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1 region suggests a genetic restriction of the autoantibody response.
2 not detectable within the strong Tg-specific autoantibody response.
3 nts; P=0.02), with marked attenuation of the autoantibody response.
4 B cell depletion reduced the PG-specific autoantibody response.
5 PAD-4 polymorphisms influence the anti-PAD-4 autoantibody response.
6 lung, the target tissue associated with this autoantibody response.
7 for examining the role of T cells in the RF autoantibody response.
8 ing a novel window into the initiation of an autoantibody response.
9 y mature, complex humoral autoimmune anti-Sm autoantibody response.
10 D4+ T cell repertoire required to induce the autoantibody response.
11 onnected group of molecules for a high-titer autoantibody response.
12 regulate two different sets of nephritogenic autoantibody responses.
13 fferentiation processes that underpin Ab and autoantibody responses.
14 ss-switched and hypermutated (mature) Ab and autoantibody responses.
15 oped for autoantigen discovery and profiling autoantibody responses.
16 ith both H(+)K(+)ATPase and intrinsic factor autoantibody responses.
17 ) regulatory T cells (Tregs) that suppressed autoantibody responses.
18 cell stimuli can influence the induction of autoantibody responses.
19 form germinal centers, and produce secondary autoantibody responses.
20 e maturation, rather than the initiation, of autoantibody responses.
21 rce of snoRNP to initiate and maintain these autoantibody responses.
22 s occurs in the face of an anti-Neu5Gc "xeno-autoantibody" response.
23 NZM2328 mice developed 1) accelerated dsDNA autoantibody response, 2) early onset and severe prolife
26 e show here that ablation of miR-155 reduced autoantibody responses accompanied by a decrease in seru
27 by ELISA, we found a consistent and specific autoantibody response against Dsg1 and other keratinocyt
28 Patients with UC, and not CD, show mucosal autoantibody response against hTM isoforms, particularly
29 4 wk, AOD progressed to ovarian atrophy with autoantibody response against multiple oocyte Ag of earl
30 e current study, we further investigated the autoantibody response against SPAG16-a protein with unkn
32 ody targets revealed marked heterogeneity in autoantibody responses against islet cell autoantigens i
33 hesis that NZW genes act to class-switch the autoantibody response, an effect that appears to contrib
34 ssion of Th1-mediated events exacerbated the autoantibody response and augmented IgG1, IgE, and IL-4
35 le manifestations, Th1 cells drive the early autoantibody response and IL-17-producing cells may be r
36 during apoptosis as potential targets of the autoantibody response and our results identify poly(ADP-
40 sulted in increased anti-mouse thyroglobulin autoantibody responses and increased expression of IFN-g
41 parations induced high-avidity anti-CCR5 IgG autoantibody responses, and all five immunized macaques
42 to study the specificity and pathogenesis of autoantibody responses, and to identify and define relev
43 tin, full-blown pathogenic maturation of the autoantibody response appears to require additional inpu
45 suggesting that at the clonal level, chronic autoantibody responses are dynamic and episodic, much li
47 on suppressed lung mucosa-associated Tfh and autoantibody responses by increasing the gut-homing alph
48 e of type I IFN-mediated signaling, systemic autoantibody responses can be dissociated from glandular
50 onged and significant increase of anti-dsDNA autoantibody responses compared with WT mice (week 4 to
51 always had reduced anti-mouse thyroglobulin autoantibody responses, compared with Tg(-) littermates,
52 bserved in vivo, suggesting that a metatypic autoantibody response could play a physiological role in
53 undertaken to determine whether this strong autoantibody response depends on T cell differentiation
54 rm large-scale multiplex characterization of autoantibody responses directed against structurally div
56 se disparate clinical outcomes, anticollagen autoantibody responses during CIA did not differ among t
59 ally incite autoimmunity, we have traced the autoantibody response in human SLE back in time, prior t
61 ur goal was to analyze the regulation of the autoantibody response in male and female W/B mice bearin
62 tal mercury elicits a genetically restricted autoantibody response in mice that targets the nucleolar
63 study, we showed that the class-switched IgG autoantibody response in MRL/Fas(lpr/lpr) and C57/Sle1Sl
64 trategy to confirm KIR4.1 as a target of the autoantibody response in multiple sclerosis and to show
65 of this type could plausibly perpetuate the autoantibody response in myasthenia gravis, and are a ra
67 pitope-specific Ab responses and alternative autoantibody responses in a model system in which an ant
68 dy identifies axopathic and/or demyelinating autoantibody responses in a subset of patients with mult
70 of Sle1b on Spt-GC, follicular Th cell, and autoantibody responses in B6.Sle1b mice was B cell auton
71 oked strong germinal centre alloantibody and autoantibody responses in C57BL/6 recipients and develop
72 ome' microarrays to profile the evolution of autoantibody responses in experimental autoimmune enceph
76 urther evidence that TLRs play a key role in autoantibody responses in SLE, we found that autoimmune-
78 FNs might be critical for amplifying overall autoantibody responses in systemic lupus erythematosus.
79 particle (VLP)-based immunogens could induce autoantibody responses in well-characterized transgenic
81 ion of linear epitopes and the complexity of autoantibody responses, including the broad spectrum of
82 further investigate the pathogenesis of the autoantibody response induced by peptide immunization, w
84 nducible regulatory T cells that can control autoantibody responses is a potential avenue for the tre
85 ection of a self-molecule as a target for an autoantibody response may be a consequence of the proinf
87 of IL-17 and IL-21 and the inflammatory and autoantibody responses observed in these autoimmune mice
88 Autoimmune ovarian disease (AOD) and oocyte autoantibody response of day 3-thymectomized (d3tx) mice
92 inea pigs not only develop antimitochondrial autoantibody responses similar to human PBC, but also de
93 CD4(+) T cells, and a robust, variegated IgG autoantibody response targeting multiple components of c
95 Overall, the highest correlations among the autoantibody responses tested were in the endemic contro
97 lyclonal and sustainable anti-mTNF-alpha IgG autoantibody response that lasts for at least 40 weeks.
98 by which a toxin such as mercury elicits an autoantibody response that predominantly targets a singl
99 Ns drove T cell-mediated inflammation and an autoantibody response that targeted abundant, tissue-res
100 its a genetically restricted, anti-nucleolar autoantibody response that targets fibrillarin, a 34-kDa
101 ritical in the initiation and maintenance of autoantibody responses that are a hallmark of systemic l
102 g linked to foreign Th epitopes induces weak autoantibody responses that are predominantly of the IgM
106 ed approach to identify the initiation of an autoantibody response to identify the sites and cell dif
109 selvagem [FS]) in which the pathogenic IgG4 autoantibody response to the self-antigen desmoglein 1 (
110 be a straightforward HLA-class II-restricted autoantibody response to the thyroid stimulating hormone
112 atosus clearly dissociate genetic control of autoantibody responses to classic lupus antigens and kid
115 uggest that measurement of T-cell as well as autoantibody responses to FcepsilonRIalpha could improve
116 e inverse relationship between IFN-gamma and autoantibody responses to FcepsilonRIalpha may signify d
120 esponses, using cellular immunoblotting, and autoantibody responses to islet proteins, before transpl
121 esponses, using cellular immunoblotting, and autoantibody responses to islet proteins, before transpl
122 observations that concomitant or coupling of autoantibody responses to proteins which are associated
123 molecular-intrastructural diversification of autoantibody responses to the components of Ul snRNPs in
127 f specific autoantigens that might stimulate autoantibody responses under proinflammatory conditions.
131 Myd88 is required for anti-DNA and anti-RNA autoantibody responses, whereas Fcer1g is not expressed
132 ete Freund's adjuvant enhanced their insulin autoantibody response with a higher level and longer per
134 clear ribonucleoprotein (snRNP) and anti-DNA autoantibody responses with some changes in isotype swit
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