor rejection in mice.

189 nts suggested that T cells were required for tumor rejection in ogr1(-/-)mice, although OGR1 expressi

190 interleukin-2 (IL-2) played the main role in tumor rejection in our model as shown by using CD4- and

191 Despite absence of tumor rejection in P14/RAG2(-/-) recipients, 2C cells di

192 nce RMA-retinoic acid early inducible-1delta tumor rejection in RAG-1(-/-) deficient mice, thereby de

193 -1) is able to overcome tolerance and induce tumor rejection in several murine syngeneic tumor models

194 leiotropic immune mechanisms that facilitate tumor rejection in several tumor models.

195 B7 costimulatory molecules fails to prevent tumor rejection in the 2C TCR/RAG(-/-) mice, suggesting

196 Blocking FasL in vivo inhibited tumor rejection in these mice.

197 The cellular requirements for tumor rejection in this therapeutic setting were strikin

198 ion for the reversal of tolerance leading to tumor rejection in transplant recipients and likely cont

199 eversal of CD8(+) TIL dysfunction and led to tumor rejection in two thirds of mice.

200 absolutely required for CD8+ T cell-mediated tumor rejection in vivo and dominantly acts at the level

201 The lack of syngeneic tumor rejection in vivo is correlated with a partial res

202 nner, NK cell degranulation/cytotoxicity and tumor rejection in vivo remained intact in the absence o

203 To determine the contribution of ICAM-1 to tumor rejection in vivo, we performed adoptive transfer

204 s and can also efficiently prime T cells for tumor rejection in vivo.

205 is by NK cells, resulting in NKG2D-dependent tumor rejection in vivo.

206 cell-surface BCMA may contribute directly to tumor rejection in vivo.

207 atural killer (NK) cell-mediated killing and tumor rejection in vivo.

208 type 1 T cell response may result in optimal tumor rejection in vivo.

209 neu-specific T cells to achieve neu-specific tumor rejection in vivo.

210 in vitro, while mutation of G226 diminished tumor rejection in vivo.

211 peptide in vitro and, after transfer, cause tumor rejection in vivo.

212 wth of different tumor types but also led to tumor rejections in mice.

213 for CD4(+) T cells in the effector phase of tumor rejection indicating a greater responsibility for

214 neutralization of IL-9 considerably impaired tumor rejection induced by DTA-1.

215 CD4(+) and CD8(+) cells were involved in the tumor rejection induced by IL-12/IL-18-cultured TDLN cel

216 However, analysis of the effector phase of tumor rejection induced by vaccination with irradiated t

217 by which homeostatic proliferation supports tumor rejection is by maintaining and/or re-establishing

218 Therefore, IFN-gamma-independent tumor rejection is excluded from the eye and may represe

219 that in certain tumor models IL-21-enhanced tumor rejection is NKG2D dependent.

220 n-specific CD8+ T cells and their subsequent tumor rejection is still vigorously debated.

221 demonstrates that one reason for the lack of tumor rejection is that tumors actively defeat host immu

222 The role of IFN-gamma in IL-12-induced tumor rejection is unclear, because after IL-12 administ

223 ect effect on tumor-specific CD8+ T cells in tumor rejection is unclear.

224 pecially effector mechanisms responsible for tumor rejection, is an important goal.

225 d that although TNF-alpha was not needed for tumor rejection, it was required for the development of

226 The pathways of donor marrow and tumor rejection lead to the development of tumor-specifi

227 icited tumor-infiltrating macrophages toward tumor rejection may hold benefit as a potential cancer t

228 e indispensable for revealing a diversity of tumor rejection mechanisms that may lack in vitro correl

229 Tumor rejection mediated by Trm cells triggers the sprea

230 immune attack has led to the hypothesis that tumor rejection, mediated through immunocompetent donor

231 , developing accurate methods for predicting tumor-rejection mediating neoepitopes (TRMNs) is critica

232 To further test if T cells alone can mediate tumor rejection, mice were immunized with pcytneu encodi

233 ved therapeutic efficacy in a murine in vivo tumor rejection model.

234 Here we report using a tumor-rejection model that ectopic B7h expression can co

235 tial cell type recruited in most, if not all tumor rejection models, including the B16 melanoma.

236 he decreased IFN-gamma production and failed tumor rejection observed in anergized NKT cells are resc

237 Finally, tumor rejection occurred after transfer of TNF-alpha, pe

238 Tumor rejection occurred in CD-1 but not in BALB/c and D

239 The results suggest that Ad5E1 tumor rejection occurs via TRAIL-induced apoptosis as fo

240 the CTL response is not suppressed, in that tumor rejection occurs.

241 Tumor rejection of melanoma was assessed after immunizat

242 s can induce protective immunity and lead to tumor rejection of some tumors in model systems of in vi

243 However, during tumor rejection, only peripheral immune cells sustained

244 s, an important gap to fill if mechanisms of tumor rejection or escape are to be understood.

245 ion with antigen-loaded AdIL18DC resulted in tumor rejection or further suppression of tumor growth w

246 c tumors resulted in CD8 and PD-L1-dependent tumor rejection or growth inhibition and a reduction in

247 an have opposing effects -- they can trigger tumor rejection or inhibit treatment after adoptive cell

248 into day 7 CMS4 or MethA tumors resulted in tumor rejection or slowed tumor growth when compared wit

249 lymphoid organs did not impair IL-10-induced tumor rejection or the activation of tumor-resident CD8(

250 We studied immunogenicity, tumor rejection potential, and safety of three vaccines:

251 However, tumor rejection rarely occurs, suggesting limited functi

252 function of myeloid lineage cells to support tumor rejection, regulating the balance between pro- and

253 lin-specific CD8+ cytotoxic T lymphocytes in tumor rejection remains elusive.

254 Intraocular tumor rejection required CD4(+) T cells, but did not req

255 Complete tumor rejection required IFNgamma-regulated Fas by the t

256 CD8(+) T cell priming and tumor rejection required tumor Ag cross-presentation, as

257 Furthermore, s.c. tumor rejection requires IL-17, which is produced by IFN

258 tion have clearly shown that immune-mediated tumor rejection requires more than simple T cell-target

259 Optimal tumor rejection requires wild-type CD80.

260 ), CD4(+), and NK cells were involved in the tumor rejection response and that CD8(+) cells had the m

261 the pancreas (in contrast to the prostate), tumor rejection responses can still be decoupled from pa

262 intimate connectivity between autoimmune and tumor rejection responses extends beyond the classic mel

263 Importantly, the DC vaccine elicited tumor rejection responses in both WT and MUC1-Tg mice.

264 A close connectivity between autoimmune and tumor rejection responses is known to exist in the case

265 lls and PD-1 on intratumoral T cells limited tumor rejection, resulting in rapid recurrence.

266 macrophages into tumors with a higher M1/M2 (tumor rejection) signature expression pattern, as well a

267 d peptides capable of mediating T cell-based tumor rejection still face important challenges.

268 gous KFERQ-like motif in murine DBY hampered tumor rejection, T cell activation, and migration into t

269 munization against a single tumor Ag induces tumor rejection that is significantly greater than HSCT

270 Although Treg cell depletion enhances tumor rejection, the ensuing autoimmune sequelae limits

271 ic proliferation may improve T cell-mediated tumor rejection, there is little direct evidence isolati

272 c effector T cells in patients can result in tumor rejection, thereby illustrating the immune system

273 ysis of cellular requirements for successful tumor rejection through an adoptive cell transfer approa

274 +) and CD4(+) T cell responses for efficient tumor rejection to occur.

275 but not after, IL-12 treatment in order for tumor rejection to occur.

276 , if anti-P1A CTL response is sufficient for tumor rejection, tumor cells must lose the antigenic epi

277 C/RAG2(-/-)/PD-1(-/-) T cells in vivo caused tumor rejection under conditions in which wild-type 2C c

278 IFN-gamma receptor 1 (IFNGR1) have impaired tumor rejection upon anti-CTLA-4 therapy.

279 tumor-induced L-selectin(high) T(S) prevent tumor rejection via blockade of sensitized, activated T(

280 gulatory T cell depletion, and which promote tumor rejection via IFN-gamma and lysis via cytotoxic gr

281 Under these conditions, tumor rejection was complete.

282 Tumor rejection was dependent on CD8(+) and NK1.1(+) cel

283 +) T cells developed cytotoxic activity, and tumor rejection was dependent on class II-restricted rec

284 B7-IgG-mediated tumor rejection was dependent on T cells, specifically C

285 Tumor rejection was enhanced through antibody-mediated C

286 The tumor rejection was mediated by NK cells, and not by CD1

287 Tumor rejection was not due to adaptive immune responses

288 To study the mechanisms controlling tumor rejection, we assessed different mouse models for

289 g the mechanisms behind CD8+ T cell-mediated tumor rejection, we discovered that antitumor CTL activi

290 nt view that Th1 cells are most important in tumor rejection, we found that Th17-polarized cells bett

291 ta cytoplasmic domain to Ag presentation and tumor rejection, we have produced a series of cell lines

292 To study the mechanisms of phthisical tumor rejection, we isolated a cell clone-designated clo

293 1 and anti-OX40 that survived after complete tumor rejection were rechallenged with KPC-Luc cells; th

294 n opportunity to study host requirements for tumor rejection when it effectively occurred.

295 f Smad4 for T-cell-mediated autoimmunity and tumor rejection, which is beyond the current paradigm.

296 Finally, since achieving tumor rejection while preserving self-tolerance is parti

297 enium-based scavenger, significantly delayed tumor rejection, while having no appreciable effect on t

298 ed IFN-gamma is critical for promoting acute tumor rejection, while host production of IFN-gamma is n

299 can circumvent immune privilege and mediate tumor rejection without inducing damage to normal ocular

300 ly engrafted with myeloma, SE cells mediated tumor rejection without inducing xenogeneic graft-versus