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1 nt in rogue B cells producing the pathogenic autoantibody.
2 ic mutations leading to an iconic pathogenic autoantibody.
3 sed in abundance before appearance of either autoantibody.
4 of immunohistopathology and normal levels of autoantibody.
5 al of autoreactive lymphocytes and increased autoantibody.
6  of FPIR over time in children with multiple autoantibodies.
7 lation-based screening of children for islet autoantibodies.
8 ntigenic proteins targeted by these maternal autoantibodies.
9 tide candidates triggering anti-Desmoglein-1 autoantibodies.
10 art failure who have positive for beta(1)-AR autoantibodies.
11  those DQB1*06:02 (+) individuals with islet autoantibodies.
12 licating a role in stimulation of pathogenic autoantibodies.
13 e complexes induced glycan-specific anti-IgE autoantibodies.
14 tment for patients who have beta(1) receptor autoantibodies.
15 rs IFN-I in pDCs and is target of pathogenic autoantibodies.
16 obalt (Co(III)) and exposed to anti-ADAMTS13 autoantibodies.
17 id tissues and the pancreas while inhibiting autoantibodies.
18 ineage leads to production of the pathogenic autoantibodies.
19 known circulating G-protein coupled receptor autoantibodies.
20 eloped autoimmunity associated with elevated autoantibodies.
21 pecifically target and neutralize beta(1)-AR autoantibodies.
22 ownregulated by glycan-specific IgG anti-IgE autoantibodies.
23 ti-thymocyte globulin (after absorption), or autoantibodies.
24  presence of autoimmune disease and positive autoantibodies.
25 count for the intrathecal synthesis of these autoantibodies.
26  study in children with and without multiple autoantibodies.
27 eatment, suggesting a role for anti-ADAMTS13 autoantibodies.
28 pared with mothers of children without islet autoantibodies (2 [1-4]) (P = .002), but declined after
29                              We investigated autoantibody (AAb) profiles in febrile children (<= 5 ye
30  and IGF2 levels were significantly lower in autoantibody (AAb)(+) compared with AAb(-) relatives of
31                     Endogenous self-reactive autoantibodies (AAs) recognize a range of G-protein-coup
32 of acetylcholine receptor (AChR) function by autoantibodies (Abs) is considered a rare pathogenic mec
33  The developed method of characterization of autoantibody activity by recording the kinetics of their
34 susceptible children with the development of autoantibodies against (pro)insulin in early childhood.
35                   In this study, we detected autoantibodies against AGE-modified proteins with ELISA
36 dings show a weak link between the levels of autoantibodies against AGEs and diabetes mellitus (DM 44
37 tem, presumably triggering the production of autoantibodies against AGEs.
38                The C105F mutation results in autoantibodies against aggregated misfolded protein with
39  Within the CNS autoimmunity control cohort, autoantibodies against aquaporin 4 and high-titer Abs ag
40        Acquired hemophilia A (AHA) is due to autoantibodies against coagulation factor VIII (FVIII) a
41  to assess serum levels of IgG, IgM, and IgA autoantibodies against FceRIalpha and investigated wheth
42 hether such patients also exhibit IgM or IgA autoantibodies against FceRIalpha.
43  is a neurological disorder characterized by autoantibodies against IgLON5 and pathological evidence
44                                              Autoantibodies against leucine-rich glioma inactivated 1
45                                        Thus, autoantibodies against M(3) acetylcholine receptors caus
46 ration of exogenous sialic acids, leading to autoantibodies against N-glycolylneuraminic acid in huma
47    The aim of this study was to test whether autoantibodies against neurologic surface Ags are found
48                                         Most autoantibodies against neuronal surface antigens show ro
49 B cell tolerance, resulting in production of autoantibodies against nucleic acids and other cellular
50 e patients showed high levels of IgG and IgM autoantibodies against numerous autoantigens, and some a
51 ns decades, beginning with the production of autoantibodies against post-translationally modified pro
52                                          IgG autoantibodies against the high-affinity IgE receptor, F
53                            Circulating serum autoantibodies against the M-type phospholipase A2 recep
54                              GD is caused by autoantibodies against the thyroid-stimulating hormone (
55                                We identified autoantibodies against TRIM72 (also known as MG53), a mu
56 tyric acid (GABAs) associated with the first autoantibody against insulin (IAA-first).
57                                          The autoantibody against the pore domain of the L-type volta
58         We used six clinical parameters (GAD autoantibodies, age at diabetes onset, HbA(1c), BMI, and
59 n and native kinetic parameters that reflect autoantibody aggressiveness to the organism's tissues.
60 ation but also on quantitative evaluation of autoantibody aggressiveness.
61                             Serum anti-heart autoantibodies (AHAs) and anti-intercalated disk autoant
62 antibodies (AHAs) and anti-intercalated disk autoantibodies (AIDAs) are autoimmune markers in myocard
63 terpretation is difficult or impossible when autoantibodies, alloantibodies, or therapeutic antibodie
64                                Compared with autoantibodies alone, the combined model dramatically im
65                                         TSHR autoantibodies also underlie Graves' orbitopathy (GO) an
66  findings, aid the identification of surface autoantibodies among unselected people with new-onset fo
67                            In the absence of autoantibodies, an incompatible crossmatch in a sensitiz
68  anti-U1 small nuclear ribonucleoprotein 70k autoantibodies and a high incidence of life-threatening
69 Rn targeted therapeutics aimed at pathogenic autoantibodies and alloantibodies.
70 asma cells that secrete disease-causing AChR autoantibodies and although thymectomy improves clinical
71 ovarian insufficiency, and between anti-RFX6 autoantibodies and diarrheal-type intestinal dysfunction
72 are the major source of pathogenic allo- and autoantibodies and have historically demonstrated resist
73 , transcriptomics, lipidomics, metabolomics, autoantibodies and immune cell profiling, complemented w
74 is study aimed to characterise both neuronal autoantibodies and levels of interferon alpha, two propo
75 notyping, we find novel associations between autoantibodies and organ-restricted autoimmunity, includ
76 munity, including a link between anti-KHDC3L autoantibodies and premature ovarian insufficiency, and
77  secrete high titers of germline-encoded IgM autoantibody and hypermutating germinal center B cells.
78 atients with the DAP1 genotype have distinct autoantibody and transcription profiles, supporting the
79 suggest a possible link between HLA alleles, autoantibodies, and environmental triggers in the pathog
80 ell burden, decreased serum and tissue-bound autoantibodies, and increased DSG3-CAART engraftment.
81 lasma revealed both known disease-associated autoantibodies (anti-La) and novel candidates that recog
82  work investigated the detection of anti-p53 autoantibodies (anti-p53aAbs) using nanomagnetic beads c
83 istence subgroup, the prevalence of positive autoantibodies (antinuclear or ACPA) was significantly h
84 ciency-often begins early in life when islet autoantibody appearance signals high risk(1).
85 ether, these findings demonstrate that NMDAR autoantibodies are detectable in a subgroup of CHR subje
86             We aimed to unravel how anti-IgE autoantibodies are induced and we aimed to understand th
87                                              Autoantibodies are key biomarkers in clinical diagnosis
88 n many autoimmune diseases, disease-specific autoantibodies are produced by B cells in response to so
89                                   Pathogenic autoantibodies arise in many autoimmune diseases, but it
90              The researchers implicate these autoantibodies as a possible pathogenic mechanism respon
91 nt work supports further evaluation of NMDAR autoantibodies as a possible prognostic biomarker and ae
92 stinfectious GN by identifying anti-factor B autoantibodies as contributing factors in alternative co
93 activity >50% and undetectable anti-ADAMTS13 autoantibodies, as well as after rituximab treatment, su
94 history of anti-interferon-gamma (IFN-gamma) autoantibody-associated immunodeficiency syndrome is not
95      Data of 74 patients with anti-IFN-gamma autoantibodies at Srinagarind Hospital, Thailand, were c
96 tial data for 4 patients with anti-IFN-gamma autoantibodies at the US National Institutes of Health w
97 giotensin receptor type 1 receptor agonistic autoantibody (AT(1) -AA)-induced mouse model of PE.
98 onia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-omega (IFN-
99 new immunofluorescence (IF) pattern in serum autoantibody (autoAb) screening of laboratory-confirmed
100 ine a general mechanism of autoimmunity with autoantibodies being produced by ignorant B cells on pro
101 sponses against pathogenic DSG3 epitopes and autoantibody binding to epithelial tissues, leading to c
102 mic lupus erythematosus because they secrete autoantibodies, but they are unresponsive to standard im
103         11/14 (79%) patients with detectable autoantibodies, but without encephalitis, showed excelle
104                             Removal of these autoantibodies by immunoadsorption has been shown to imp
105  subsets to induce desmoglein (Dsg)-specific autoantibodies by memory B cells was evaluated in cocult
106 18 (78%) samples, proving that anti-ADAMTS13 autoantibodies can induce an open ADAMTS13 conformation.
107 e screened a panel of anticomplement protein autoantibodies, carried out related functional character
108 e growth factor 1 receptor (IGF1R) with TSHR autoantibodies, causing retro-orbital tissue expansion a
109 human serum both critical characteristics of autoantibody: concentration and native kinetic parameter
110                                 Anti-Drebrin autoantibodies define a chronic syndrome of recurrent se
111  for immunopathologic confirmation of MMP by autoantibody detection is inappropriate for DIF- ocular-
112      Understanding the mechanisms underlying autoantibody development will accelerate therapeutic tar
113  disease characterized by mutually exclusive autoantibodies directed against distinct nuclear antigen
114                                 Importantly, autoantibody discovery in APS1 can illuminate fundamenta
115 es and long-lived plasma cells as sources of autoantibodies, discuss data that indicate migration of
116 enerally decreased with time, anti-IFN-gamma autoantibody disease had a chronic clinical course with
117                                  A subset of autoantibodies (DNRAbs) cross-react with the GluN2A and
118           We find that SAP is essential when autoantibody-driven immune complexes promote inflammatio
119 therapeutic value to patients suffering from autoantibody-driven immune disorders.
120 upus pathology by reducing serum antinuclear autoantibodies, dsDNA titers, and the number of circulat
121  of the lung in the generation of RA-related autoantibodies during a period of disease development te
122 arises only under pathological conditions in autoantibodies endowed with stereospecific binding sites
123                     Prospective clinical and autoantibody evaluations in a cohort of 219 consecutive
124              To address B cell tolerance and autoantibody formation to TG2, we generated immunoglobul
125      This effect is associated with impaired autoantibody formation, and mitigates experimental autoi
126 ine monolayer, replicating a key activity of autoantibodies found in patients with antiphospholipid s
127 T cells increased the serum concentration of autoantibodies, frequency of germinal center (GC) B cell
128 conclusion, we have shown that anti-ADAMTS13 autoantibodies from iTTP patients induce an open ADAMTS1
129 z and Wong et al. assessed the prevalence of autoantibodies from the sera of 51 adult ICL patients (o
130  Two risk associations were related to GAD65 autoantibody (GADA) and IA-2 autoantibody (IA-2A) but in
131                 Patients with high levels of autoantibodies had a higher body mass index (BMI 28.6 vs
132 dherins, including human and mouse pemphigus autoantibodies, had no effect on monolayer integrity and
133 orefront of this effort is the modulation of autoantibody half-life and blocking access of autoantibo
134          The prevalence and breadth of their autoantibodies, however, and their potential contributio
135 ividuals were positive for one or more islet autoantibodies; however, there was a greater proportion
136  children having early onset of each initial autoantibody, i.e., IAA-first by 12 months and GADA-firs
137 xposures, heralding the development of islet autoantibodies (IA) and type 1 diabetes (T1D).
138 ental exposures may develop pancreatic islet autoantibodies (IA) at a very young age.
139 elated to GAD65 autoantibody (GADA) and IA-2 autoantibody (IA-2A) but in opposite directions.
140 rocarriers to selectively capture anti-dsDNA autoantibodies (IgG, IgA and IgM AAbs) present in the se
141 vidence strongly supports the involvement of autoantibodies in arrhythmogenesis, a large-panel autoan
142 pecific tyrosine kinase (MuSK)-specific IgG4 autoantibodies in autoimmune myasthenia gravis (MG) are
143 s are still needed to guarantee detection of autoantibodies in complex matrices.
144   PAD2 and PAD4 are additionally targeted by autoantibodies in distinct clinical subsets of patients
145   The generation of MAR-ASD-specific epitope autoantibodies in female mice prior to breeding created
146            Finally, we investigated anti-IgE autoantibodies in human sera.
147 r data demonstrate that a high prevalence of autoantibodies in ICL, some of which are specific for CD
148 s, and increases germinal center B cells and autoantibodies in mice aged over 15 months.
149  CD20 has emphasized the role of B cells and autoantibodies in MS pathogenesis.
150 eases; our data confirms the presence of AGE-autoantibodies in patients with CAD and that in parallel
151 ee-triiodothyronine levels, and TSH-receptor autoantibodies in patients with GD.
152                    Of note, disease-specific autoantibodies in patients with rheumatoid arthritis dis
153 0, a ring-shaped protein that is a target of autoantibodies in patients with systemic lupus erythemat
154         Anti-desmoglein (Dsg) 1 and Dsg3 IgG autoantibodies in pemphigus foliaceus and pemphigus vulg
155 f an FO-SPR immunoassay for the detection of autoantibodies in plasma samples from immune-mediated th
156 mmunologic study revealed high titers of IgG autoantibodies in serum and cerebrospinal fluid directed
157   The finding of mildly increased neurologic autoantibodies in SLE may be consistent with a broader l
158                 Patients with anti-IFN-gamma autoantibodies in Thailand and the United States had dis
159 ion and activity characterization of several autoantibodies in the same serum sample have been demons
160 s needed to understand the effects of THSD7A autoantibodies in this disease.
161 ution series of a cloned human anti-ADAMTS13 autoantibody in ADAMTS13-depleted plasma resulting in an
162 d LAMP3 expression and the presence of serum autoantibodies including anti-Ro/SSA, anti-La/SSB, anti-
163 hages and suggest a therapeutic strategy for autoantibody-induced inflammation, including lupus nephr
164 in barrier (BBB) breakdown, extravasation of autoantibodies into the CNS, and loss of excitatory syna
165 ssociated with positivity for multiple islet autoantibodies, irrespective of class II HLA DR-DQ genot
166              The development of these unique autoantibodies is not well understood.
167 clinical role of epitope regions targeted by autoantibodies is unclear.
168 unotherapy-responsive seizure syndromes with autoantibodies largely fall under the umbrella of autoim
169                               Anti-IFN-gamma autoantibody levels decreased over time in Thailand (P <
170 t is also associated with lower anti-insulin autoantibody levels in part by inhibition of T follicula
171                               Anti-IFN-gamma autoantibody levels were measured in plasma samples.
172 arthritis model without reducing circulating autoantibody levels, providing support for FcRn's direct
173 e deaminase induction, and boosts IgG Ab and autoantibody levels.
174  have demonstrated effectiveness in reducing autoantibody levels.
175 T cell functions and reduce serum anti-dsDNA autoantibody levels; 2) differentially regulate autophag
176 ) and the pathogenic, GD-specific monoclonal autoantibody, M22, robustly induce IL-23 in human fibroc
177 omes included IA cases positive for multiple autoantibodies (mAb+).
178    We examined MG patient-derived monoclonal autoantibodies (mAbs), their corresponding germline-enco
179 , we investigated the role of SAP in T1D and autoantibody-mediated arthritis.
180                                              Autoantibody-mediated diseases have been treated by nons
181                                     In human autoantibody-mediated diseases, the detailed characteriz
182 idence that IgG is a primary driver in these autoantibody-mediated diseases.
183 mmunotherapy-treated patients with confirmed autoantibody-mediated encephalitis (p<0.05).
184 how that synovial NK cells produce GM-CSF in autoantibody-mediated inflammatory arthritis.
185 spontaneous arthritis depended on SAP in the autoantibody-mediated K/BxN model, organized insulitis a
186 st common autoimmune encephalitis related to autoantibody-mediated synaptic dysfunction.
187  the Sle1 interval leading to anti-chromatin autoantibodies; Mfge8(-/-) , leading to defective cleara
188 he majority of patients under 50 y with AChR autoantibody MG have thymic lymphofollicular hyperplasia
189 herefore critical for selective CNS entry of autoantibodies, microglial activation, and neural circui
190 s.RESULTSAll ICL patients had a multitude of autoantibodies mostly directed against private (not shar
191 here was a greater proportion who were islet autoantibody negative compared with those T1D DQB1*06:02
192 rapy, patients with these neuroglial surface autoantibody (NSAb)-mediated diseases often experience c
193        We grouped children having an initial autoantibody only against insulin (IAA-first) or GAD (GA
194 h encephalitis, by contrast to 0/196 without autoantibodies (p<0.0001).
195                               Differences in autoantibody patterns could relate to disease progressio
196 oming tolerized and repressed from secreting autoantibody, Pik3cd gain-of-function B cells are activa
197 inding with free native antigens is based on autoantibody polyvalency.
198 ed from whole genome sequencing of 160 islet autoantibody positive subjects, including 87 who had pro
199 cestry; T1D (n = 262 clinically defined, 200 autoantibody positive), T2D (n = 345) and controls (n =
200 ellent immunotherapy-independent outcomes of autoantibody-positive patients without encephalitis sugg
201 to identify patients with so-called 'active, autoantibody-positive SLE'.
202 ysis identified six features which predicted autoantibody positivity (area under the curve=0.83): age
203 inical features of encephalitis, rather than autoantibody positivity.
204                          High-affinity islet autoantibodies predict type 1 diabetes (T1D) but do not
205     Families of children with multiple islet autoantibodies (presymptomatic type 1 diabetes) were inv
206 primary care-based screening showed an islet autoantibody prevalence of 0.31%.
207                                 The anti-IgE autoantibodies prevented effector cell sensitization, re
208 e that ASD-specific antigen-induced maternal autoantibodies produced alterations in a constellation o
209  deletion of alphav from B cells accelerates autoantibody production and autoimmune kidney disease in
210 c impact on B cells extends to inhibition of autoantibody production and autoimmunity in mouse lupus
211 precipitated fatal autoimmunity with intense autoantibody production and dysregulated T follicular he
212 ed the contributions of BAFF to aberrant IgG autoantibody production and hepatic fibrosis.
213 over, female ALX/FPR2 KO mice show increased autoantibody production and loss of salivary gland funct
214 lls led to hyperactivation of B and T cells, autoantibody production and lupus-like disease in mice.
215  that c-Rel overexpression in B cells caused autoantibody production and renal immune complex deposit
216 geting BAFF specifically for attenuating the autoantibody production associated with cholestatic live
217 marily responsible for inducing Dsg-specific autoantibody production by B cells.
218 ntibodies, and provided spontaneous help for autoantibody production ex vivo.
219                                              Autoantibody production occurs when these checkpoints ar
220 ecific Tlr9 deficiency unlinked disease from autoantibody production.
221 e, including Th17 CD4 T cell development and autoantibody production.
222 e in the skin and kidneys without effects on autoantibody production.
223  such that monovalent IgG4 Fab-arm-exchanged autoantibodies reach a high-affinity threshold required
224 nd their families, including the presence of autoantibodies reactive to fetal brain proteins in nearl
225 ertoire with immunodominant clones and serum autoantibodies reactive to oncogenic signaling pathway p
226                                              Autoantibody reactivity detected by any 1 or more of the
227                        Desmoglein 3 chimeric autoantibody receptor T cells (DSG3-CAART) expressing th
228 -tolerance checkpoints to secrete pathogenic autoantibodies remains incomplete.
229 h different forms of IgE and tested anti-IgE autoantibody responses and their specificities.
230 , as central to the maturation of the Ab and autoantibody responses.
231 in the formation of public rheumatoid factor autoantibodies responsible for mixed cryoglobulinemic va
232  primary hippocampal neurons to anti-Drebrin autoantibodies resulted in aberrant synapse composition
233 ay lead to antibodies against self-antigens (autoantibodies), resulting in organ-specific or systemic
234 ntibodies in arrhythmogenesis, a large-panel autoantibody screening was performed in patients with ca
235 nresolved etiology and equivalent results in autoantibody screening were subjected to epitope identif
236 itro functional studies confirmed that these autoantibodies selectively blocked M(3) receptor activat
237            Moreover, the study identified an autoantibody signature specific to patients with cardiac
238 ettings they are enriched for characteristic autoantibody specificities.
239 s have been reclassified incorporating their autoantibody status.
240                                         DSG3 autoantibodies stimulated DSG3-CAART IFN-gamma secretion
241  We examined HLA associations in SSc and its autoantibody subsets in a large, newly recruited African
242                  Conditional analysis in the autoantibody subsets of SSc revealed several associated
243 mphasizing the importance of HLA in defining autoantibody subtypes.
244                               Serum neuronal autoantibodies, such as those to the NMDA receptor (NMDA
245     However, newborn serum contains abundant autoantibodies, suggesting that B cell tolerance during
246  patient sera with elevated levels of TRIM72 autoantibodies suppress sarcolemmal resealing in healthy
247                                              Autoantibody surveillance programs effectively prevent m
248 n Drebrin as a pathophysiologically relevant autoantibody target in patients with recurrent seizures
249 opathy, and previous studies described three autoantibody-targeted PLA(2)R1 epitope regions.
250 t inflammatory pathways, genetic influences, autoantibodies targeting brain proteins, and exposure to
251                             Hitherto unknown autoantibodies targeting extracellular sequences of card
252                                    At onset, autoantibodies targeting factor B (a component of the al
253                                              Autoantibodies targeting TRIM72 lead to skeletal muscle
254 ods: Clinical examination, CT, PET, MRI, and autoantibody testing were performed.
255                             Pemphigoid serum autoantibody tests did not provide immunopathologic evid
256 ot more frequently seropositive for neuronal autoantibodies than controls (8.3% vs. 5.2%; OR = 1.50;
257 oup of CNS diseases are caused by pathogenic autoantibodies that target neuroglial surface proteins.
258  neuromuscular, autoimmune disease caused by autoantibodies that target postsynaptic proteins, primar
259                    In children with multiple autoantibodies, the change in FPIR over time was signifi
260 ive to immunoadsorption is neutralization of autoantibodies through the intravenous application of sm
261 t ensures a constant exposure to the salient autoantibodies throughout gestation in C57BL/6J mice.
262 anage symptoms, and marginal changes in AChR autoantibody titer.
263 ation in the pancreas, decreased circulating autoantibody titers against citrullinated glucose-regula
264 AP1 risk allele exhibit significantly higher autoantibody titers and altered expression of the immune
265                                              Autoantibody titers correlated with IgG responses to bac
266 both TM strains had significant increases in autoantibody titers, Ag spread, and IgG deposition in th
267 s have generally resulted in reduced thyroid autoantibody titre without apparent improvements in the
268 nts, NMO is caused by pathogenetic serum IgG autoantibodies to aquaporin 4 (AQP4), the most abundant
269 ering skin disease caused by pathogenic IgG4 autoantibodies to desmoglein 1 (DSG1).
270                    The role and relevance of autoantibodies to FceRIalpha in CSU can and should be fu
271 oped competitive ELISA for IgG, IgM, and IgA autoantibodies to FceRIalpha.
272 utoantibody half-life and blocking access of autoantibodies to fragment cystallizable gamma receptors
273 n to acquired immunodeficiencies like HIV or autoantibodies to IFN, variants in specific genes have b
274 ew-onset focal epilepsy had detectable serum autoantibodies to known or novel cell surface antigenic
275  and are characterized by the development of autoantibodies to the neutrophil proteins leukocyte prot
276         Graves' hyperthyroidism is caused by autoantibodies to the thyroid-stimulating hormone recept
277                                              Autoantibodies to transglutaminase 2 (TG2) are hallmarks
278 autoimmune skin-blistering disease driven by autoantibodies to type VII collagen.
279 d pathogenicity by causing the antigen-bound autoantibodies to undergo phase transition to insoluble
280 tage (presence of anti citrullinated-peptide autoantibody) to diagnosis of rheumatoid arthritis (RA),
281 of clinically relevant concentrations of the autoantibodies up to 1000 IU/mL.
282 function, immune responses to transgenes and autoantibodies, vector copy number, and integration were
283 TTING, AND PARTICIPANTS: Screening for islet autoantibodies was offered to children aged 1.75 to 5.99
284 up (p < 0.05) and the presence of a neuronal autoantibody was associated with larger amygdala volumes
285 anin were measured by ELISA, and presence of autoantibody was detected by microarray.
286               Plasma 25(OH)D prior to either autoantibody was lower in T1D progressors compared with
287                             Serum pemphigoid autoantibodies were detected in 29 of 76 MMP patients (3
288                                    9/23 with autoantibodies were diagnosed with encephalitis, by cont
289  circulating B lymphocytes making pathogenic autoantibodies were found to comprise clonal trees accum
290 3 activity >50%, although free anti-ADAMTS13 autoantibodies were not always detected.
291        Furthermore, glycan-specific anti-IgE autoantibodies were present in sera from subjects with a
292            Elevated IgM, but not IgG or IgA, autoantibodies were significantly more frequent in ASST-
293 dies against numerous autoantigens, and some autoantibodies were specific for lymphocytes.
294    In acute postinfectious GN, anti-factor B autoantibodies were transient and correlated with plasma
295      Respiratory allergy and the presence of autoantibodies were unrelated (12% concurrence versus th
296 ignorant to their antigen, and they produced autoantibodies when provided T cell help.
297 sts such as nerve ultrasound and testing for autoantibodies, which are not yet part of the guidelines
298 n, associated with a higher frequency of IgG autoantibodies with an agalactosylated, proinflammatory
299 e immunoassay for detection of anti-ADAMTS13 autoantibodies with FO-SPR.
300  type 1 diabetes, defined by 2 or more islet autoantibodies, with categorization into stages 1 (normo

 
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