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1 therothrombotic status, further modulated by specific autoantibodies.
2 to isolate several dozen unique IgG platelet-specific autoantibodies.
3 haracterized by a variety of circulating SSc-specific autoantibodies.
4 provided new information about many of these specific autoantibodies.
5  solid supports for the selective capture of specific autoantibodies.
6 dromes of which many are closely linked with specific autoantibodies.
7 ausally related to the deposition of antigen-specific autoantibodies.
8 NIK, RELB or NF-kappaB2 have very few tissue-specific autoantibodies.
9 s with critical disease producing type I IFN-specific autoantibodies.
10 CVD in APS and SLE; 2) assess the effects of specific autoantibodies.
11 fector T cells, and the production of kidney-specific autoantibodies.
12 creened to identify peptides targeted by MGO-specific autoantibodies.
13 sting of T1D subjects with and without organ-specific autoantibodies.
14 tion recognized by rheumatoid arthritis (RA)-specific autoantibodies.
15 d spinal cords of MHV-infected mice with CNS-specific autoantibodies.
16 titer of anti-RNA binding protein (anti-RBP)-specific autoantibodies.
17  of microarrays was used to identify disease-specific autoantibodies.
18 y as demonstrated by the presence of disease-specific autoantibodies.
19  recent progress, including the discovery of specific autoantibodies, a significant number of adult-o
20 produced lower levels of mouse thyroglobulin-specific autoantibodies after immunization with MTg and
21  patients with chronic prostatitis possessed specific autoantibodies against the human SVS2-like semi
22            Recently, we identified a new SSc-specific autoantibody against portions of fibrillin-1, a
23 I were mimicked by the induction of ACBP/DBI-specific autoantibodies, an inducible Acbp/Dbi knockout
24 re, and have provided evidence that myositis-specific autoantibodies and autoreactive T cells are pre
25                                              Specific autoantibodies and class II HLA genotypes were
26 e SSc families tend to be concordant for SSc-specific autoantibodies and HLA haplotypes; familial SSc
27 O mice is preceded by the development of OVA-specific autoantibodies and is delayed in B cell-deficie
28 ritis; and immunologic measures, such as SLE-specific autoantibodies and low complement levels.
29 lude recent findings related to the myositis-specific autoantibodies and magnetic resonance imaging o
30 ter criteria is proposed to include myositis-specific autoantibodies and magnetic resonance imaging.
31 n of increased expression of ISGs with lupus-specific autoantibodies and nephritis in humans.
32  treated with anti-CD20 Ab at a time when PG-specific autoantibodies and T cell activation were evide
33  autoimmune condition, given the presence of specific autoantibodies and the immune response against
34  immune complexes of ribonucleoprotein (RNP)-specific autoantibodies and TLR-engaging or BCR-engaging
35 ether IFNalpha induction was associated with specific autoantibodies and/or clinical features of the
36 dependent Ab production, have reduced GM-CSF-specific autoantibody and do not develop PAP.
37 plement-dependent pathogenic role of dry-eye-specific autoantibodies, and suggest autoantibody deposi
38 atched for both genetic ancestry and disease-specific autoantibodies (anti-citrullinated protein anti
39 y index, a history of nephritis, and disease-specific autoantibodies (anti-dsDNA, anti-Smith (Sm), an
40                    TMPD did not induce lupus-specific autoantibodies (anti-RNP, anti-Sm, anti-double-
41  Anti-GP2 IgG and IgA, constituting novel CD specific autoantibodies, appear to be associated with di
42 ts driving CDC in NMO using recombinant AQP4-specific autoantibodies (AQP4 rAbs) derived from affecte
43 ve been recently associated with the disease-specific autoantibody aquaporin-4, thought to be pathoge
44 B cell-mediated autoimmune diseases, disease-specific autoantibodies are enriched for Fab glycans.
45         In many autoimmune diseases, disease-specific autoantibodies are produced by B cells in respo
46 cells and the occurrence of certain myositis-specific autoantibodies are striking features.
47 port a role for a complement activating AQP4-specific autoantibody as the initiator of the NMO lesion
48 anding of immunopathogenesis, histology, and specific autoantibody associations has broadened our und
49 une component has been proposed, but disease-specific autoantibodies, autoantigens, or autoreactive T
50 subjects, including the presence of pancreas-specific autoantibodies, autoreactive CD4+ and CD8+ T ce
51 e course, with a progressive accumulation of specific autoantibodies before the onset of SLE, while p
52 (FH) cell subsets to induce desmoglein (Dsg)-specific autoantibodies by memory B cells was evaluated
53                               Thus, myositis-specific autoantibodies can be used to subset JIIMs into
54 e, myelin oligodendrocyte glycoprotein (MOG)-specific autoantibodies can initiate disease bouts by co
55 ta demonstrate that a precursor of a disease-specific autoantibody can be present in the preimmune re
56 oma, or both for clinical features and organ-specific autoantibodies characteristic of APS-I patients
57 We hypothesized that the presence of antigen-specific autoantibodies could be used as a "surrogate ma
58                                     Myositis-specific autoantibodies define clinical phenotypes in JI
59 ce produce high level of serum TNF-alpha and specific autoantibodies deposited onto brain blood vesse
60 tion of GL7+ CD95+ GC-like B cells and brain-specific autoantibody deposition.
61 en accompanied by the development of disease-specific autoantibodies directed against the SNF2-superf
62                    Our data show how beta1AR-specific autoantibodies elicit DCM by agonistically indu
63                                          SLE-specific autoantibodies emerged in a sequential manner t
64 eport that children who present with insulin-specific autoantibodies first have distinct transcriptio
65                                         Less specific autoantibodies for systemic sclerosis and limit
66 he families of SLE probands, suggesting that specific autoantibody formation is partly genetically de
67                      Anti-Sm is a common and specific autoantibody found in systemic lupus erythemato
68 t to other inflammatory myopathies, myositis-specific autoantibodies had not been found in sIBM patie
69  specific and sensitive determination of p53-specific autoantibodies has been developed for the first
70   In dogs with inflammatory myopathy, muscle-specific autoantibodies have been found, especially in m
71                           Different myositis-specific autoantibodies have been identified and, on the
72                           Different myositis-specific autoantibodies have been identified that are as
73                             Interferon (IFN)-specific autoantibodies have been implicated in severe c
74 nd tested for association with seven disease-specific autoantibodies in a large cross-sectional cohor
75                                        Organ-specific autoantibodies in motor unit disorders with wea
76 ical activity of SP077 in the recognition of specific autoantibodies in multiple sclerosis patients'
77                           Aquaporin 4 (AQP4)-specific autoantibodies in neuromyelitis optica (NMO) ar
78  unlipoylated peptides are able to recognize specific autoantibodies in patients sera.
79 cs-based approach, we identified neurofascin-specific autoantibodies in patients with MS.
80 h unique specificities may represent disease-specific autoantibodies in patients with RA.
81                             Of note, disease-specific autoantibodies in patients with rheumatoid arth
82  once disease was evident, we detected heart specific autoantibodies in PD-L1(-/-);MRL-Fas(lpr) mice.
83  patients with COVID-19, we found type I IFN-specific autoantibodies in peripheral blood samples from
84 inated peptides are major targets of disease-specific autoantibodies in rheumatoid arthritis.
85             Dramatic reductions in 23 myelin-specific autoantibodies in the 0.5 mg BHT-3009 arm were
86  self tolerance, including the deposition of specific autoantibodies in the respective target organs,
87  is extremely sensitive in detecting disease-specific autoantibodies in the sera of bullous pemphigoi
88 AMAs represents the most highly directed and specific autoantibody in autoimmune diseases.
89                          In PF, desmoglein-1-specific autoantibodies induce blistering.
90                      The concentration of PG-specific autoantibody is similar in mice sufficient or d
91     Here we show that TrkA-, TrkB-, and TrkC-specific autoantibodies isolated from the sera of four i
92                         We hypothesized that specific autoantibodies may associate with IPF manifesta
93                Defining additional phenotype-specific autoantibodies may identify such circumstances.
94 we define a causal mechanism whereby beta1AR-specific autoantibodies mediate noninflammatory cardiomy
95 mphigus vulgaris (PV) is a prototypic tissue-specific autoantibody-mediated disease, in which anti-de
96 1, detected by DNA oligotyping) and myositis-specific autoantibodies (MSA) were determined in 224 pat
97 ong correlations between particular myositis-specific autoantibodies (MSAs) and clinical subsets.
98                                     Myositis-specific autoantibodies (MSAs) are directed against cell
99                                     Myositis-specific autoantibodies (MSAs) have become pivotal bioma
100            IFNalpha production is induced by specific autoantibody-nuclear antigen immune complexes,
101  differences in the proportion of DM- and DM-specific autoantibodies observed around the world are no
102                                     Myositis-specific autoantibodies or myositis-associated autoantib
103 autoantibodies, revealed the presence of MOG-specific autoantibodies over vesiculated myelin networks
104                              The presence of specific autoantibodies, particularly anti-dsDNA, anti-R
105 e factor in Korean patients without myositis-specific autoantibodies (Pcorr = 0.004, OR 0.046).
106 he treatment of juvenile DM in both myositis-specific autoantibody-positive and -negative patients.
107 , and TrkC, but not T. cruzi, are targets of specific autoantibodies present in the sera of patients
108 ls as primarily responsible for inducing Dsg-specific autoantibody production by B cells.
109 attenuate, but did not completely abolish HA-specific autoantibody production in an adoptive transfer
110 nchymal destruction, hypergammaglobulinemia, specific autoantibody production, and hepatic fibrosis a
111 llular responses, and with elevated collagen-specific autoantibody production.
112  to PGIA is not due to the suppression of PG-specific autoantibody production.
113 s also limits the potential to identify a CV-specific autoantibody profile.
114 se symptoms and clinical course, scleroderma-specific autoantibody profiles associate strongly with d
115 ations but are more strongly correlated with specific autoantibody profiles.
116               The identification of myositis-specific autoantibodies provides both diagnostic and pro
117 from a multiple sclerosis patient and by MBP-specific autoantibodies purified from multiple sclerosis
118 phy that these glucose-6-phosphate isomerase-specific autoantibodies rapidly localize to distal joint
119 lular staining patterns were determined, and specific autoantibody reactivities were assessed by immu
120                   The discovery of increased specific autoantibody reactivity in MDS patients, provid
121  study reveals features of a disease- and Ag-specific autoantibody repertoire with preferred VH:VL us
122 rol sera by ELISA, we found a consistent and specific autoantibody response against Dsg1 and other ke
123                         The association of a specific autoantibody response with distinct disease phe
124  IgG are not detectable within the strong Tg-specific autoantibody response.
125              B cell depletion reduced the PG-specific autoantibody response.
126 logy was used to study islet and other organ-specific autoantibody responses in parallel.
127 caused by the development of IgG(4)- and IgE-specific autoantibody responses.
128                    Patients without myositis-specific autoantibodies showed a significant peak in sum
129 harbors, on average, fourfold higher disease-specific autoantibody signals compared with plasma from
130                           Sjogren's syndrome-specific autoantibodies (SSA/Ro and SSB/La) were detecte
131 M, regardless of disease subtype or myositis-specific autoantibody status.
132 l autoimmunity is presented in which epitope-specific autoantibody stimulates de novo autoimmune path
133 ritical COVID-19 with and without type I IFN-specific autoantibodies supports a unifying model for di
134                                     Myositis-specific autoantibodies target intracellular proteins in
135     Here, we investigated the feasibility of specific autoantibody targeting in pemphigus.
136                                              Specific autoantibody testing can help identify these pa
137 ic thrombocytopenic purpura caused by a GPVI-specific autoantibody that mediates clearance of the GPV
138 eth cells and were seropositive for defensin-specific autoantibodies; the presence of autoantibodies
139 highlights the recent work on novel myositis-specific autoantibodies, their autoantigen targets, the
140 n pregnant dams harbored DNA-specific, NMDAR-specific autoantibodies throughout gestation.
141  is the presence of high-titer and extremely specific autoantibodies to the E2 component of the pyruv
142 in-4 (AQP4) antibody (AQP4-antibody), an NMO-specific autoantibody to AQP4, the dominant water channe
143  been described recently in which an epitope-specific autoantibody to murine zona pellucida 3 induces
144 adic IIM, although the frequency of myositis-specific autoantibodies was lower in familial than in sp
145  patterns were seen in 6.1%; the most common specific autoantibodies were anti-Ro (3.9%) and anti-Su
146                                          MOG-specific autoantibodies were identified in a subset of A
147                              Furthermore, HA-specific autoantibodies were induced in the absence of v
148                              Putative ROHHAD-specific autoantibodies were orthogonally validated usin
149 with active SLE, although the association of specific autoantibodies with chemokine score, a combined
150                     Although associations of specific autoantibodies with immune-related adverse even
151 l studies have implicated the association of specific autoantibodies with morphea subtype or severity
152 tures, such as autoimmune manifestations and specific autoantibodies, with patients affected by autoi

 
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