ライフサイエンスコーパス: autoantigen

1 atients only, supporting a role as psoriatic autoantigen.

2 dehydrogenase complex is considered the main autoantigen.

3 nd was independent of the endogenous retinal autoantigen.

4 e in the presence or absence of the IgG2a(a) autoantigen.

5 likely activated and perpetuated by cognate autoantigen.

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

7 -forming cells (AFCs) in the presence of the autoantigen.

8 ere activated upon instillation of exogenous autoantigen.

9 ested FL Igs recognized vimentin as a shared autoantigen.

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

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

12 to pathogens, other foreign substances, and autoantigens.

13 luence repertoire responsiveness to specific autoantigens.

14 riety of environmental allergens and also to autoantigens.

15 r MS patients and identified three different autoantigens.

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

17 d the cleavage of many nucleolar proteins or autoantigens.

18 n regulating the expression of the major T1D autoantigens.

19 about what regulates the expression of these autoantigens.

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

21 The nucleoli are abundant with autoantigens.

22 subjects to discover sarcoidosis-associated autoantigens.

23 ation to sarcoidosis and potentially related autoantigens.

24 genase and epoxide hydrolase-2 as additional autoantigens.

25 to mice either carrying or lacking relevant autoantigens.

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

27 ell responses that spread to other beta-cell autoantigens.

28 ased Abs targeting a broad range of systemic autoantigens.

29 IL-10 (but not IL-4) responses to beta-cell autoantigens.

30 maintenance of self-tolerance to AC-derived autoantigens.

31 peripheral B cell tolerance to cell surface autoantigens.

32 of B cells expressing antibodies recognizing autoantigens.

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

34 y by broadly degrading nucleolar proteins or autoantigens.

35 that showed increased specificity to peptide autoantigens.

36 which presents multiple vitiligo melanocyte autoantigens.

37 Cell division autoantigen 1 (CDA1) enhances TGF-beta signaling in rena

38 pontaneous type 1 T-helper cell responses to autoantigens, ABT-induced IL-4 and humoral responses, an

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

40 Th cells sensitized against autoantigens acquire pathogenicity following two sequent

41 une complexes (ICs) containing nucleoprotein autoantigens activate plasmacytoid dendritic cells (PDCs

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

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

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

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

46 reduced frequencies of T cells responding to autoantigen and alloantigen peptide-MHC tetramers in TCR

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

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

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

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

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

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

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

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

55 immune responses to microbial infection and autoantigens and contributes to intestinal immune homeos

56 -cell clonal expansion against allergens and autoantigens and demonstrate how hypersensitive response

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

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

59 Apoptotic cells are a source of autoantigens and impairment of their removal contributes

60 B cells, reduced antibodies against nuclear autoantigens and improved kidney pathology.

61 of clinical and experimental systems, novel autoantigens and neoepitopes involved in RA have been re

62 measurement of multiple serum antibodies to autoantigens and peptides.

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

64 n processing of pathogen-derived proteins or autoantigens and we find distinct paths for peptide proc

65 MOG (rhMOG), a T cell- and B cell-dependent autoantigen, and exhibited diminished Th1 and Th17 respo

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

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

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

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

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

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

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

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

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

75 Many autoantigens are components of multimolecular complexes,

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

77 Four major autoantigens are established (insulin, glutamate decarbo

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

79 The autoantigens are ubiquitous and partition with mitochond

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

81 rst case of a pathophysiologically important autoantigen as a ubiquitin-independent substrate of the

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

83 ion failed to break tolerance to the gastric autoantigen, as migratory DCs presenting the gastric aut

84 ll activation implied the presentation of an autoantigen, as the weakly pathogenic T cells, which rem

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

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

87 th IL-7 or IL-15 enabled T cell responses to autoantigens associated with RA.

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

89 ly driving the inappropriate localization of autoantigen-bearing DCs.

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

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

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

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

94 These abnormalities lead to an increased autoantigen burden and antigen modifications, such as nu

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

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

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

98 osttranslational modification (PTM) of islet autoantigens can cause lack of central tolerance in type

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

100 lated properties and suggest that pathogenic autoantigens, capable of efficiently priming CTLs while

101 Thus, EXOs could be the autoantigen carrier with potent adjuvant activities and

102 ropil brain immunostaining were selected for autoantigen characterization.

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

104 rsen into autoimmune disease?" The theory of autoantigen complementarity posits that the initiating i

105 n how components delineated in the theory of autoantigen complementarity potentially promote the acqu

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

107 cally distinct and potentially have separate autoantigens contributing to pathogenesis.

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

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

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

111 Autoantigen-derived immunodominant epitopes are resistan

112 ystem using human CD4(+) T cells pulsed with autoantigen-derived peptides.

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

114 ing, autoimmune-initiating potential of this autoantigen (designated autoantigenicity) was impaired.

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

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

117 CRP bound to autoantigen did not induce IFNalpha in PBMCs or PDCs, wh

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

119 antigen microarrays have been developed for autoantigen discovery and profiling autoantibody respons

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

121 ed in gene silencing associate with aberrant autoantigen expression.

122 cells into endogenous islets requires local autoantigen expression.

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

124 HSP70 protein was an autoantigen for IPF CD4 T cells, inducing lymphocyte pro

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

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

127 imited adenoviral infection with the hepatic autoantigen formiminotransferase cyclodeaminase (FTCD).

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

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

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

131 bacteria for controlled secretion of the T1D autoantigen GAD65370-575 and the anti-inflammatory cytok

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

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

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

135 ire induces the expression of a large set of autoantigen genes in the thymus, driving immunological t

136 erases and to activate ectopic expression of autoantigen genes in the thymus.

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

138 g Msr1 were inefficient at taking up the key autoantigen glucose-6-phosphate isomerase and that Msr1-

139 tetanus toxoid, beta-lactoglobulin, and the autoantigens glutamic acid decarboxylase 65, heat shock

140 and beta-lactoglobulin) and diabetes-related autoantigens (glutamic acid decarboxylase 65, insulin, h

141 n blood and skin, but the search for natural autoantigens has been confounded by background T cell re

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

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

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

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

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

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

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

149 Because cardiac myosin (CM) is a dominant autoantigen in autoimmune heart disease, we hypothesized

150 of TG2 activity and the enzyme's role as an autoantigen in celiac disease, we have addressed structu

151 HSP70 was identified as a potential IPF autoantigen in discovery assays.

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

153 atory cytokines and to proteinase 3, a major autoantigen in GPA, and analyzed the effects on NK cell

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

155 of PR3, scavengers, and clearers of the PR3 autoantigen in granulomatosis with polyangiitis.

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

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

158 ting the endogenous gastric H(+)/K(+) ATPase autoantigen in its normal physiological context.

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

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

161 Thus, we uncover a role of LL37 as a T-cell autoantigen in psoriasis and provide evidence for a role

162 omal cadherin desmoglein 3 (Dsg3), the major autoantigen in PV, cause loss of epidermal keratinocyte

163 rullinated collagen II (CII) is a well-known autoantigen in rheumatoid arthritis (RA).

164 ulating autoantibody against a 43 kDa muscle autoantigen in sporadic inclusion body myositis (IBM) an

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

166 Threonyl-tRNA synthetase (TARS) is an autoantigen in the autoimmune disorder myositis, and bor

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

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

169 ntral nervous system myelin, is an important autoantigen in the neuroinflammatory disease multiple sc

170 The target autoantigen in this disease is the noncollagenous domain

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

172 ating the notion that insulin is the primary autoantigen in type 1 diabetes.

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

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

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

176 Specific autoantigens in experimental autoimmunity-associated ath

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

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

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

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

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

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

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

184 The target autoantigens in several organ-specific autoimmune diseas

185 ring an attractive candidate modifying islet autoantigens in T1D.

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

187 date for the long-time hypothesized role of autoantigens in the pathogenesis of CLL.

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

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

190 tients make antibodies to a limited group of autoantigens, including RPC1, encoded by the POLR3A gene

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

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

193 prevalent epitope of the beta-cell-specific autoantigen islet-specific glucose-6-phosphatase catalyt

194 As insulin is the major autoantigen leading to T1D, we tested the capacity of in

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

196 sponses toward unknown arterial wall-derived autoantigens may be organized by artery tertiary lymphoi

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

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

199 ent the I-A(b)-immunodominant peptide of the autoantigen myelin oligodendrocyte glycoprotein (MOG).

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

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

202 Oily autoantigens naturally coat the surface of the skin; thu

203 d by autoantibodies directed against nuclear autoantigens normally concealed from immune recognition

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

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

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

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

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

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

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

211 cell leukemia (TCL)1 cells reactive with the autoantigen phosphatidylcholine (PtC).

212 An autoantigen piezoelectric sensor to quantify specific ci

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

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

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

216 oimmune response against melanocytes through autoantigen presentation.

217 urally accumulate in epidermis and sebum, as autoantigens presented by CD1a.

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

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

220 ined poly(ADP-ribose) polymerase 1, Lupus Ku autoantigen protein p70, and glyceraldehyde 3-phosphate

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

222 data show that injection of small numbers of autoantigen-reactive CD4(+) T cells can cause a targeted

223 Autoantigen reactivity was present in most BAL and serum

224 anged TCRalpha endowed unprimed T cells with autoantigen reactivity.

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

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

227 sue microenvironment control the dynamics of autoantigen recognition by T cells and their resulting p

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

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

230 pha5 is also an important component of islet autoantigen recognition.

231 othesis, we examined the presentation of the autoantigen recognized in autoimmune gastritis, gastric

232 , particularly through the identification of autoantigens recognized by patient sera.

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

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

235 Interestingly, RNA helicase A and La autoantigen relocated from a nuclear location to form cy

236 gen, as migratory DCs presenting the gastric autoantigen remain tolerogenic under such conditions, de

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

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

239 Interrogation of established autoantigens revealed highly reliable detection of autoa

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

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

242 therapeutic potential of orally administered autoantigen-secreting LL for tolerance induction in T1D.

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

244 erimental autoimmune encephalomyelitis, that autoantigen-sensitized XX lymph node cells, compared wit

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

246 The high levels of autoantigen specific peripheral plasmablasts indicate re

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

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

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

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

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

252 Autoantigen-specific immunological tolerance represents

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

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

255 Autoantigen-specific regulatory immunity emerges in the

256 an autoimmune uveitis, with the emergence of autoantigen-specific regulatory immunity in the spleen t

257 Importantly, autoantigen-specific T-cell frequencies in the periphery

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

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

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

261 ation of effector-memory T cells of multiple autoantigen specificities in the periphery of type 1 dia

262 chanism by which Sjogren syndrome-associated autoantigen (SSA), an estrogen receptor (ER) coactivator

263 Our results suggest autoantigen-stimulated BCR signaling in secondary tissue

264 Peripheral cytokines from autoantigen-stimulated splenocytes were measured, and ce

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

266 ated atherosclerosis and identified vascular autoantigens targeted by autoimmunity.

267 Autoantigen targeting by mAb123 increased RAG-2 expressi

268 une etiology for their symptoms.1 Additional autoantigen targets continue to be identified, and the p

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

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

271 ptide of the TRIM21 (TRIM: tripartite motif) autoantigen that is recognized by a polyclonal antibody

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

273 s include uncovering previously unrecognized autoantigens, the improved classification of patient cli

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

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

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

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

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

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

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

281 The primary autoantigen triggering spontaneous type 1 diabetes melli

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

283 s for AIRE and 16 peripheral tissue-specific autoantigens (TSAgs) by quantitative PCR.

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

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

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

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

288 Furthermore, antibody responses to the ECGF autoantigen were more common in patients with post-Lyme

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

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

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

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

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

294 ptor, and a repertoire of known cell surface autoantigens were used to identify additional antibodies

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 We screened islet autoantigens with the tTG substrate motif for candidate-

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

299 GAD65, but not GAD67, is a prevalent autoantigen, with autoantibodies to GAD65 being detected

300 was to identify frequently targeted retinal autoantigens within the 60-70-kDa molecular weight range