ライフサイエンスコーパス: autoantibody

1 gens common to both recipient and donor (ie, autoantibody).

2 and reduced the amount of GCs and pathogenic autoantibody.

3 yer's patches, and thus reduced the systemic autoantibodies.

4 g in the production of tumor-associated (TA) autoantibodies.

5 cur before transplant in the form of natural autoantibodies.

6 GADA), and commercial (125)I-GAD65 (RSRGADA) autoantibodies.

7 diseases from a dry eye practice have these autoantibodies.

8 e 1 diabetes than full-length GAD65 (fGAD65) autoantibodies.

9 hildren positive for two or more biochemical autoantibodies.

10 cumulative incidence of diabetes-associated autoantibodies.

11 t potential pathogenic mechanism mediated by autoantibodies.

12 an be caused by fetal-specific AChR-blocking autoantibodies.

13 dren identifiable by positivity for multiple autoantibodies.

14 sponse to pressure overload independently of autoantibodies.

15 leoli were broadly reactive with SLE patient autoantibodies.

16 n, and development of double-strand (ds) DNA autoantibodies.

17 slet autoimmunity revealed by specific islet autoantibodies.

18 disease indicated by markers such as insulin autoantibodies.

19 o BP blister formation in the presence of BP autoantibodies.

20 the dry eye patients expressed one of these autoantibodies.

21 cally from studies of the properties of some autoantibodies.

22 phocytes in SLE beyond the production of IgG autoantibodies.

23 C1 treatment was estimated using SLE patient autoantibodies.

24 t z scores and development of multiple islet autoantibodies (1 year: HR 1.21, 95% CI 1.08-1.35, P = 0

25 A cell-penetrating, anti-DNA, lupus autoantibody, 3E10, was previously shown to inhibit HDR,

26 n CSU and elevated levels of IgG antithyroid autoantibodies (AAbs), with most of a large number of st

27 To determine the prevalence of neurological autoantibodies (Abs) among adult patients with epilepsy

28 mechanism behind their induction and monitor autoantibodies accumulation in various tissues.

29 cepsilonRI and IgE, reducing activity of IgE autoantibodies against an antigen or autoantigen that ha

30 ring skin disease pemphigus is caused by IgG autoantibodies against desmosomal cadherins, but the pre

31 ctivation and autoantigens secretion induced autoantibodies against dsDNA and heat shock protein 60 a

32 The presence of autoantibodies against eosinophil peroxidase (EPX) and a

33 can be identified by the presence of sputum autoantibodies against EPX and autologous cellular compo

34 receptor function, reducing activity of IgG autoantibodies against FcepsilonRI and IgE, reducing act

35 e here ascertain the presence of circulating autoantibodies against glutamate NMDA receptor (NMDAR-Ab

36 Circulating autoantibodies against glutamatergic N-methyl-D-aspartat

37 neurons revealed the presence of circulating autoantibodies against glutamatergic NMDAR in approximat

38 However, the prevalence of circulating autoantibodies against glutamatergic NMDAR in psychotic

39 methods to detect the presence of low-titer autoantibodies against glutamatergic NMDAR in seropositi

40 Besides, the occurrence of autoantibodies against IgE or its receptor, FcepsilonRI,

41 hat patients with CSU frequently exhibit IgE autoantibodies against many autoantigens and that IL-24

42 erythematosus patients were shown to acquire autoantibodies against MARCO, this highlights a mechanis

43 Autoantibodies against myelin oligodendrocyte glycoprote

44 The identification of circulating autoantibodies against neuronal receptors in neuropsychi

45 d miscarriages in the persistent presence of autoantibodies against phospholipid-binding proteins (aP

46 Autoantibodies against TG2 are a hallmark of CD, and ant

47 likely drive aggregation as well as generate autoantibodies against the aggregates.

48 mucous membrane pemphigoid patients generate autoantibodies against the alpha3 chain of laminin 332 (

49 immunoproteomic approach, we discovered that autoantibodies against the cell-cycle kinase inhibitor p

50 Autoantibodies against the extracellular domains of the

51 N) is an autoimmune disease mainly caused by autoantibodies against the recently discovered podocyte

52 The presence of IgE autoantibodies against the transmembrane protein BP anti

53 ced basophil activation, increased levels of autoantibodies against thyroid peroxidase, and also exhi

54 Preformed non-HLA autoantibodies alone did not impact outcomes.

55 n in six patients (11 alloantibodies and two autoantibodies), among whom three developed antibodies i

56 Levels of autoantibodies and B2A-CIC were quantified immediately b

57 -reactive protein; immune cells; antibodies, autoantibodies and comorbid autoimmune disorders; comple

58 e initiation of two or more diabetes-related autoantibodies and continue to contribute to type 1 diab

59 ighly relevant in RA, since patients express autoantibodies and depleting this cell type is a success

60 Mice also presented with elevated autoantibodies and evidence of immune-mediated glomerulo

61 germinal centers, increased titers of serum autoantibodies and excessive accumulation of B cells.

62 factor T-bet promote the rapid appearance of autoantibodies and germinal centers in spontaneous murin

63 ctrum disorders (ASD) are positive for these autoantibodies and high-dose folinic acid is beneficial

64 deling, the combination of preformed non-HLA autoantibodies and HLA-DSA were associated with an incre

65 at least 2 autoantibodies, including insulin autoantibodies and normal glucose tolerance, were enroll

66 sial findings about the effects of pemphigus autoantibodies and other inflammatory mediators into per

67 eristics and often with disease progression, autoantibodies and other soluble mediators are considere

68 tration of leptin accelerated development of autoantibodies and renal disease.

69 ophils provide the cellular link between IgE autoantibodies and skin blistering in this murine model

70 se C1 genetic deficiency causes anti-nuclear autoantibodies and SLE disease.

71 However, the role of non-HLA autoantibodies and the interaction between HLA DSA and n

72 ed a correlation between the presence of IgA autoantibodies and worse disease course.

73 4 years off IS) with serial liver tests and autoantibody and alloantibody assessments.

74 After conditioning on autoantibody and disease duration, time-averaged DAS28 s

75 Identifying women positive for the autoantibody and treating them with high-dose folinic ac

76 tigens revealed highly reliable detection of autoantibodies, and by exploring the full panel of more

77 chain, CD45RO(+)CD4(+) effector T cells, and autoantibodies, and this was predictive of favorable cli

78 mplexes composed of ribonucleotide proteins, autoantibody, and complement.

79 gnetic resonance imaging correlations of the autoantibody, and immunotherapy responsiveness.

80 Recent studies have identified autoantibodies, anti-salivary gland protein 1 (SP1), ant

81 tic genotype (HLA-DQ2 and HLA-DQ8 genes) and autoantibodies (antitissue transglutaminase and antiendo

82 morbidity in patients with antiphospholipid autoantibodies (aPLs).

83 ceptor and anti-endothelin-1 type A receptor autoantibodies are associated with an increased risk of

84 Interferon-gamma (IFNgamma) neutralizing autoantibodies are associated with disseminated nontuber

85 Non-HLA alloantibodies and autoantibodies are involved in allograft rejection in ki

86 itional immune modulators targeting ADAMTS13 autoantibodies are mainly based on steroids and the huma

87 The autoantibodies are pathogenic, but whether their generat

88 TA autoantibodies are present in a clinically significant n

89 as a T cell-driven autoimmune disease, islet autoantibodies are the best currently available biomarke

90 ity and demyelinating properties of anti-MAG autoantibodies are well established, current treatments

91 e the generation, evolution and functions of autoantibodies, as well as their target autoantigens.

92 To identify autoantibodies associated with chemokine score, we devel

93 Only 30% expressed one of the autoantibodies associated with long-standing SS, which a

94 from 11 children (cases) who developed serum autoantibodies associated with T1D (of whom five develop

95 with these properties, patients with active autoantibody-associated vasculitis, a chronic relapsing

96 ositive for islet or tissue transglutaminase autoantibodies at 2 consecutive clinic visits at least 3

97 s, relationship to a family member with T1D, autoantibody at seroconversion, INS gene (rs1004446_A),

98 Agonistic angiotensin II type 1 receptor autoantibodies (AT1RaAbs) have not been associated with

99 Previous epitope-mapping of autoantibodies (AutoAbs) from prostate cancer patients i

100 However, autoantibodies bind to specific rodent hippocampal subfi

101 atory (bullous pemphigoid-like) EBA variant, autoantibody binding is followed by a lesional inflammat

102 tes allograft injury in proximity to non-HLA autoantibody binding.

103 ciation and blister formation in response to autoantibody binding.

104 activation in the presence or absence of BP autoantibodies, brefeldin A, diphenyleneiodonium, DNase

105 ncy is most frequently acquired via ADAMTS13 autoantibodies, but rarely, it is inherited via mutation

106 l subjects (7 of each) were screened for IgE autoantibodies by using an array of more than 9000 prote

107 recent data show that production of non-HLA autoantibodies can occur before transplant in the form o

108 A non-HLA autoantibody combined with a preformed HLA DSA is associ

109 n or pathological states in which GC-derived autoantibodies contribute to the pathology.

110 an anti-IL-21 blocking Ab reduced titers of autoantibodies, delayed progression of glomerulonephriti

111 Clinical remission was associated with autoantibody depletion and with recovery of conduction b

112 ncurable autoimmune disease characterized by autoantibody deposition in tissues such as kidney, skin

113 The MAP1B (PCA-2) autoantibody detection rate, among approximately 70,000

114 ent antigen challenge, immune spectratyping, autoantibody detection, and detailed tissue immunohistoc

115 toimmune blistering disease characterized by autoantibodies directed against basement membrane protei

116 In this context, the detection of autoantibodies directed against nodal and perinodal targ

117 anifestations, such as skin infiltration and autoantibodies, dramatically improved in GT mice with a

118 senting a potential therapeutic strategy for autoantibody-driven diseases such as systemic lupus eryt

119 apeutic targets for these and possibly other autoantibody-driven disorders.

120 In humans, exposure to FRalpha autoantibodies during fetal development and infancy coul

121 tivation with IL-5 and in the presence of BP autoantibodies, eosinophils induced separation along the

122 ly 70,000 patients undergoing service neural autoantibody evaluation in 2015, was 0.024%, equaling am

123 sting in comprehensive paraneoplastic neural autoantibody evaluation.

124 ients were identified through service neural autoantibody evaluation.

125 Furthermore, IgE autoantibodies fail to induce BP in eosinophil-deficient

126 zed, allowing the selective determination of autoantibodies for diagnosis and prognosis of Systemic L

127 ty and specificity between fGAD65 and tGAD65 autoantibodies for type 1 diabetes in relation to HLA-DQ

128 the immunopathology and the determinants of autoantibody formation and keratinocyte susceptibility i

129 nteraction, whereas IL-10 production and IgM autoantibody formation were CD40L independent.

130 he presence of maternally derived anti-brain autoantibodies found in 20% of mothers whose children a

131 Circulating autoantibodies from patients with THSD7A-associated MN h

132 oaffinity purified from brain extracts using autoantibodies from the sera of patients with diabetes b

133 We defined IA as positivity for at least one autoantibody (GADA, IAA, or IA-2A) on two or more visits

134 nd to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 agai

135 tes in adults (LADA) usually refers to GAD65 autoantibodies (GADAb)-positive diabetes with onset afte

136 in CD4(+) Tfh, Treg, and Tfr populations and autoantibody generation, and how this is related to bnAb

137 m the late endocytic pathway compartments in autoantibody generation.

138 Folate receptor alpha (FRalpha) autoantibodies have been associated with fetal abnormali

139 More recently, IgE autoantibodies have been recognized to participate in th

140 Age at developing multiple autoantibodies (hazard ratio = 0.96 per 1-month increase

141 as not associated with the appearance of any autoantibody (hazard ratio [HR], 0.98; 95% CI, 0.95-1.01

142 R], 0.98; 95% CI, 0.95-1.01), multiple islet autoantibodies (HR, 0.99; 95% CI, 0.95-1.03), or the tra

143 95% CI, 0.95-1.03), or the transglutaminase autoantibody (HR, 1.00; 95% CI, 0.98-1.02).

144 leles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-

145 y and flow cytometry were used to screen for autoantibodies, identify their main targets, investigate

146 investigations implicating autoimmunity and autoantibodies in ASD.

147 mmonly examined by the levels of circulating autoantibodies in clinical practices.

148 ins and citrullinates them, is the target of autoantibodies in early RA.

149 ably, this protein is frequently targeted by autoantibodies in experimental models of prostatic autoi

150 6 and neurofascin-140 as the main targets of autoantibodies in five patients presenting IgG reactivit

151 tric sensor to quantify specific circulating autoantibodies in human serum is developed.

152 We observed higher levels of all 10 CV autoantibodies in hypertensive subjects (n = 77) compare

153 SFB induce autoantibodies in lung during the pre-arthritic phase, a

154 r revision, RAG expression, and polyreactive autoantibodies in lupus-prone mice.

155 dies focusing on the pathogenic role of ANO2 autoantibodies in MS.

156 holine receptor (nAChR) is a major target of autoantibodies in myasthenia gravis (MG), an autoimmune

157 After earlier studies discovering autoantibodies in patients with CRS, we sought to invest

158 tion did not generate anti-type VII collagen autoantibodies in patients' blood or skin.

159 n 1, and neurofascin-155) are the targets of autoantibodies in subsets of patients showing distinct c

160 ation was increased in patients with non-HLA autoantibodies in the location of C4d positivity.

161 macrophages, splenomegaly, lymphadenopathy, autoantibodies (including anti-DNA IgG), and a type I in

162 December 21, 2015, relatives with at least 2 autoantibodies, including insulin autoantibodies and nor

163 urthermore, we found that assessing KIAA1199 autoantibody increased the sensitivity of detecting panc

164 characterized by the presence of circulating autoantibodies, increasing concentration and range of in

165 s, IFN-gamma-dependent IgG2c production, and autoantibodies, indicating that Tfh cell-derived IL-21 i

166 Thus, we identify a critical role for Kal in autoantibody-induced arthritis with pleiotropic effects,

167 for plasma kallikrein in the pathogenesis of autoantibody-induced arthritis.

168 Kal and HK and determined the role of KKS in autoantibody-induced arthritis.

169 tated the elucidation of the pathogenesis of autoantibody-induced, cell-mediated subepidermal blister

170 IgG autoantibodies infer the presence of antigen/disease-spe

171 with healthy participants (n = 30), and the autoantibodies investigated were related to each other,

172 and shows that the antigenic target of these autoantibodies is LRP2.

173 with other recognized paraneoplastic neural autoantibodies, justifies its testing in comprehensive p

174 US is associated primarily with mutations or autoantibodies leading to dysregulated complement activa

175 ion of complement-activating GC-specific IgG autoantibodies, leading to complement activation and C5a

176 opulation that had the highest anti-vimentin autoantibody levels (University of Alabama at Birmingham

177 osome IgG into AID(-/-)MRL/lpr mice elevated autoantibody levels and promoted lupus nephritis by indu

178 Anti-vimentin autoantibody levels in IPF patients were HLA biased and

179 immunoglobulins from patients with increased autoantibody levels triggered eosinophil degranulation i

180 Circulating anti-vimentin IgG autoantibody levels were much greater in IPF subjects fr

181 bility of response and/or relapse rate, AChR autoantibody levels, adverse effects, and inflammatory m

182 ed, current treatments are aimed at reducing autoantibody levels.

183 Circulating autoantibodies, lung perivascular lymphoid tissue, and e

184 haracterization of a recombinantly expressed autoantibody (mAb 131) previously isolated from a myasth

185 2 was often accompanied by additional neural autoantibody markers of small-cell carcinoma, including

186 IgG autoantibodies marking humans at future risk for T1D ind

187 Testing for these autoantibodies may allow early recognition of patients w

188 The related autoantibodies may be now divided into likely pathogenic

189 terminally truncated (96-585) GAD65 (tGAD65) autoantibodies may better delineate type 1 diabetes than

190 here that eosinophils are necessary for IgE autoantibody-mediated BP blister formation in a humanize

191 Mucous membrane pemphigoid is an autoantibody-mediated disease predominantly affecting th

192 ory mediators on mucosal and skin lesions in autoantibody-mediated diseases.

193 us erythematosus (lupus) is characterized by autoantibody-mediated organ injury.

194 into the role of PLA2R in podocytes and how autoantibodies might disrupt PLA2R function.

195 as to investigate the prevalence of neuronal autoantibodies (NAbs) in a large consecutive series with

196 When commenced in already insulin autoantibody(+) NOD mice, continuous BAFFR-Fc treatment

197 ing the keywords of either 'autoantigen' or 'autoantibody' or their lexical variants, which were furt

198 rbored extremely high-affinity, neutralizing autoantibodies, particularly against specific cytokines.

199 Synaptic autoantibodies, particularly those reactive with ion cha

200 time in situ, that in pancreas sections from autoantibody-positive (Ab+) donors, insulin area and bet

201 b in the treatment of acetylcholine receptor autoantibody-positive (AChR+) generalized MG.

202 in children with newly diagnosed T1D and in autoantibody-positive at-risk children with impaired glu

203 ntribute to type 1 diabetes (T1D) risk among autoantibody-positive children in The Environmental Dete

204 l insulin delays onset of type 1 diabetes in autoantibody-positive relatives of patients with type 1

205 Among autoantibody-positive relatives of patients with type 1

206 We examined a cohort of 3,358 autoantibody-positive relatives of T1D patients in the P

207 sal of hyperglycemia, and decline in insulin autoantibody positivity was an immune biomarker of thera

208 cose concentrations (<350 mg/dL) and insulin autoantibody positivity were predictors of the stable re

209 iduals with type 1 diabetes (T1D) defined by autoantibody positivity, establishing evidence for diffe

210 Characteristics included are age at multiple autoantibody positivity, sex, selected high-risk HLA-DR-

211 -1 receptor and endothelin-1 type A receptor autoantibodies pre-LT, and year 1 post-LT.

212 ich have been shown to mainly target S-MGCA, autoantibodies produced by normal mice with transient Tr

213 and Th17 responses in the spleen, the major autoantibody producing site known to correlate with K/Bx

214 ematosus by acting not only as precursors of autoantibody-producing cells but also as antigen-present

215 a strong genetic component characterized by autoantibody production and a type I interferon signatur

216 Strikingly, autoantibody production in HgIA was not dependent on the

217 way and the proinflammatory cytokine IL-6 in autoantibody production, but not IFN regulatory factor 7

218 uce elevated levels of factors known to fuel autoantibody production, including IL-6 and B cell survi

219 ew ways to prevent early deaths by targeting autoantibody production, replenishing ADAMTS13, and bloc

220 y B cell development and plasma cell-derived autoantibody production.

221 ing that Prdm1 functions in TECs to regulate autoantibody production.

222 ti-organ autoimmune disease characterized by autoantibody production.

223 nhibit the germinal center reaction to limit autoantibody production.

224 uld otherwise limit B cell hyperactivity and autoantibody production.

225 the potency of T cell help needed to promote autoantibody production.

226 cells are known to promote inflammation and autoantibody production.

227 o both sustain protective immunity and avoid autoantibody production.

228 mits the potential to identify a CV-specific autoantibody profile.

229 (n = 114) and strata 3 (n = 3) had different autoantibody profiles and first-phase insulin release th

230 d that this platform can be used to evaluate autoantibody profiles in hypertensive subjects at risk f

231 nanotechnology-based plasmonic gold chip for autoantibody profiling.

232 Autoantibodies raised against tumor-associated antigens

233 hese diseases and linking comorbidities with autoantibody reactivities and clinical variants, for exa

234 e further studies on the association of fine autoantibody reactivities with clinical features of BP.

235 Autoantibodies refer to antibodies that target self-anti

236 that SLE neutrophils exposed to TLR7 agonist autoantibodies release interferogenic DNA, which we now

237 the interaction between HLA DSA and non-HLA autoantibodies remains uncharacterized.

238 Measurement of autoantibodies remains, however, challenging because of

239 the transglutaminase 2 (TG2)-specific VH:VL autoantibody repertoire of celiac disease (CD) patients.

240 veals features of a disease- and Ag-specific autoantibody repertoire with preferred VH:VL usage and p

241 for anti-TRIM21 and anti-TROVE2 circulating autoantibodies, respectively.

242 tested for islet and tissue transglutaminase autoantibodies, respectively.

243 ral tolerance permits a cross-reactive HIV-1 autoantibody response able to neutralize HIV-1.

244 on suppressed lung mucosa-associated Tfh and autoantibody responses by increasing the gut-homing alph

245 Myd88 is required for anti-DNA and anti-RNA autoantibody responses, whereas Fcer1g is not expressed

246 Biopsies with de novo non-HLA autoantibodies revealed a new sinusoidal C4d staining pa

247 deletion and triggered differentiation into autoantibody secreting plasmablasts.

248 f-antigens and the impact of this process in autoantibody secretion in lupus.

249 creased serum levels of IgM anti-histone H2A autoantibodies significantly correlated with tier 2 HIV-

250 s, islet inflammation (i.e., insulitis), and autoantibodies specific for beta-cell antigens.

251 Anti-hinge antibodies (AHAs) are an autoantibody subclass that, following proteolytic cleava

252 In some cases, certain autoantibodies, such as anti-NMDAR or anti-phospholipid

253 ntuberculous mycobacterial infections due to autoantibodies targeting interferon-gamma are an emergin

254 uishable types based on whether they produce autoantibodies targeting the acetylcholine receptor (ACh

255 oach allowed simultaneous detection of 10 CV autoantibodies targeting the structural myocardial prote

256 dysregulation, inflammation, and endogenous autoantibodies that all persist within the affected indi

257 al immune responses that produce circulating autoantibodies that can be used clinically for diagnosti

258 GC storage induces complement-activating IgG autoantibodies that drive a pathway of C5a generation an

259 actor T-bet, which become major producers of autoantibodies that promote malarial anaemia.

260 ripheral neuropathy caused by monoclonal IgM autoantibodies that recognize the carbohydrate epitope H

261 of complement is frequently overactivated by autoantibodies that stabilize the C3 convertase C3bBb.

262 is (MG) is an autoimmune disease mediated by autoantibodies that target proteins at the neuromuscular

263 of desmoglein-specific versus nondesmoglein autoantibodies, the contribution of nonautoantibody fact

264 Measures: Frequency and definition of novel autoantibody, the autoantigen's immunochemical identific

265 along with other interventions to lower the autoantibody titer are effective strategies that may be

266 se duration, and glutamic acid decarboxylase autoantibody titers.

267 d B-cell/antibody response indicated by high autoantibody titers.

268 This process produced serum autoantibodies to a breadth of self-antigens, leading to

269 asses, and apparent affinities of anti-FVIII autoantibodies to assess their prognostic value for the

270 sion of cryptic autoantigens, allowing these autoantibodies to bind antigenic targets and further enh

271 Autoantibodies to citrullinated proteins (ACPAs) are pre

272 ng evidence suggesting an important role for autoantibodies to cryptic antigens as novel accelerators

273 more variable, but correlated strongly with autoantibodies to endothelial cell growth factor, matrix

274 Half of the patients with CSU have IgG autoantibodies to FcepsilonRIalpha on dermal mast cells

275 toimmunity (ie, IgE to autoallergens and IgG autoantibodies to IgE or its receptor, respectively) hav

276 Of these, only IgE autoantibodies to IL-24 were found in all patients with

277 BACKGROUND, METHODS AND Maternal autoantibodies to neuronal proteins may be one cause of

278 zed by T cells, which help the production of autoantibodies to proteins bound by PADs, according to a

279 yocarditis or dilated cardiomyopathy develop autoantibodies to SERCA2a suggesting that they may have

280 ormation due to tissue-bound and circulating autoantibodies to the hemidesmosomal antigens BP180 and

281 y further linking these three significant CV autoantibodies to the innate and growth factors, we reve

282 aled a positive but weak association between autoantibodies to troponin I and proinflammatory cytokin

283 In addition, we established that autoantibodies to troponin I, annexin-A5, and beta 1-adr

284 of thyroid-stimulating hormone or the human autoantibody to TSHR.

285 s for development of tissue transglutaminase autoantibodies (tTGA).

286 Sera were assessed for autoantibodies using ELISA assays.

287 rative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using ELISA.

288 Finally, the presence of these autoantibodies was confirmed in human EBOV survivors.

289 microenvironment in patients with detectable autoantibodies was examined.

290 A single de novo non-HLA autoantibody was associated with an increased risk for T

291 first autoantibody (when more than a single autoantibody was the first-appearing indication of seroc

292 sts for IgG and complement component 3; warm autoantibodies were identified in all these patients.

293 Autoantibodies were measured in four groups of participa

294 These autoantibodies were not increased in mothers of children

295 ingerprint pattern or profile of circulating autoantibodies, what allows scoring accurately SLE patie

296 0.95, 0.97; P < 0.001) and the type of first autoantibody (when more than a single autoantibody was t

297 y, characterised by production of anti-PLA2R autoantibodies which bind to the podocyte.

298 Anti-nuclear autoantibodies, which frequently target the nucleoli, ar

299 Unlike postvasectomy autoantibodies, which have been shown to mainly target S

300 plaques revealed essential colocalization of autoantibodies with endothelial cells, their adherence t