ライフサイエンスコーパス: self-antigen

1 d human cells by engaging a stress-regulated self antigen.

2 and may be required for B cell tolerance to self-antigen.

3 these cells display medium/high avidity for self-antigen.

4 they do not bind (or bind limited amount of) self-antigen.

5 s irrespective of the presence or absence of self-antigen.

6 gand-stabilized model protein expressed as a self-antigen.

7 that were otherwise tuned down to a systemic self-antigen.

8 ally overcame memory CD8 T-cell ignorance of self-antigen.

9 in anergic B cells repeatedly stimulated by self-antigen.

10 GSIS-dependent surface exposure of the ZnT8 self-antigen.

11 n the expression of their endogenous cognate self-antigen.

12 ulations specific for endogenously expressed self antigens.

13 ance of unwarranted immune responses against self antigens.

14 requencies similar to those specific for non-self antigens.

15 hat increases the inflammatory properties of self antigens.

16 ogenic versus tolerogenic characteristics of self antigens.

17 to draining lymph nodes charged with tissue self antigens.

18 limit the immunostimulatory presentation of self antigens.

19 ure (MARCO), which has affinity for modified self-antigens.

20 dly elevated levels of surface-bound nuclear self-antigens.

21 IL-2-positive T cells that are activated by self-antigens.

22 mechanisms that mediate immune tolerance to self-antigens.

23 hat arise during disease-driven oxidation of self-antigens.

24 ounts of foreign antigen present in a sea of self-antigens.

25 ognizing a plethora of self-antigens and non-self-antigens.

26 d allows responses against pathogens but not self-antigens.

27 pecific effector T cells by expressing tumor self-antigens.

28 hese cells and serve as a source of modified self-antigens.

29 loned and assessed for their ability to bind self-antigens.

30 ch includes the diverse spectra of alien and self-antigens.

31 verall repertoire of promiscuously expressed self-antigens.

32 ility epitope (SE) and the citrullination of self-antigens.

33 dust mites to microbial products as well as self-antigens.

34 -based cancer immunotherapies are unmodified self-antigens.

35 B cells capable of responding to sequestered self-antigens.

36 ersus establishment of tolerance to tumor or self-antigens.

37 naive phenotype in response to low-affinity self-antigens.

38 for T-cell-based cancer immunotherapies are self-antigens.

39 iated attack directed against both viral and self-antigens.

40 ngages self-antigens and the nature of these self-antigens.

41 f the 108 recipients developed antibodies to self-antigens.

42 eby Tregs control the immune response to non-self-antigens.

43 s (pMHC) to discriminate between foreign and self-antigens.

44 at is important for maintaining tolerance to self-antigens.

45 ion of signals from systemically distributed self-antigens.

46 ot fixed, but are evolving as they encounter self-antigens.

47 the production of antibodies against nuclear self-antigens.

48 active GCs generated B cells targeting other self-antigens.

49 hly diverse and skewed toward recognition of self-antigens.

50 of B cells that are continuously exposed to self-antigens.

51 at mediates central T cell tolerance to many self-antigens.

52 y capable of breaking tolerance toward these self-antigens.

53 racterized by pathogenic immune responses to self-antigens.

54 ral specificity resulting in presentation of self-antigens.

55 trolling the TCR repertoire breadth to a non-self-antigen, a TCRbeta transgenic mouse model (EF4.1) e

56 riggers", i.e., specific this should be 'non-self antigens' accompanying infectious agents, might dis

57 e investigate how developing T cells measure self-antigen affinity.

58 embrane protein to serve as a ubiquitous neo self-antigen (Ag) were transplanted with a human immune

59 peripheral B cell survival and tolerance to self-antigens (Ags), a gene modifier screen was performe

60 igate whether protection could be induced by self-antigens alone, we injected apoptotic cells that ca

61 ile simultaneously inhibiting the release of self antigens and danger signals from apoptotic cell-der

62 which ensures more effective presentation of self antigens and favors diversity of self-tolerance bet

63 connection between an autoimmune response to self-antigen and an immune response to foreign Ag prompt

64 that occurs when autoantibodies complex with self-antigen and form immune complexes that accumulate i

65 ted during immune responses to infection and self-antigen and have been implicated in the pathogenesi

66 e, requiring continuous BCR interaction with self-antigen and resultant regulatory signaling for its

67 For example, defects in the clearance of self-antigens and chronic stimulation of type 1 interfer

68 at TEIPPs derive from ubiquitous, nonmutated self-antigens and constitute a class of immunogenic neoa

69 e T cell tolerance by ectopically expressing self-antigens and eliminating autoreactive T cells in th

70 As expected, Abs against self-antigens and germinal center formation were not dev

71 ts innate and adaptive immunity to apoptotic self-antigens and IDO-mediated regulation inhibits infla

72 ant role in induction of immune responses to self-antigens and immunopathogenesis of OAD following th

73 Immune tolerance to both self-antigens and innocuous non-self-antigens is essenti

74 lyreactive with additional specificities for self-antigens and it has been proposed immunological tol

75 rtoires capable of recognizing a plethora of self-antigens and non-self-antigens.

76 play a key role in controlling reactivity to self-antigens and onset of autoimmunity.

77 hich contributes to maintaining tolerance to self-antigens and persisting foreign antigens, averting

78 ry T cells (Tregs) maintain tolerance toward self-antigens and suppress autoimmune diseases, although

79 Here, we examined whether FDCs retain self-antigens and the impact of this process in autoanti

80 itself, how the NKT T cell receptor engages self-antigens and the nature of these self-antigens.

81 f the TCR expressed by T-cell precursors for self-antigens and the proper development of a unique pop

82 , homing potentials, and their reactivity to self-antigens and viral antigens in healthy subjects and

83 ide:MHC complexes that can be generated from self-antigens and/or foreign Ags in vivo remains poorly

84 ure and aberrant processing of nucleoprotein self antigens, and discuss their role in the SLE pathoge

85 involved in cytokine production, removal of self-antigens, and responses to autoreactive IgE antibod

86 ss Fezf2 and Aire, regulators of intrathymic self-antigens, and support T-reg development despite los

87 cell antigen receptor repertoire tolerant to self-antigens, and thus for avoiding autoimmunity.

88 cell receptors (TCRs) with high affinity for self-antigen are eliminated.

89 secreted by CD4+Th17 cells specific to lung self-antigens are critical mediators of autoimmunity lea

90 weak, and high avidity T cells specific for self-antigens are deleted in the thymus, but tumor respo

91 In systemic lupus erythematosus (SLE), many self-antigens are found in apoptotic cells (ACs), and de

92 ritic cells (DCs) and macrophages (MFs), the self-antigens are part of IgG-ICs that promote FcgammaRI

93 verse TCR-mediated interactions with cognate self-antigens are required for these processes.

94 current efforts, we utilize a mammalian non-self-antigen as an immunogen.

95 electing common, apparently lineage-specific self-antigens as targets for TCR-based immunotherapies.

96 es recycling and the accumulation of nuclear self-antigens at the membrane 72 h after internalization

97 Once tolerance was broken for one self-antigen, autoreactive GCs generated B cells targeti

98 patibility complex (MHC) class II-restricted self antigens by autoreactive T cell antigen receptors (

99 ected host cells enabled the presentation of self antigens by major histocompatibility complex class

100 ression of self-antigens or presenting a neo-self-antigen by medullary TECs, displaying decreased neg

101 ll receptor of higher functional avidity for self-antigen by Treg cells than Tconv cells, a differenc

102 tating the direct presentation of endogenous self-antigens by mTECs.

103 reasing evidence suggest that recognition of self-antigens by these cells plays an important role not

104 Here, we established that abnormal self-antigens can serve as targets for tumor rejection.

105 In particular, modified self-antigens can trigger CD4(+) T-cell responses that m

106 in TCR signalling thresholds or affinity for self-antigens, can explain the data.

107 (L265P) In B cells chronically stimulated by self-antigen, CD79B and MYD88(L265P) mutations in combin

108 sozyme epitope displayed on both foreign and self-antigens, cell transfers revealed that anergic IgM(

109 orepletion even in the absence of tolerogen (self-antigen), challenging the prevailing paradigm that

110 ese cells restrain inflammatory responses to self antigens, commensal microorganisms, allergens, and

111 cells, which express and present peripheral self-antigen, DC must acquire self-antigen to mediate th

112 Our study documents how self-antigens define the repertoire of thymus-derived Tr

113 rs, and shared specificity for a non-mutated self-antigen derived from U2AF2.

114 pathogenic IgG4 autoantibody response to the self-antigen desmoglein 1 (Dsg1) cross-reacts with the L

115 dy, we investigated how memory to AC-derived self-antigens develops and the contribution of self-memo

116 Interestingly, high-affinity soluble self-antigen did cause B cells to adopt many of the clas

117 In this article, we show that self-antigen displayed on FDCs mediates effective elimin

118 d, thus, may modulate the T-cell response to self-antigens displayed on dying cells.

119 for safe, subcutaneous delivery of the high self-antigen doses required for effective tolerance indu

120 affinity of the T cell antigen receptor for self antigen drives the differentiation of Treg cells in

121 3 (B:9-23), which are known to be a critical self-antigen-driving disease progress in animal models o

122 tivation of dendritic cells (DCs) presenting self-antigens during inflammation may lead to activation

123 earance of apoptotic debris, modification of self-antigens during inflammatory responses, and molecul

124 , suggesting that they are poised to present self-antigens efficiently.

125 cells, thereby controlling the repertoire of self-antigens encountered by differentiating thymocytes.

126 Transfusion of red blood cells expressing self-antigen epitopes can alleviate and even prevent sig

127 g responses to low-affinity or low-abundance self-antigens even in the context of an inflammatory mil

128 st selection' of functionally differentiated self-antigen-experienced T cells.

129 is is positively regulated by encounter with self-antigen expressed on peripheral tissues, which is l

130 aris (PV) harbor antibodies reactive against self-antigens expressed at the surface of keratinocytes,

131 Here we show that recognition of self-antigens expressed by endothelial cells in target t

132 or (Aire) prevents autoimmunity by promoting self-antigen expression in medullary thymic epithelial c

133 rus reactivation and immune responses to the self-antigens fibronectin (FN) and collagen type-IV (Col

134 beta-GlcCer in mammals functions as a lipid self antigen for iNKT cells.

135 ing the immunogenicity of poorly immunogenic self-antigens for cancer therapy.

136 et-specific zinc transporter ZnT8 is a major self-antigen found in insulin granules of pancreatic bet

137 is granular zinc transporter is also a major self-antigen found in type 1 diabetes patients.

138 on, remain unresponsive to the low levels of self-antigen generally expressed by some normal tissues.

139 ll receptor transgenic mice specific for the self-antigen glucose-6-phosphate isomerase, we show that

140 ntified indicating T-cell activation against self-antigens (graft versus self).

141 T-cell receptor affinity for self-antigen has an important role in establishing self-

142 lerance for inducing immune response against self-antigen has hindered the wide application of the st

143 s, and a breakage of immune tolerance to CNS self-antigens has been suggested to initiate CNS autoimm

144 Polyspecific T cells targeting distinct self-antigens have been identified in healthy individual

145 dulatory molecule IDO2 modifies responses to self-antigens; however, the mechanisms involved are obsc

146 Although insulin is a critical self-antigen in animal models of autoimmune diabetes, du

147 or the loss of immunologic tolerance to this self-antigen in autoimmunity.

148 Insulin represents a key self-antigen in disease pathogenesis, as recent studies

149 ymic expression of TRP-1 (TYRP1), which is a self-antigen in melanocytes and a cancer antigen in mela

150 studies suggest that prolonged expression of self-antigen in skin in a non-inflammatory context is be

151 active T cells encountering large amounts of self-antigen in the target organ of the autoimmune disea

152 e T cells encountering very small amounts of self-antigen in the thymus.

153 al expression and presentation of ocular neo-self-antigen in transgenic mice expressing hen egg lysoz

154 s (MPs) encapsulating denatured insulin (key self-antigen in type 1 diabetes; T1D), and PuraMatrix(TM

155 Thymus-derived Treg cells were selected by self-antigens in a specific manner, while autoreactive T

156 The BCR of another ABC line reacted with self-antigens in apoptotic debris, and the survival of a

157 ificantly impact the immune response against self-antigens in autoimmune disease, including type 1 di

158 ects but responded instead to myelin-derived self-antigens in patients with MS.

159 of inflammation and to promote tolerance to self-antigens in steady-state.

160 n, yet retain the ability to be activated by self-antigens in target organs.

161 the temporal and spatial (re)presentation of self-antigens in the medulla in the context of tolerance

162 The use of self-antigens in the study and treatment of a range of a

163 subsequent autoimmunity caused by release of self-antigens in the wake of infection.

164 to a major role for TLR7 in the response to self-antigens in this model of experimental autoimmunity

165 terized by adaptive immune responses against self-antigens, including humoral responses resulting in

166 differences in adaptive immune responses to self-antigens independent of external stimuli, including

167 speculated that binding of lymphoma BCRs to self-antigens initiates and maintains chronic active BCR

168 cells with a sufficiently high affinity for self-antigen interacting with peripheral IL-15.

169 The nature of the self-antigens involved in the development and maturation

170 immune response and maintaining tolerance to self-antigens involves a complex network of co-stimulato

171 mosaic pattern (i.e., at a given time, each self-antigen is expressed only in 1-3% of mTECs).

172 and RNA molecules derived from pathogens or self-antigen is one way the mammalian immune system sens

173 Tolerance to self-antigens is achieved through thymic deletion of hig

174 ance to both self-antigens and innocuous non-self-antigens is essential to protect the host against c

175 active cellular phenotype where tolerance to self-antigens is lost.

176 Hence, a diverse set of self-antigens is responsible for maintaining the maligna

177 An abnormal response to self-antigens is thought to drive the development of SLE

178 JC viruria) on antibodies to kidney-specific self-antigens is unknown.

179 , the sharing of epitopes among self and non-self antigens, is extraordinary common and provides the

180 the intrinsic reactivity of naive T cells to self-antigens, it did not cause spontaneous autoimmunity

181 undergo a positive selection step driven by self-antigens, kept in control by Tregs.

182 We previously identified a class of hidden self-antigens known as T cell epitopes associated with i

183 roduced serum autoantibodies to a breadth of self-antigens, leading to antibody deposition in the kid

184 results from a break in immune tolerance to self-antigens, leading to multi-organ destruction.

185 Persistent expression of Ag, a mimic of self-antigen, leads to functional inactivation and loss

186 naturally occurring polyclonal Tregs for any self-antigen, let alone MOG, has not been analyzed in th

187 In these responses, the selecting self-antigens likely derive from the remains of dead and

188 n autoimmune process directed at aortic wall self-antigens may play a central role in the immunopatho

189 T cells (Tregs), suggesting oral delivery of self-antigens might represent an effective means for mod

190 bility of CD4 cells to target tumor-specific self-antigens modified by citrullination, which converts

191 Using a human-Her2 self-antigen mouse model, we report here that alpha-4-1B

192 t with multiple sclerosis and recognizes the self-antigen myelin basic protein.

193 s for Treg generation in vivo, we targeted a self antigen, myelin oligodendrocyte glycoprotein, using

194 A highly conserved self-antigen, nonmuscle myosin heavy chain II, has been

195 particle-associated chromatin is a potential self-antigen normally digested by circulating DNASE1L3.

196 ntravenous injection of hapten conjugated to self-antigens of syngeneic erythrocytes and subsequent c

197 el to conditionally express a membrane-bound self-antigen on FDCs and to monitor the fate of developi

198 The majority of CAR targets have been normal self-antigens on dispensable hematopoietic tissues or ov

199 to inefficiency in promiscuous expression of self-antigens or presenting a neo-self-antigen by medull

200 NK cells recognize the loss of self-antigens or up-regulation of stress-induced ligands

201 fficiently this occurs for tissue-restricted self antigens, or how immune tolerance is maintained for

202 Thus, HLA-B27-restricted immune responses to self-antigens, or arthritogenic peptides, might drive im

203 n of defective and rapidly degraded forms of self-antigen, possibly as a mechanism to diminish the pr

204 ery step of immunosurveillance, particularly self-antigen presentation and apoptosis.

205 MHC-II self-antigen presentation by lymph node stromal cells al

206 ive T cells are abundant in human blood, but self-antigens presented by CD1c to the T-cell receptors

207 Lysophospholipids are self-antigens presented by CD1d that are generated throu

208 between developing or mature lymphocytes and self-antigen-presenting cells.

209 We determined that self-antigens processed by tissue-specific proteases, in

210 R), it remains unclear whether engagement of self-antigen provides a positive impact for most B cells

211 ults demonstrate that ZnT8 is a cell surface self-antigen, raising the possibility of a direct involv

212 nse based on recognition of the peptide as a self-antigen rather than a viral Ag.

213 s a protein complementary (antisense) to the self-antigen, rather than a response to the native prote

214 lls to recognize MDM2 in vitro, the improved self-antigen recognition abolished their ability to prov

215 s the response of CD4(+)CD8(-) thymocytes to self-antigen recognition, which affects the quantity of

216 Identification of UBE3A as a self-antigen recognized by CD4bs bNAbs offers a mechanis

217 (SF3B3) as the primary conserved, vertebrate self-antigens recognized by the 2F5 and 4E10 antibodies,

218 The major self-antigens recognized by Treg cells remain undefined,

219 d Treg cells are biased towards self and non-self antigens, respectively, but their relative contribu

220 sis, which are driven by foreign antigens or self-antigens, respectively.

221 logy, over-reactive T cell responses against self-antigens result in autoimmunity and, in a transplan

222 (+) Treg formation but is unable to activate self-antigen-selected Tregs to modulate an antiviral imm

223 However, these self-antigen-selected Tregs were unable to suppress the

224 nting peptides derived from tumor-associated self-antigens (self-TAA) are attractive targets for T-ce

225 with an emphasis on: (i) T cell tolerance to self-antigens (self-tolerance); (ii) T cell exhaustion d

226 reg cell development and function in certain self-antigen specific animal models.

227 pheral tissues driven by innate immunity and self antigen-specific pathogenic T and B cells.

228 rgic polyclonal CD4(+) T cells, enriched for self antigen-specific T cell antigen receptors, was also

229 mined PD-1/PD ligand 1 (PD-L1) regulation of self-antigen-specific CD4 and CD8 T cells in autoimmune-

230 digms, but a visual framework is lacking for self-antigen-specific T cells at the effector phase in t

231 Deletion of self-antigen-specific T cells during thymic development

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

233 s, or how immune tolerance is maintained for self-antigen-specific T cells that routinely escape dele

234 A), which were transferred with effector neo-self-antigen-specific T cells to assess whether an autoi

235 identify and select other shared tumor- and self-antigen-specific TCRs and ensure selective antitumo

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

237 Thus, a subset of fully committed self-antigen-specific Treg cells lost Foxp3 expression d

238 expressing the hemagglutinin (HA) as a "neo-self-antigen" specifically in hypothalamic orexin(+) neu

239 l response against the endogenous antigen or self-antigen still remains a major challenge.

240 T (TFH) cells can induce the GC response to self-antigens, subsequently leading to autoimmunity.

241 Moreover, self- and non-self-antigens, such as apolipoprotein B-100 and heat sho

242 s, such as those of microbial pathogens, and self-antigens, such as those targeted in autoimmunity, a

243 lustered B-cell receptors likely recognizing self-antigens, suggesting that SLAM/SAP regulate B-cell

244 y and autoimmunity in vivo, we used a unique self-antigen system comprising seven human melanoma gp10

245 that was dependent on cross-reactivity with self-antigen, TGF-beta1, and MHC class II Ag presentatio

246 m whereby alphabeta T cells indirectly sense self antigens that are bound to an antigen-presenting mo

247 Under these conditions the only response to self-antigen that could be unambiguously identified was

248 t only expands the range of tumor-associated self-antigens that are amenable for T-cell therapy, but

249 Furthermore, these data demonstrate that self-antigens that are expressed at high levels on healt

250 est that they can act as decoy receptors for self-antigens that are recognized by membrane bound BCRs

251 thogenic autoantibodies have specificity for self-antigens that are TLR ligands.

252 extrafollicular (EF) plasmablast response to self-antigens that contain Toll-like receptor (TLR) liga

253 ss I antigens can induce immune responses to self-antigens that contributes to immunopathogenesis of

254 l death, indicating the potential release of self-antigens that favor autoimmunity.

255 velopment can be induced by the same agonist self-antigens that induce negative selection, perturbati

256 tes with immune responses to kidney-specific self-antigens that may increase the risk for acute rejec

257 s invading parasites while strictly avoiding self-antigens that would result in autoimmunity.

258 If a thymocyte is activated by a self-antigen, the cell undergoes either deletion or dive

259 T cells specific for these modified self-antigens then produce cytokines that promote blood

260 deleted or inactivated in the thymus if the self antigens they recognize are ubiquitously expressed.

261 ted arthritogenic TCRs and characterized the self antigens they recognized.

262 For pancreatic self antigen, this resulted in an absence of steady-stat

263 17 cells recognizing both an SFB epitope and self-antigen, thus augmenting autoimmunity.

264 T cells must be tolerant of self antigens to avoid autoimmunity but responsive to fo

265 ytes must productively signal in response to self antigens to mature and enter the peripheral T cell

266 tory receptor 2 (DCIR2) or DEC-205 to target self-antigen to CD11b(+) (cDC2) DCs and CD8(+) (cDC1) DC

267 gulatory T cells are activated by peripheral self-antigen to increase their suppressive function, and

268 ent peripheral self-antigen, DC must acquire self-antigen to mediate thymic negative selection.

269 ave indicated that the selective delivery of self-antigen to the endocytic receptor DEC205 on steady-

270 m by which these proteins enable foreign and self-antigens to be tolerated is unresolved.

271 lpha(+) DCs for presentation of Aire-induced self-antigens to developing thymocytes.

272 esponses and facilitated the presentation of self-antigens to T cells, whereas it inhibited the activ

273 Targeted delivery of self-antigens to the immune system in a mode that stimul

274 dings reveal that for some tissue-restricted self antigens, tolerance relies entirely on nondeletiona

275 In this article, we examined the self-antigen-tolerized DC phenotype, function, and mecha

276 rges individual tissue-restricted peripheral self-antigens (TRA) from the total thymic ectopic TRA re

277 c expression of tissue-restricted peripheral self-antigens (TRA), which is in mature medullary thymic

278 and by antibodies reactive to gluten or the self-antigen transglutaminase 2 (TG2).

279 Expression of tissue-restricted self antigens (TRAs) in medullary thymic epithelial cell

280 ous expression of numerous tissue-restricted self-antigens (TRAs) in medullary thymic epithelial cell

281 In 2 syngeneic HER2+ self-antigen tumor models, we found that either genetic

282 f the TIL TCRs were specific for non-mutated self-antigens, two of which were present in separate pat

283 ate leukocytes can recognize a wide array of self-antigens via pattern recognition receptors, adaptiv

284 e CD4(+) T cells through the presentation of self-antigens via transferred peptide-MHCII complexes of

285 follicular lymphoma patient, the recognized self-antigen was identified as myoferlin.

286 tolerance, T-cell tolerance against hepatic self-antigens was also broken and CD4(+) T cells were id

287 del of negative selection against ubiquitous self-antigen, we previously found that one of the princi

288 h specificity for a set of tissue-restricted self antigens were not deleted at all.

289 n the maintenance of peripheral tolerance to self-antigens whereas under inflammation LCs efficiently

290 ient mice showed heightened sensitivity to a self-antigen, whereas increasing CS content by intrathym

291 immunogenic characteristics of intracellular self antigens, which all participate in development of l

292 toantibodies refer to antibodies that target self-antigens, which can play pivotal roles in maintaini

293 t by promoting expression of tissue-specific self-antigens, which include many cancer antigens.

294 d antibody (Ab) response to pancreatic islet self-antigens, which is a biomarker of progressive islet

295 associated antibodies often cross-react with self-antigens, which leads to autoimmunity, and B1 cells

296 antigen receptor (TCR) by weak agonists and self antigens while not impeding responses to strong ago

297 hese cells was impaired in mice lacking this self-antigen, while Tconv cell development was not negat

298 Tmu receptor specific to hen egg lysozyme (a self-antigen with respect to chicken B cells) induced, i

299 hat underlies progression of the response to self-antigens with implications for SLE development ther

300 that developing T cells that recognize these self-antigens within the thymus undergo clonal deletion.