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1 pearance of immune complexes (IC) containing autoreactive Abs and TLR-activating nucleic acids, whose
2 patients with systemic lupus erythematosus, autoreactive Abs secreted by autoreactive plasma cells (
3 IgM and class-switched IgG1, IgG2b, and IgG3 autoreactive Abs that depended on the epitope density.
5 Moreover, mAbs bearing this clonotype are autoreactive against CD4 T cells and inhibit insulin tet
7 terparts, only a few of the tested BCRs were autoreactive, although the cell-based assay sensitively
8 results of single-antigen antibody testing, autoreactive and alloreactive flow cytometry crossmatche
9 unity, and with unique effects on priming of autoreactive and arthritogenic T cells, provides new ins
10 a stand-alone signal to trigger secretion of autoreactive and class-switched IgG in vivo in the absen
12 ell therapy did not alter the frequencies of autoreactive and polyreactive B cells, which remained el
13 e hypothesized that the HA stem bnAbs may be autoreactive and thus eliminated through the mechanisms
14 a human B-cell population that is naturally autoreactive and tolerized by functional anergy (BND cel
15 lammasomes, and independent of infection and autoreactive antibodies or antigen-specific T cells.
16 mic lupus erythematosus (SLE) is mediated by autoreactive antibodies that damage multiple tissues.
17 These include IGHV4-34, known to produce autoreactive antibodies, and IGKV3-20, a feature describ
18 of BTK in both the production and sensing of autoreactive antibodies, inhibitors of BTK kinase activi
19 ways involved in balancing protective versus autoreactive antibody responses in humans are incomplete
20 ce that lack surface MHC-I, however, are not autoreactive as predicted by the missing-self hypothesis
23 echanisms whereby BAFF/APRIL signals promote autoreactive B cell activation, discuss whether altered
24 ystemic lupus erythematosus (SLE), including autoreactive B cell activation, T effector cell function
26 ther deficiency of such molecule(s) disrupts autoreactive B cell anergy and causes B cell-mediated di
28 l mouse model where the presence of a single autoreactive B cell clone drives the TLR7-dependent acti
30 e immature B cells, but in contrast promotes autoreactive B cell expansion in the germinal center and
31 n of kinases, for instance, downstream of an autoreactive B cell receptor (BCR) or a transforming onc
32 irected against an exogenous Ag can cause an autoreactive B cell response and participate in the lice
33 e iNKT cells to regulate potentially harmful autoreactive B cell responses during inflammasome-driven
36 reover, the limited proliferative history of autoreactive B cells after treatment revealed that these
37 uals with SLE are unmutated, supporting that autoreactive B cells also differentiate outside germinal
38 permits quick and accurate quantification of autoreactive B cells and plasma cells in vivo within a n
39 ed the antiapoptotic protein survivin in the autoreactive B cells and plasma cells of MG patients.
40 ist throughout B cell development to control autoreactive B cells and prevent the generation of patho
41 triggers a checkpoint for the elimination of autoreactive B cells and represents a new strategy to ov
45 universal strategy for specific targeting of autoreactive B cells in antibody-mediated autoimmune dis
47 expansion, retention, and class-switching of autoreactive B cells in GCs under conditions where ACs a
53 nergy is one tolerance mechanism; it renders autoreactive B cells insensitive to stimulation by self-
56 ctive form of PI3K-P110alpha by high-avidity autoreactive B cells of mice completely abrogates centra
58 e data suggest that proper identification of autoreactive B cells requires the membrane-bound BCR, as
60 ation of the PI3K pathway leads high-avidity autoreactive B cells to breach central, but not late, st
62 However, conventional assays to identify autoreactive B cells usually employ in vitro-generated A
64 lonal expansion of immunoglobulin M (IgM)(+) autoreactive B cells, and also have an increased B-cell
65 way, a mechanism previously shown to silence autoreactive B cells, as a key physiological target to c
66 germinal centers that formed contained fewer autoreactive B cells, suggesting that IL-17 signaling is
76 We sought to explore alternative targets of autoreactive B lymphocytes through manipulation of affin
77 c immunoreceptors can direct T cells to kill autoreactive B lymphocytes through the specificity of th
78 e B cells restored the positive selection of autoreactive B-1 B cells by self-antigen in adult bone m
82 It has long been appreciated that highly autoreactive BCRs are actively removed from the developi
84 ntify the molecular mechanism of how anergic autoreactive BND cells escape functional anergy and whet
88 sed myeloid cell infiltration contributes to autoreactive CD4 T cell-mediated skin autoinflammation.
89 macrophages and neutrophils is required for autoreactive CD4 T cell-mediated skin disease pathogenes
90 een widely used to study the contribution of autoreactive CD4 T cells and relevant Ags to autoimmune
91 models of how specific cytokines produced by autoreactive CD4 T cells contribute to the pathogenesis
92 stable DQ8 complexes and potently stimulates autoreactive CD4 T cells from T1D patients, but not heal
96 -21-induced Th17 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as
98 to be dependent on high-level production by autoreactive CD4(+) and CD8(+) T cells of interferon-gam
101 an H2s haplotype showed increased numbers of autoreactive CD4(+) T cells and elevated IL-21 and IFN-g
104 miting supply of paracrine IL-2 generated by autoreactive CD4(+) T cells in response to MHC class II-
105 gest that identification of most potentially autoreactive CD4(+) T cells in the peripheral repertoire
106 Nod2(-/-) CD4(+) T cells or retina-specific autoreactive CD4(+) T cells lacking Nod2 reveals a T cel
108 These results suggest that the induction of autoreactive CD4(+) T cells triggers an opposing mobiliz
109 Although reactivation and accumulation of autoreactive CD4(+) T cells within the CNS are considere
110 y response that accompanies atherosclerosis, autoreactive CD4(+) T-helper cells accumulate in the ath
112 important for the accumulation of beta cell-autoreactive CD8 T cells but was dispensable for their a
113 t increased precursor frequency of beta cell-autoreactive CD8 T cells in NY8.3 mice obviated a role f
114 tion, and provide evidence for the escape of autoreactive CD8 T cells to the periphery when phagocyto
115 the expansion and accumulation of beta cell-autoreactive CD8 T cells, and in the absence of CD137 or
118 Although DC-mediated peripheral deletion of autoreactive CD8(+) T cells has been demonstrated using
119 analyses of insulitis, the identification of autoreactive CD8(+) T cells in situ, in islets of human
120 go is an autoimmune skin disease mediated by autoreactive CD8(+) T cells that destroy the pigment-pro
122 of IFNalpha/beta to modulate human activated autoreactive CD8(+) T-cell (cytotoxic T lymphocyte) resp
123 "blocking" anti-CD8 antibodies can suppress autoreactive CD8(+) T-cell activation in a relatively se
125 This relationship between properties of autoreactive CD8+ T cells and the rate of T1D disease pr
126 ressed whether the phenotype and function of autoreactive CD8+ T cells influence disease progression.
128 echanisms by which LNSC regulate low-avidity autoreactive cells in the NOD mouse model of type 1 diab
129 to target survivin through Ab recognition of autoreactive cells offers the potential for a highly spe
133 ies can originate from the pool of poly- and autoreactive clones that populate the naive B cell compa
134 n contrast, thymic B cells were enriched for autoreactive clones that showed increased specificity to
141 e tolerance was broken for one self-antigen, autoreactive GCs generated B cells targeting other self-
147 sophil activation status and the presence of autoreactive IgE were assessed in peripheral blood of a
150 ammaRIIb enhances the deletion and anergy of autoreactive immature B cells, but in contrast promotes
151 nTreg activities, which include blockade of autoreactive immune cells by cell-cell contact, Th17 and
152 owth factors promoting tumor development and autoreactive immune cells to reach the insulin-producing
154 critical checkpoint balancing protective and autoreactive immune responses, linking infection with in
157 e progressors had an increased proportion of autoreactive, islet-specific CD8(+) T cells expressing a
158 memory CD4(+) T cells that associate with an autoreactive-like profile involving IL-17 and Ccr7.
160 hanced autophagy, leading to the survival of autoreactive lymphocytes and increased autoantibody.
162 may be easily performed by IF and alert for autoreactive-mediated complications such as thrombotic o
163 upus they promote aberrant GC responses with autoreactive memory B cell development and plasma cell-d
165 eficiency can have dysregulated T cells, and autoreactive mouse thymocytes with weak Zap-70 signaling
167 new evidence suggests that this reservoir of autoreactive naive B cells contains clones that may deve
168 utoantibodies can originate from the pool of autoreactive naive B cells, which develops as a conseque
169 ignificantly higher frequencies of poly- and autoreactive new emigrant/transitional and mature naive
173 ymphocyte repertoire by increasing levels of autoreactive pathogenic T cells while suppressing develo
175 is, are neuroinflammatory diseases driven by autoreactive pathogenic TH cells that elicit demyelinati
179 erythematosus, autoreactive Abs secreted by autoreactive plasma cells (PCs) are considered to play a
181 ive selection in the thymus, thymocytes with autoreactive potential are either deleted or differentia
182 T cells in type 1 diabetes (T1D) sustains an autoreactive potential despite having access to a consta
183 nctionally equivalent to acute activation of autoreactive pre-B cell receptor signaling, which engage
185 ural antibodies (Nabs) with polyreactive and autoreactive properties have recently emerged as potenti
186 because it is a mechanism known to generate autoreactive receptors, this implies that shark lymphocy
188 Here we show that Plasmodium DNA induces autoreactive responses against erythrocytes by activatin
189 ent is a formative stage in the spleen where autoreactive specificities are censored as B cells gain
192 ants were polyreactive and four (66.7%) were autoreactive, suggesting that pathogenic anti-AQP4 autoa
193 odies are not inherently polyspecific and/or autoreactive, suggesting that polyreactivity of MPER-spe
194 ese disorders, such as molecules that target autoreactive T and B cells and anti-inflammatory mediato
195 g the presence of a continuous generation of autoreactive T and B cells within the pituitary gland.
197 inally, we identified TCR sequences from the autoreactive T cell clones, suggesting possible pathogen
200 lly, it thus seems that the expression of an autoreactive T cell receptor is a shared characteristic
201 erance eliminates most immature T cells with autoreactive T cell receptors (TCR) that recognize self
202 s, both HLA-DR15 allomorphs jointly shape an autoreactive T cell repertoire by serving as antigen-pre
204 selves and that this might suffice to elicit autoreactive T cell responses that lead to autoimmunity.
205 ytes play an important role as APC-expanding autoreactive T cell responses ultimately causing type 1
206 s immune tolerance by ensuring that distinct autoreactive T cell specificities differentiate into the
207 is being targeted therapeutically to inhibit autoreactive T cell trafficking, and these findings sugg
208 Consistently, transgenic mice harbored fewer autoreactive T cells and a higher proportion of regulato
210 ntral nervous system (CNS) that is caused by autoreactive T cells and associated with viral infection
212 ed system, we isolated human CD1c-restricted autoreactive T cells and characterized them at the molec
215 f T cells and results in both an increase in autoreactive T cells and decrease in regulatory T cells
216 actions needed for sufficient suppression of autoreactive T cells and helps to understand how MSCs am
220 regions to which DC may draw attention from autoreactive T cells are largely distinct and more restr
221 at acute GVHD blocks peripheral tolerance of autoreactive T cells by impairing lymph node (LN) displa
222 e key factor in thymic negative selection of autoreactive T cells by promoting the ectopic expression
225 uggests that despite impaired TCR signaling, autoreactive T cells exposed to chronic antigen stimulat
228 nize MHC, CD1a, CD1c, or CD1d proteins, CD1b autoreactive T cells have been difficult to isolate in h
229 itiate disease bouts by cooperating with the autoreactive T cells in helping them to recognize their
230 g Apoe-/- mice) to determine the role of CD1-autoreactive T cells in hyperlipidemia-associated inflam
232 Pbx1-d is associated with the production of autoreactive T cells in mice carrying the Sle1a1 lupus-s
233 as and may suppress the activity of pancreas autoreactive T cells in newly hyperglycemic non-obese di
234 As it can recognize and eliminate effector autoreactive T cells in the inflamed target tissue, the
235 oprotein 35-55 peptide, which induces myelin autoreactive T cells in the periphery, resulted in massi
236 ted with increased accumulation of beta-cell autoreactive T cells in the spleen and pancreatic lymph
237 ation are mediated by peripherally generated autoreactive T cells infiltrating into the central nervo
238 romote the differentiation of disease-primed autoreactive T cells into TR1-like cells, which in turn
239 ting a multi-hit model in which emergence of autoreactive T cells is a pinnacle pathogenic event.
242 differing self and foreign structures, CD1b autoreactive T cells recognize lipids with dual self and
243 y that central nervous system (CNS)-targeted autoreactive T cells required a process of licensing in
246 rview of recent progress in our knowledge of autoreactive T cells that has emerged from experimental
247 fy a link between metabolic disturbances and autoreactive T cells that promotes development of autoim
248 NA splicing variants) has been reported, and autoreactive T cells that target these neoantigens have
249 tolerance by mediating negative selection of autoreactive T cells through the collective expression o
251 hat Idd22 regulates the ability of beta cell-autoreactive T cells to traffic into the pancreatic isle
253 has demonstrated the pathogenic role of CD1b-autoreactive T cells under hyperlipidemic conditions in
254 erfering with the presentation of antigen to autoreactive T cells using a peptide approach; a recepto
255 In psoriatic patients, the frequency of CD1b-autoreactive T cells was increased compared with that in
257 ize and composition of polyclonal cohorts of autoreactive T cells with shared specificity is poorly u
258 tify and characterize potentially pathogenic autoreactive T cells, as well as protective antiviral T
259 types, including impaired central tolerance, autoreactive T cells, chronic fungal infection, and ESCC
260 s to actively adapt and effectively suppress autoreactive T cells, which are not fixed, but are evolv
272 lished a role for Smad7 in the generation of autoreactive T cells; however, the function of Smad7 in
274 ed coexpression on B cells coincided with an autoreactive T helper cell phenotype in MS patients.
276 s reveal an important role for miR-223-3p in autoreactive T(h)17 cell responses and suggest a potenti
279 nderstanding the pathobiology related to the autoreactive T-cell and microglial/macrophage demyelinat
280 g cells, of total T cells and of cells of an autoreactive T-cell clone found in inflamed organs, whil
283 by self-antigens in a specific manner, while autoreactive Tconv cells were produced through degenerat
284 nd CD1c molecules (hCD1Tg) as well as a CD1b-autoreactive TCR (HJ1Tg) in the ApoE-deficient backgroun
288 here gluten-reactive T cells provide help to autoreactive TG2-specific B cells by involvement of glut
289 erosis, the pathological interaction between autoreactive Th cells and mononuclear phagocytes in the
291 d natalizumab therapies efficiently targeted autoreactive TH1/TH17CM cells but also blocked virus-spe
293 immune reactions, but its role in regulating autoreactive Th17 cells and organ-specific autoimmunity
294 This was sufficient for the generation of an autoreactive TH17 subset of helper T cells, prominently
298 A large proportion of human T cells are autoreactive to group 1 CD1 proteins, which include CD1a
299 egulatory activity, but not the retention of autoreactive TR1 cells, requires local autoantigen expre