ライフサイエンスコーパス: self-antigen

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

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

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

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

5 ction against B cells with high affinity for self-antigen.

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

7 e associated with the presence or absence of self-antigen.

8 to a tissue-restricted, melanoma-associated self-antigen.

9 issue, and undergo activation in response to self-antigen.

10 limit the immunostimulatory presentation of self antigens.

11 ulations specific for endogenously expressed self antigens.

12 ance of unwarranted immune responses against self antigens.

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

14 hat increases the inflammatory properties of self antigens.

15 sent on the surfaces of common pathogens and self antigens.

16 oduction, even in response to exogenous, non-self antigens.

17 anergy via unresponsiveness of their BCRs to self-antigens.

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

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

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

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

22 the production of antibodies against nuclear self-antigens.

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

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

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

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

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

28 racterized by pathogenic immune responses to self-antigens.

29 ral specificity resulting in presentation of self-antigens.

30 ells recognizing nonmutated tumor-associated self-antigens.

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

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

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

34 mechanisms that mediate immune tolerance to self-antigens.

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

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

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

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

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

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

41 reign antigens vs. induction of tolerance to self-antigens.

42 athogens, while also sustaining tolerance to self-antigens.

43 defines adaptive response to infections and self-antigens.

44 (Tregs) to maintain peripheral tolerance to self-antigens.

45 oth commensal bacteria and hematopoietic I/i self-antigens.

46 tic hypermutations that improve affinity for self-antigens.

47 ty alloantigens but generally fail to target self-antigens.

48 olyclonal T cell population directed against self-antigens.

49 ve immune responses against microbial and/or self-antigens.

50 a critical mechanism of immune tolerance to self-antigens.

51 on the availability of peptide repertoire of self-antigens.

52 V-2-neutralizing mAbs reacted with mammalian self-antigens.

53 by overloading of the organism with altered self-antigens.

54 ese antibody mutations decrease affinity for self-antigen 19-fold and increase foreign affinity 67-fo

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

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

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

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

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

62 cells (T(reg) cells) able to respond to both self antigens and non-self antigens remain unclear.

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 fide bond-containing proteins, including the self-antigen and melanoma Ag tyrosinase-related protein

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

67 ctivated circulatory cells and was shaped by self-antigen and the peripheral microbiome.

68 nd instead encode antibodies that react with self-antigens and antigens of other species.

69 onspecific B cells with reactivities against self-antigens and antigens of other species.

70 motifs, which recognize both erythrocyte I/i self-antigens and commensal bacteria.

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

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

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

74 (NCRs) temper the T cell immune response to self-antigens and limit the development of autoimmunity.

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

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

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

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

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

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

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

82 mune system activity, such as in response to self-antigens, and are switched on by tumor necrosis fac

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

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

85 ion of this initial BCR repertoire reacts to self-antigens, and these "forbidden" B cells are culled

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

87 -specific recognition of microbial antigens, self-antigens, and tumor-associated carbohydrate antigen

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

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

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

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

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

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

94 esearch implicates autoimmunity to nonmyelin self-antigens as important contributors to disease patho

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

96 on is restricted to mTECs, DCs still present self-antigens at least as frequently as mTECs.

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

98 une responses may lead to antibodies against self-antigens (autoantibodies), resulting in organ-speci

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

100 can be positively or negatively selected by self-antigens, but the mechanisms that determine these o

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

102 ts specific processing and presentation as a self-antigen by antigen-presenting cells.

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

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

105 rates from damaging immune responses against self-antigens by mature lymphocytes, i.e., peripheral to

106 Loss of immune tolerance to self-antigens can promote chronic inflammation and disru

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

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

109 Immunization for EAU with a retinal self-antigen caused selective downregulation of LXA(4) i

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

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

112 the collective expression of the peripheral self-antigen compartment, including tissue-specific anti

113 However, it is not clear how insulin self-antigen controls the selection of autoimmune and re

114 ) IgD(+) phenotype, which is associated with self-antigen cross-reactivity.

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

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

117 ergo clonal proliferation and expansion in a self-antigen dependent manner, which supports the shared

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

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

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

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

122 chronic exposure of self-reactive B cells to self-antigen, did not take place.

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

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

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

126 3 (B:9-23), which are known to be a critical self-antigen-driving disease progress in animal models o

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

128 Although many DUX4 target genes encode self-antigens, DUX4-expressing cancers were paradoxicall

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

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

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

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

133 lso called Mi-2beta, plays a key role in the self-antigen expression in medullary thymic epithelial c

134 t study, we used a murine model of inducible self-antigen expression in the epidermis to elucidate th

135 To maximize the diversity of self-antigen expression, Fezf2 and Aire utilized complet

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

137 (NPSLE), autoimmune responses against neural self-antigens find expression in neurological and cognit

138 We focus on the evidence for a self-antigen-focused T(reg) cell repertoire as well as t

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

140 ute substantially to presentation of diverse self-antigens for establishing central tolerance.

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

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

143 tion immunopathology through presentation of self-antigen from necrotic cardiac cells to cytotoxic CD

144 involves loss of tolerance against modified self-antigens generated in response to hypercholesterole

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

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

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

148 apable of recognizing weak cancer-associated self-antigens have employed altered peptide antigens to

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

150 ive selection of autoreactive B-1 B cells by self-antigen in adult bone marrow.

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

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

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

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

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

156 s driven by intrathymic encounter of agonist self-antigens in a similar manner to the clonal deletion

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

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

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

160 Deposition of self-antigens in glomeruli was examined by staining with

161 promiscuous expression of tissue-restricted self-antigens in medullary thymic epithelial cells.

162 l role in regulating B cell TLR signaling to self-antigens in mice.

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

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

165 avidity to recognize naturally overexpressed self-antigens in the context of self-HLA can be found in

166 ctivating CTL capable of recognizing weak or self-antigens in the context of self-MHC.

167 Clonal deletion of T cells specific for self-antigens in the thymus has been widely studied, pri

168 Aire (-/-) mice fail to express self-antigens in the thymus, exhibit reduced central tol

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

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

171 gnaling as a result of cross-reactivity with self-antigens in vivo.

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

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

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

175 l-autonomous subversion of their response to self-antigen: instead of becoming tolerized and represse

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

177 data indicate that BCR cross-reactivity with self-antigen is a common feature of populations of naive

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

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

180 Identifying TCRs directed against bona fide self-antigens is made difficult by the extraordinary div

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

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

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

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

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

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

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

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

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

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

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

192 d serum antibodies predominately reactive to self antigens, like phosphatidylcholine (PtC), or antige

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

194 utoimmune diseases in which C3 deposition on self-antigens may serve to activate self-reactive B cell

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

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

197 can produce an antibody response to any non-self-antigen molecule in the appropriate context.

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

199 Administration of self-antigen (mouse thyroglobulin; mTg) loaded multi-lig

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

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

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

203 lls become dysfunctional when they encounter self antigens or are exposed to chronic infection or to

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

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

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

207 virus-like particles that displayed the same self-antigen peptide at comparable epitope densities.

208 to the size of viruses, that display a model self-antigen peptide at defined surface densities.

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

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

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

212 eal ligand specificity patterns that include self-antigens presented in an age- and inflammation-depe

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

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

215 ertoire that is biased towards bacterial and self-antigens, promoting a rapid response to infection a

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

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

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

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

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

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

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

223 ble to respond to both self antigens and non-self antigens remain unclear.

224 o less efficient T cell selection, decreased self-antigen representation and increased T cell recepto

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

226 l death protein 1), control the threshold of self-antigen responses directed against cardiac TnI (tro

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

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

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

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

231 itory pathways is an effective way to induce self-antigen specific T cell tolerance to suppress ongoi

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

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

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

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

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

237 or in vitro expansion of the low numbers of self-antigen-specific T cells of sufficient avidity to r

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

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

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

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

242 ncer Ag GUCY2C to establish a model to study self-antigen-specific tolerance mechanisms.

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

244 4(+) T cells that regulate CD4(+) and CD8(+) self-antigen specificities and autoimmune diabetes in NO

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

246 hat self-HLA-restricted T cells specific for self-antigens such as MiHA in MiHApos donors and TAAs ar

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

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

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

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

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

252 r-associated antigens (TAAs) are monomorphic self-antigens that are proposed as targets for immunothe

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

254 encountered antigens such as tissue-specific self-antigens that are regionally drained and through dr

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

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

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

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

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

260 letion and by the identification of multiple self-antigens that promote B cell expansion.

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

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

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

264 17 cells recognizing both an SFB epitope and self-antigen, thus augmenting autoimmunity.

265 , we found that a human TCR specific for the self-antigen thyroid peroxidase (TPO) is positively sele

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

267 cd gain-of-function B cells are activated by self-antigen to form plasmablasts that secrete high tite

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

269 ote autoimmunity through the presentation of self-antigen to T cells.

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

271 well as the APCs responsible for presenting 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 and by antibodies reactive to gluten or the self-antigen transglutaminase 2 (TG2).

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

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

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

281 ell responses against tumor-derived neo- and self-antigens via dermal DCs.

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

283 ntributing to the Aire-mediated induction of self-antigens via super-enhancers.

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

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

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

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

288 active B cells insensitive to stimulation by self-antigen, whereas Toll-like receptor (TLR) signaling

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

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

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

292 ced by specific antigens, possibly including self-antigens, which is consistent with an autoimmune in

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

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

295 ease relies on tolerization of thymocytes to self-antigens whose expression and presentation by thymi

296 ates of apoptosis and interacted with thymic self antigens with higher affinity than did Foxp3(lo) T(

297 Autoreactive B cells that bind self-antigen with high avidity in the bone marrow underg

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.