ライフサイエンスコーパス: autoantigen

1 es both T and B cell recognition of a myelin autoantigen.

2 atients only, supporting a role as psoriatic autoantigen.

3 dehydrogenase complex is considered the main autoantigen.

4 nd was independent of the endogenous retinal autoantigen.

5 verse sources including its homologous human autoantigen.

6 ted from induction of EAE by the appropriate autoantigen.

7 s of autoantibodies, as well as their target autoantigens.

8 d the cleavage of many nucleolar proteins or autoantigens.

9 for reactivity against a panel of 44 non-HLA autoantigens.

10 stroma cells, in the presence or absence of autoantigens.

11 y by broadly degrading nucleolar proteins or autoantigens.

12 that showed increased specificity to peptide autoantigens.

13 which presents multiple vitiligo melanocyte autoantigens.

14 gnize insulin or HEL as foreign, rather than autoantigens.

15 to pathogens, other foreign substances, and autoantigens.

16 luence repertoire responsiveness to specific autoantigens.

17 riety of environmental allergens and also to autoantigens.

18 r MS patients and identified three different autoantigens.

19 s) can target and affect the levels of these autoantigens.

20 n regulating the expression of the major T1D autoantigens.

21 about what regulates the expression of these autoantigens.

22 g cells (APCs) displaying a diverse array of autoantigens.

23 The nucleoli are abundant with autoantigens.

24 subjects to discover sarcoidosis-associated autoantigens.

25 ation to sarcoidosis and potentially related autoantigens.

26 genase and epoxide hydrolase-2 as additional autoantigens.

27 to mice either carrying or lacking relevant autoantigens.

28 e miRNAs modulate the mRNA levels of the T1D autoantigens.

29 activity to spread from EGFP to other B-cell autoantigens.

30 ew ICIS patients were seropositive for these autoantigens.

31 immune tolerance to both food allergens and autoantigens.

32 Type 1 diabetes islet cell autoantigen 512 (ICA512/IA-2) is a tyrosine phosphatase-

33 ed with increased circulating apoptotic cell autoantigens (AC-Ags) as well as increased type I IFN si

34 Th cells sensitized against autoantigens acquire pathogenicity following two sequent

35 cells in response to MHC class II-restricted autoantigen activation by 33D1(+)CD11b(int) dendritic ce

36 s include direct damage on tissue-containing autoantigens, activation and migration of basophils to l

37 d ARFNDLRFV) and an analogue of a melanocyte autoantigen (ADAMTSL5, VRSRR-abu-LRL) implicated in psor

38 ic TSHR Abs following the release of thyroid autoantigens after radio-iodine therapy in Graves patien

39 ive conditions for the expression of cryptic autoantigens, allowing these autoantibodies to bind anti

40 d discovered that the transcriptomes of both autoantigen and anti-CD3/CD28 stimulated CD4(+) T lympho

41 e T cells in helping them to recognize their autoantigen and become efficiently reactivated within th

42 Co-delivery of both autoantigen and dexamethasone increased B-cell populatio

43 rmore, proliferative responses to endogenous autoantigen and diabetogenic function were impaired in B

44 Our findings suggest that both Dsg1 autoantigen and LJM11 environmental Ag could be the init

45 vy chain alpha (MYHCA) is a dominant cardiac autoantigen and that T cells with T cell receptor (TCR)

46 Toll-like receptor 7 (TLR7) mediates autoantigen and viral RNA-induced cytokine production.

47 Finally, we identified 1126 genes as human autoantigens and 1071 related human diseases, with which

48 ich are predicted to target the mRNAs of T1D autoantigens and 12 of which are glucose-sensitive.

49 with respect to modulating responses against autoantigens and alloantigens after kidney transplant.

50 These observations suggest that both autoantigens and certain classes of pathogens provide th

51 ing new methods and technologies to identify autoantigens and characterize immune responses toward th

52 ivation drives the removal of damaged cells, autoantigens and environmentally derived antigens.

53 s of self-tolerance and formation of nuclear autoantigens and immune complexes resulting in inflammat

54 ss-induced exosomal release of intracellular autoantigens and immunostimulatory chaperones may play a

55 le dampening immune reactivity to allergens, autoantigens and microbiome determinants.

56 n the innate immune response to self-derived autoantigens and pathogen-derived danger signals and ant

57 and tolerability of administration of islet autoantigens and peptides thereof into recipients with o

58 measurement of multiple serum antibodies to autoantigens and peptides.

59 ntly exhibit IgE autoantibodies against many autoantigens and that IL-24 is a common, specific, and f

60 mmunity provides induced tolerance to ocular autoantigen, and requires melanocortin 5 receptor (MC5r)

61 CD1a itself rather than lipids serves as the autoantigen, and various mechanisms by which the activat

62 contain FRC-like cells expressing beta-cell autoantigens, and are able to induce systemic and antige

63 and IgE responses to vaccines, allergens and autoantigens, and exert critical immunoregulatory functi

64 e dehydrogenase, and catalase as the primary autoantigens, and glutamate dehydrogenase and epoxide hy

65 m, psoriasis-associated susceptibility loci, autoantigens, and multiple environmental factors.

66 IgG and IgM autoantibodies against numerous autoantigens, and some autoantibodies were specific for

67 cal tolerance to clinically relevant gastric autoantigens, and Th2 responses can be a pathogenic mech

68 -producing Bregs maintain tolerance to islet autoantigens, and that hyperglycemic nonobese diabetic (

69 hat AD patients produce IgE Abs specific for autoantigens, and we described Th as well as CD8(+) T ce

70 leads to the breakdown of tolerance to these autoantigens, and we have an incomplete understanding of

71 Autoantibodies to these autoantigens appear years before disease onset and are w

72 The genes encoding these autoantigens are abnormally expressed in peripheral gran

73 Many autoantigens are components of multimolecular complexes,

74 In this technology the target autoantigens are derived from a protein/nucleoprotein mi

75 Four major autoantigens are established (insulin, glutamate decarbo

76 rts of these countless previously identified autoantigens are randomly dispersed in the literature.

77 aimed at antigen-specific tolerance to these autoantigens are thus indicated for these diseases.

78 The autoantigens are ubiquitous and partition with mitochond

79 e cell surface of the allograft endothelium, autoantigens are usually cryptic.

80 ,000-human-proteome array and to a 128-known-autoantigen array, respectively.

81 eniently browse, retrieve and download human autoantigens as well as their associated diseases.

82 e polyspecific and not focussed on essential autoantigens, as described for other APS-1-related autoi

83 To discover novel autoantigens associated with Lyme arthritis (LA), we ide

84 AM14 Vkappa8 B cells can respond robustly to autoantigen/autoadjuvant immune complexes and could ther

85 autoimmune disease pemphigus vulgaris (PV), autoantigen-based chimeric immunoreceptors can direct T

86 odimer's likelihood of productively engaging autoantigen, because they are pervasive and often high f

87 Ralphabeta heterodimer productively engaging autoantigen, because they are widely present in the popu

88 t), and T and B cell autoepitopes in the APS autoantigen beta(2)-glycoprotein I (beta(2)GPI).

89 rather than developing, and are enriched for autoantigen binding.

90 Here we speculated that differences in autoantigen-binding repertoires between a heterozygote's

91 ficity is independent from the nature of the autoantigen, but rather relies on the disease-specific m

92 cell development in the presence/absence of autoantigen by crossing the Ig KI mice to Tgm2-/- mice.

93 Tetraspanin-7 was confirmed as an autoantigen by demonstrating binding to autoantibodies i

94 atured Bregs may maintain tolerance to islet autoantigens by selectively suppressing autoreactive T-c

95 of a limited group of ubiquitously expressed autoantigens by the immune system.

96 These mediators, combined with exposure of autoantigens, can lead to an adaptive T cell-mediated re

97 inity CD4(+) mimotope (BDC2.5(mim)) of islet autoantigen chromogranin A (ChgA) with or without calcit

98 , derived from major prevalent citrullinated autoantigens (citrullinated filaggrin, fibrinogen, vimen

99 AMR patients exhibited greater reactivity to autoantigens compared to DSA-negative (P < .0001) and AM

100 tage of patients with elevated reactivity to autoantigens compared to non-AMR (P = .002) and healthy

101 perties and enhanced expression of beta-cell autoantigens compared with nontransgenic NOD TLOs found

102 presence of autoantibodies to multiple-islet autoantigens confers high risk for the development of ty

103 diseases, with which we constructed a human autoantigen database (AAgAtlas database 1.0).

104 The autoantigen, defined in mouse brain lysate by Western bl

105 The extent of nucleolar autoantigen degradation upon C1 treatment was estimated

106 ve AA pathobiology independent of classical, autoantigen-dependent CD8(+) T-cell functions.

107 of the multiplicity of target citrullinated autoantigens described for ACPA, we generated a multiepi

108 tibody receptor (CAAR), consisting of the PV autoantigen, desmoglein (Dsg) 3, fused to CD137-CD3zeta

109 Of the 31 IgE autoantigens detected in more than 70% of patients, 8 we

110 ially accumulated in diseased skin and these autoantigens directly activated CD1b-autoreactive HJ1 T

111 These findings indicate that the autoantigen drives autoimmunity in MuSK MG through the a

112 AART) expressing the pemphigus vulgaris (PV) autoantigen DSG3 fused to CD137-CD3zeta signaling domain

113 e produced by B cells in response to soluble autoantigens due to defects in B cell tolerance mechanis

114 ated by factors outside the B cell including autoantigen engagement of the B-cell receptor (BCR) with

115 proinsulin is a major source for HLA class I autoantigen epitopes implicated in CD8 T cell (CTL)-medi

116 These novel APS1 autoantigens exhibit tissue-restricted expression, inclu

117 ellular regulatory networks by reprogramming autoantigen-experienced CD4+ T cells into autoimmune dis

118 rential upregulation of Kv1.3 over KCa3.1 on autoantigen-experienced effector memory T cells, whether

119 ive inhibitory mechanisms induced by chronic autoantigen exposure in vivo.

120 ed in gene silencing associate with aberrant autoantigen expression.

121 on of autoreactive TR1 cells, requires local autoantigen expression.

122 Chromogranin A (ChgA) is an autoantigen for CD4(+) T cells in the nonobese diabetic

123 (pDCs)-Type I interferon (IFN-I) and acts as autoantigen for pathogenic Th17-cells.

124 of common mammalian lipids that function as autoantigens for alphabeta and gammadelta T cells, a nov

125 hich have been implicated in presentation of autoantigens for negative selection of T cell progenitor

126 expressing proinsulin and GAD to protect the autoantigens from degradation in an oral vaccine and tes

127 nderlying disease propagation, with specific autoantigens functioning as the hubs around which amplif

128 gnificantly reduced the mRNA levels of all 3 autoantigens, further confirming the importance of miRNA

129 epigenetic gene silencing modification, and autoantigen gene expression and disease status in ANCA-a

130 e likelihood of stable remission and explain autoantigen gene regulation.

131 Low-affinity BCR interactions with autoantigens generated during apoptosis are also positiv

132 easured gene-specific DNA methylation of the autoantigen genes myeloperoxidase (MPO) and proteinase 3

133 ating that loss of SNERV underlies the lupus autoantigen gp70 overproduction that promotes nephritis

134 ne repertoires are limited and reactivity to autoantigens has not been demonstrated.

135 ew patients but collectively targeting >1000 autoantigens have been attributed to false positives (La

136 In both diseases, the autoantigens have been cloned and characterized; pemphig

137 om these, 19 plasma membrane proteins and 10 autoantigens identified from gene ontology analysis were

138 An unbalance between Abs that recognize an autoantigen (idiotypes; IDs) and Igs that bind such Abs

139 thyroid autoimmunity may include IgE against autoantigens, immune complexes, and complement.

140 spholipase A2 receptor 1 (PLA2R) is a target autoantigen in 70% of patients with idiopathic membranou

141 Myeloperoxidase (MPO) is a well defined autoantigen in ANCA-associated vasculitis.

142 has accumulated in the artery wall is a key autoantigen in atherosclerosis, and activation of antige

143 ance of transcriptional dysregulation of the autoantigen in autoimmune disease.

144 tite motif (TRIM) protein family, is a major autoantigen in autoimmune diseases and a modulator of in

145 r La) is a 48 kDa RNA-binding protein and an autoantigen in autoimmune disorders such as systemic lup

146 Our results identify DNAJB9 as a putative autoantigen in fibrillary GN and suggest IgG1 and classi

147 Proteinase 3 (PR3), the autoantigen in granulomatosis with polyangiitis, is expr

148 The peripheral membrane protein GAD65 is an autoantigen in human T1D.

149 spholipase A2 receptor (PLA2R1) is the major autoantigen in idiopathic membranous nephropathy.

150 e clonotype that encodes a potent CD4 T cell autoantigen in its antigen binding site.

151 or has been recently proposed as a potential autoantigen in manifestations of Lyme disease that are t

152 Ro60 was first described as an autoantigen in patients with rheumatic disease, and Ro60

153 spholipase A2 receptor (PLA2R1) is the major autoantigen in primary membranous nephropathy.

154 either dead or damaged cells serves as a key autoantigen in rheumatoid arthritis (RA).

155 Insulin is a major autoantigen in T1D, but how its peptides are presented t

156 t proinsulin is an early and integral target autoantigen in T1D.

157 yelin oligodendrocyte glycoprotein (MOG), an autoantigen in the EAE model.

158 ese data indicate that SERCA2a is a critical autoantigen in the mediation of atrial inflammation in m

159 We found that both Trm and Tcm sensed autoantigen in the skin long after stabilization of dise

160 ion of GRP78 in beta-cells generates a novel autoantigen in type 1 diabetes, opening new avenues for

161 Insulin is a major autoantigen in type 1 diabetes, targeted by both CD8 and

162 ule protein, chromogranin A (ChgA), as a new autoantigen in type 1 diabetes.

163 system to facilitate intradermal delivery of autoantigens in a minimally invasive manner.

164 TGs are also autoantigens in a number of immune diseases, resulting i

165 r identified MAGEB2 and PDILT as novel major autoantigens in APS1.

166 anslocator 1 (ANT1), have been identified as autoantigens in cardiac autoimmunity.

167 Specific autoantigens in experimental autoimmunity-associated ath

168 c islets release the intracellular beta-cell autoantigens in human T1D, GAD65, IA-2, and proinsulin i

169 stigated whether enteric alpha-defensins are autoantigens in humans and mice with AIRE deficiency.

170 cardiac mitochondrial proteins can be target autoantigens in myocarditis, supporting the notion that

171 ing patient-derived mAbs identifies relevant autoantigens in patients with IgG(4)-RD.

172 PR3) and myeloperoxidase (MPO) are two major autoantigens in patients with vasculitis with ANCA.

173 d transcription results in newly synthesized autoantigens in peripheral neutrophils of patients.

174 ain-containing 7A (THSD7A) are the two major autoantigens in primary membranous nephropathy (MN), and

175 Finally, it appears likely that other autoantigens in primary MN exist.

176 The target autoantigens in several organ-specific autoimmune diseas

177 , La (SSB), and alpha-fodrin protein, common autoantigens in Sjogren's syndrome, via extracellular ve

178 chains reactivity toward disease-associated autoantigens in the context of diverse TCRalpha.

179 nd glutamate decarboxylase (GAD65) are major autoantigens in type 1 diabetes (T1D).

180 g antibody responses to foreign antigens and autoantigens in vivo is still unclear due to a lack of s

181 PO and PRTN3 and increased expression of the autoantigens; in remission, DNA methylation generally in

182 ammatory, IL-17-driven skin disease in which autoantigen-induced CD8(+) T cells have been identified

183 y fibrosis (IPF); however, the repertoire of autoantigens involved in this disease and the clinical r

184 Autoimmunity against pancreatic beta-cell autoantigens is a characteristic of childhood type 1 dia

185 Identifying T cell epitopes of islet autoantigens is important for understanding type 1 diabe

186 impairment of antigenic responses, including autoantigens, is a hallmark of sepsis-induced immunopara

187 cell receptor (TCR) specific for a beta cell autoantigen leads to activation of islet-reactive T cell

188 into TR1-like cells, which in turn suppress autoantigen-loaded antigen-presenting cells and drive th

189 BCR) stimulation in conjunction with ligand (autoantigen)- mediated BCR signaling in chronic lymphocy

190 ugh the membrane comprising the high density autoantigen mixture to induce rapid binding of patient a

191 ilieu driving T-cell subset polarization and autoantigen modifications.

192 ed with reduced number, but not function, of autoantigen (MOG)-specific pathogenic CD4 T cells in the

193 ific clearance of antibodies recognizing the autoantigen, myelin oligodendrocyte glycoprotein and tum

194 ral blood mononuclear cells and identified 2 autoantigens, N-acetylglucosamine-6-sulfatase (GNS) and

195 IL-24 is a common, specific, and functional autoantigen of IgE antibodies in patients with CSU.

196 se complex (PDC-E2), the major mitochondrial autoantigen of PBC and xenobiotic cross reactive chemica

197 m with a mimotope of the major mitochondrial autoantigen of PBC, 2-octynoic acid (2-OA) coupled to BS

198 essed how tolerance to a naturally expressed autoantigen of the central nervous system shapes the CD4

199 SL5) as an HLA-C*06:02-presented melanocytic autoantigen of the Valpha3S1/Vbeta13S1 TCR.

200 nerate citrullinated proteins - the hallmark autoantigens of RA.

201 ed the Ig gene repertoires and reactivity to autoantigens of single-sorted B cells from pediatric thy

202 s show that maximal T-cell responses against autoantigen or repeated tetanus toxoid stimulations requ

203 es from PubMed using the keywords of either 'autoantigen' or 'autoantibody' or their lexical variants

204 ties between viral peptide sequences and T1D autoantigen peptide sequences.

205 An autoantigen piezoelectric sensor to quantify specific ci

206 is work, dexamethasone was co-delivered with autoantigen (PLP) in vivo to create effective ASIT for t

207 The ADAMTSL5 autoantigen possessed a P7-Leu instead of the P7-Arg res

208 -DQ8/8 on dendritic cells pulsed with islet autoantigens preproinsulin (PPI), GAD65, and IA-2, follo

209 engulfment of dying cells and prevention of autoantigen presentation to other immune cells.

210 lls has the potential to reduce the risk for autoantigen presentation while retaining the phagocytic

211 oimmune response against melanocytes through autoantigen presentation.

212 ently express TCRs activatable by ubiquitous autoantigens presented by class II MHCs on conventional

213 Barr virus and Akkermansia muciniphila), and autoantigens presented by DR2a and DR2b.

214 he T cells scan the leptomeningeal space for autoantigen-presenting cells (APCs).

215 -1 diabetes, treatment with the glycosylated autoantigens prevented T-cell-mediated diabetes, expande

216 proves neonatal immune tolerance against the autoantigen (pro)insulin.

217 ported mucosal administration of T1D-related autoantigens [proinsulin or glutamic acid decarboxylase

218 ce of a variety of islet-infiltrating, islet-autoantigen reactive T cells in individuals with T1D, an

219 Autoantigen-reactive CD4(+) memory T cell clones and an

220 Finally, profiling the autoantigen reactivity of MIS-C plasma revealed both kno

221 Autoantigen reactivity was present in most BAL and serum

222 anged TCRalpha endowed unprimed T cells with autoantigen reactivity.

223 ly affects only the B1a cell population with autoantigen receptors rather than the entire pool of B1a

224 ction; in particular, B1a cells that express autoantigen receptors, such as anti-phosphatidylcholine

225 ociated with BCR replacement that eliminated autoantigen recognition in a proportion of developing an

226 BCR signal induction and the involvement of autoantigen recognition remain unclear.

227 proton pump, H(+)/K(+) ATPase, is the major autoantigen recognized by autoreactive T cells.

228 We extracted 45 830 autoantigen-related abstracts and 94 313 sentences from

229 us and partly directed against intracellular autoantigens released during tissue destruction.

230 The identification of autoantigens remains a critical challenge for understand

231 ynthesis of p24(PR3/MBN) seems to expand the autoantigen repertoire, because immunoblots showed that

232 INTERPRETATION: MAP1B, the PCA-2 autoantigen, represents a novel target in paraneoplastic

233 Interrogation of established autoantigens revealed highly reliable detection of autoa

234 se findings establish a link among the lupus autoantigen Ro60, Alu retroelements, and type I interfer

235 cy and definition of novel autoantibody, the autoantigen's immunochemical identification, clinical an

236 ce and NHP, polyclonal B cell activation and autoantigens secretion induced autoantibodies against ds

237 MC from AIH patients with the AIH-associated autoantigen SEPSECS resulted in significant TNF producti

238 Most of the stem bnAbs we examined bound autoantigens; several showed staining of HEp-2 cells.

239 that catalyzes gluten deamidation is also an autoantigen, something that is hardly coincidental.

240 iseases, accompanied by high serum levels of autoantigen-specific antibodies.

241 Fundamentally, the autoantigen-specific B cell lineage leads to production

242 easible strategy for the characterization of autoantigen-specific B cell subsets in different models

243 These autoantigen-specific B cells have been consistently iden

244 Ab-mediated diseases contains high levels of autoantigen-specific B cells that are likely to account

245 Moreover, TCRB CDR3 clonotypes expressed by autoantigen-specific CD4(+) T cells are shorter compared

246 ed immunogenic potential and failed to prime autoantigen-specific CD4+ T cells to mediate autoimmunit

247 ombinatorial therapy promotes engraftment of autoantigen-specific donor T(regs) and controls islet au

248 ajor caveats, including the low frequency of autoantigen-specific Foxp3(+) Tregs and lack of understa

249 c mice, we provide direct evidence for human autoantigen-specific Foxp3(+)Treg-induction in vivo.

250 Autoantigen-specific immunological tolerance represents

251 nts for central tolerance can be overcome by autoantigen-specific immunomodulatory therapy.

252 ics exist in the affinity matured peripheral autoantigen-specific memory pools of individuals, both o

253 Here, we investigated autoantigen-specific plasma cells, CD4(+) T cells, and I

254 PD-L2(+) B1a cell subset, are enriched with autoantigen-specific receptors.

255 Autoantigen-specific regulatory immunity emerges in the

256 of human autoimmune uveitis marked by ocular autoantigen-specific regulatory immunity in the spleen.

257 Here, we show that such ubiquitous autoantigen-specific T cells are also awakened by extrah

258 However, infusion of autoantigen-specific T(regs) after alphaCD3 alone result

259 goal for type 1 diabetes (T1D) is to induce autoantigen-specific tolerance of T cells.

260 The development of autoantigen-specific vaccination strategies for Foxp3(+)

261 with established age-associated profiles of autoantigen specificities and autoantibody class switchi

262 patients produce IgE autoantibodies against autoantigens, such as thyroperoxidase or double-stranded

263 ated atherosclerosis and identified vascular autoantigens targeted by autoimmunity.

264 Glycosylated autoantigens targeted to hepatic antigen-presenting cell

265 Autoantigen targeting by mAb123 increased RAG-2 expressi

266 ritis (RA), and are thought to have distinct autoantigen targets.

267 s had significantly greater reactivity to 13 autoantigens than individuals with low chemokine scores.

268 re protein of low-density lipoprotein, is an autoantigen that drives the generation of pathogenic T-h

269 of IgE autoantibodies against an antigen or autoantigen that has yet to be definitively identified,

270 uced by T-cell receptor signaling implicates autoantigens that have not yet been identified in this c

271 The nature of autoantigens that trigger autoimmune diseases has been m

272 Our data suggest oral autoantigen therapy alone does not effectively influence

273 (e.g., the spleen) where, in the absence of autoantigen, they establish transient contacts with stro

274 wed self-reactivity upon testing with common autoantigens, they recognized 1547 proteins present on a

275 by presenting the same foreign peptides and autoantigens to autoreactive CD4(+) T cells in MS.

276 a role of thymic B cells in presentation of autoantigens to developing T cells during negative selec

277 tase to covalently attach disease-associated autoantigens to genetically engineered and to unmodified

278 r function, providing a continuous source of autoantigens to promote autoimmunity and further amplify

279 tory cytokines and chemokines, presenters of autoantigens to T cells, producers of pathogenic antibod

280 roach, coupled with epitope mapping of known autoantigens, to identify and characterize autoepitopes

281 Antibodies to the autoantigen transglutaminase 2 (TG2) are a hallmark of c

282 rs (BCR) specific for gluten peptides or the autoantigen transglutaminase 2 (TG2).

283 mmune disease, but the precise nature of the autoantigens triggering T-cell activation remains poorly

284 as an "adjuvant" during the presentation of autoantigens, tying together genetic variation in the MH

285 utoreactive IgE raised against the main MCTD autoantigen U1 small nuclear ribonucleoprotein 70k were

286 atherogenesis and identified specific aortic autoantigens using serologic proteomic studies.

287 The introduction of beta-cell autoantigens via the gut through Lactococcus lactis (L.

288 on of Neu5Gc (from red meat) acts as a "xeno-autoantigen" via metabolic incorporation into endogenous

289 as discovered that the controlled release of autoantigen was important for the suppression of clinica

290 n monitoring (QCM-D) where TRIM21 and TROVE2 autoantigens were covalently immobilized, allowing the s

291 proteolysis, but many nucleolar proteins and autoantigens were degraded by C1 proteases; >20 nucleola

292 leoli were targeted by C1q and two nucleolar autoantigens were degraded by C1r/C1s proteases, we cons

293 By using array analyses, more than 200 IgE autoantigens were found in patients with CSU that were n

294 Antibodies to Borrelia burgdorferi or autoantigens were measured by enzyme-linked immunosorben

295 Immune effector pathways generate additional autoantigen, which feeds further immune response.

296 tibodies predominantly detect RNA-associated autoantigens, which are commonly targeted in TLR7-domina

297 studies to date have employed single peptide autoantigens, which would restrict ASI to patients expre

298 named nucleolar RNA helicase 2) is a nuclear autoantigen with undefined roles in cancer.

299 It is unknown whether autoantigens with weak cross-linking potential, such as

300 al protein C receptor, a clonally restricted autoantigen, with minimal CDR1, CDR2, or HV4 contributio