ライフサイエンスコーパス: tumor rejection

1 pact of systemic immune responses that drive tumor rejection.

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

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

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

5 regs and Teffs that directly correlated with tumor rejection.

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

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

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

9 temic tumor immunity resulting in indigenous tumor rejection.

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

11 nderstanding the dynamics of immune-mediated tumor rejection.

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

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

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

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

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

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

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

19 oxicity is additionally required for optimal tumor rejection.

20 ermine the particular mechanisms involved in tumor rejection.

21 12 (IL-12) induced CD8+ T-cell responses and tumor rejection.

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

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

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

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

26 1BB-specific Abs can lead to T cell-mediated tumor rejection.

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

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

29 y correlate with the occasional instances of tumor rejection.

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

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

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

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

34 the roles of these activities in subsequent tumor rejection.

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

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

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

38 N elicits prolonged survival times and brain tumor rejection.

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

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

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

42 a biologic response modifier that stimulated tumor rejection.

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

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

45 beta to subcutaneous sites protected against tumor rejection.

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

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

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

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

50 ression of free L chain secretion reinstated tumor rejection.

51 re subsequently rejected, implying a role in tumor rejection.

52 n of tissue autoantigens can actually induce tumor rejection.

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

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

55 tissue to induce CTL dysfunction and prevent tumor rejection.

56 th prevention of autoimmunity and failure of tumor rejection.

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

58 at together facilitate immune cell-dependent tumor rejection.

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

60 nevertheless generally impotent in eliciting tumor rejection.

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

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

63 significantly diminished, thereby impairing tumor rejection.

64 nd M1 macrophages were involved in mediating tumor rejection.

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

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

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

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

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

70 in the connectivity between autoimmunity and tumor rejection.

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

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

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

74 ynergized with vaccination to achieve potent tumor rejection.

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

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

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

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

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

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

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

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

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

84 CTL were directed toward molecularly defined tumor rejection Ags.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 resents the first demonstration that a human tumor rejection antigen can be generated from a normal c

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

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

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

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

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

114 ith cancer, and a 24-amino acid product as a tumor rejection antigen recognized by T cells.

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

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

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

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

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

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

121 small number of cancers where candidates for tumor rejection antigens have been identified.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 Tumor rejection correlated with changes in the lymphocyt

156 Because tumor rejection correlates with expression of class II w

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

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

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

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

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

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

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

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

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

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

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

168 1(+) CD3(-) cells were responsible for acute tumor rejection, establishing the relationship of NK1.1(

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 Recombinant soluble MULT1 stimulated tumor rejection in mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

216 in addition, tumor rejection is impaired in melanoma-immune mice chal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 Tumor rejection of melanoma was assessed after immunizat

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

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

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

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

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

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

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

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

246 However, tumor rejection rarely occurs, suggesting limited functi

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

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

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

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

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

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

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

254 Optimal tumor rejection requires wild-type CD80.

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

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

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

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

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

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

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

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

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

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

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

266 Since sensitivity to apoptosis is key to tumor rejection, these results may point to new approach

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

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

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

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

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

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

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

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

275 Under these conditions, tumor rejection was complete.

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

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

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

279 Tumor rejection was enhanced through antibody-mediated C

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

281 Tumor rejection was not due to adaptive immune responses

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

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

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

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

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

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

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

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

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

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

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

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