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1 nds to mucosal-associated invariant T cells (MAIT cells).
2 tivate polyclonal and quasi-monoclonal mouse MAIT cells.
3 ityllumazine [RL] Ags) capable of activating MAIT cells.
4 mor tissue reduced IFN-gamma production from MAIT cells.
5 cytokine expression (IFNgamma, TNF) by human MAIT cells.
6 convert to lumazines, as potent antigens to MAIT cells.
7 ssed in both circulating and intrasinusoidal MAIT cells.
8 RL-6-CH(2)OH), specifically detect all human MAIT cells.
9 ompounds, that either inhibited or activated MAIT cells.
10 eactivity in a discrete subset of TRAV1-2(+) MAIT cells.
11 exacerbations and is a plausible target for MAIT cells.
12 ts that control the generation of functional MAIT cells.
13 on of MR1 Ags as well as into the biology of MAIT cells.
14 geneous and largely distinct from TRAV1-2(+) MAIT cells.
15 tes known as mucosal associated invariant T (MAIT) cells.
16 NKT cells or mucosal-associated invariant T (MAIT) cells.
17 , were named mucosal-associated invariant T (MAIT) cells.
18 In the rabbit, which has very few NKT and no MAIT cells, a previously unrecognized iTRA was identifie
22 apy rapidly decreased liver inflammation and MAIT cell activation and cytotoxicity, and increased the
25 ment with interferon-alpha leads to specific MAIT cell activation in vivo in parallel with an enhance
27 l stereochemical and energetic influences on MAIT cell activation, enabling design of a water stable
33 otein 1 (MR1) participation, is required for MAIT cell activation; iv) MAIT cell responses to SEB can
36 ween and within individuals, suggesting that MAIT cell adaptation was a direct consequence of exposur
40 n that mucosal-associated invariant T-cells (MAIT cells), an abundant population of innate-like T-cel
41 ely activate mucosal-associated invariant T (MAIT) cells, an abundant population of innate-like T cel
42 sms dictating the interactions between human MAIT cells and DCs and demonstrate that human MAIT cells
45 enotypic characterization of human and mouse MAIT cells and revealed unanticipated TCR heterogeneity
46 l feature of mucosal associated invariant T (MAIT) cells and have been recently implicated in host de
49 resulting MR1-Ag complexes are recognized by MAIT cell antigen receptors (alphabeta T cell receptors
50 antitative and functional data indicate that MAIT cells are a specialized cell population highly adap
52 cent studies have shown that mouse and human MAIT cells are activated by antigen-presenting cells (AP
53 and velpatasvir, we found that intrahepatic MAIT cells are activated by monocyte-derived cytokines a
58 provides in vivo evidence demonstrating that MAIT cells are an important T-cell subset with activitie
63 In this article, we show that circulating MAIT cells are depleted in obese adults, and depletion i
64 T cell receptors (TCRs), we demonstrate that MAIT cells are detectable in a broad range of tissues in
66 ontrast, mature IL-18Ralpha(+) CD8alphaalpha MAIT cells are enriched in the fetal small intestine, li
68 colleagues (2014) demonstrate that, although MAIT cells are found in psoriatic skin, they are not inc
69 for the first time that: i) mouse and human MAIT cells are hyperresponsive to SAgs, typified by stap
70 ll responses, as well as that MR1-restricted MAIT cells are important for tuberculosis protective imm
74 argely contributed by IL-12 and IL-18; v) as MAIT cells are primed by SAgs, they also begin to develo
76 avin metabolite antigens have suggested that MAIT cells are relatively homogeneous and uniform in res
77 in this study reveal for the first time that MAIT cells are systemically depleted in an AIDS virus in
96 cells, called mucosa-associated invariant T (MAIT) cells, as the most powerful source of pro-inflamma
97 omes were changes in frequencies of Th17 and MAIT cells between health and asthma using Mann-Whitney
101 escribe new MR1 ligands that do not activate MAIT cells but compete with bacterial and synthetic comp
103 -OE-RU from bacterial cultures that activate MAIT cells, but not from non-activating bacteria, indica
104 molecules and their mode of presentation to MAIT cells by the major histocompatibility complex (MHC)
106 eral recent advances in our understanding of MAIT cell characteristics and functions secure their upc
111 receptor alpha (TCRalpha) repertoire in the MAIT cell compartment without redistribution to other an
112 ngs are consistent with a model in which the MAIT-cell compartment, possibly as a result of persisten
113 T cells and mucosal-associated invariant T (MAIT cells), conserved TCRs define other subsets of huma
127 lthough 5-A-RU does not bind MR1 or activate MAIT cells directly, it does form potent MAIT-activating
130 oreover, in both patient groups, circulating MAIT cells displayed an activated phenotype that was ass
139 Consistent with high IL-17A production, most MAIT cells express high levels of retinoic acid-related
144 NKT and mucosal-associated invariant T (MAIT) cells express semi-invariant TCR and restriction b
147 ified from peripheral blood, intrasinusoidal MAIT cells expressed markers of T cell activation; howev
148 pertoire, and although the majority of human MAIT cells expressed TRAV1-2-TRAJ33, some expressed TRAJ
150 ogeneous subsets of tetramer(+) Valpha19i-Tg MAIT cells expressing CXCR3 and alpha4beta1 were recruit
151 an macaques, several studies have shown that MAIT cell frequencies actually decrease in peripheral bl
152 increased in childhood obesity, and altered MAIT cell frequencies in obese children are positively a
156 tivation and cytotoxicity, and increased the MAIT cell frequency among intra-hepatic but not blood T
162 nic and/or commensal bacteria, distinguishes MAIT cells from peptide- or lipid-recognizing alphabeta
164 rvations contrast with previous reports that MAIT cells from Valpha19 TCR transgenic mice are PLZF(-)
165 te the origin and differentiation pathway of MAIT-cells from a naive type-17 precommitted CD161(++)CD
168 indings establish a novel mechanism by which MAIT cells function to promote both innate and adaptive
171 that is important in antimicrobial defense, MAIT cells have immune-modulatory functions that could e
175 bsiella pneumoniae and Escherichia coli; vi) MAIT cell hyperactivation and anergy co-utilize a signal
177 T cell receptors (TCRs)), and the subsequent MAIT cell immune responses are thought to protect the ho
178 NTHi constitutes a target for pulmonary MAIT-cell immune responses, which are significantly impa
181 es of a T cell antigen receptor (TCR) from a MAIT cell in complex with MR1 bound to the non-stimulato
182 studies have implicated MR1 presentation to MAIT cells in bacteria recognition, although the mechani
184 ls, but they had higher percentages of CD38+ MAIT cells in blood, which declined on entecavir treatme
185 uency, phenotype, and functional capacity of MAIT cells in colon adenocarcinomas and unaffected colon
187 f human MR1, forms MR1 tetramers that detect MAIT cells in human PBMCs, and stimulates cytokine expre
190 lyzed the frequency and function of CD161++ /MAIT cells in peripheral blood and tissue from patients
195 inverse correlation between the frequency of MAIT cells in the liver and histologically determined le
196 ata provide evidence for a cytotoxic role of MAIT cells in the lung and highlight important differenc
197 Together our data highlight the role of MAIT cells in the maintenance of gut integrity and the c
199 analyses showed significant accumulation of MAIT cells in tumor tissue, irrespective of tumor stage
204 of Th17 and mucosal associated invariant T (MAIT) cells in airway inflammation; to characterise asso
205 ogy of mucosal-associated invariant T cells (MAIT cells) in mice have been hampered by a lack of spec
206 tic (NOD) strain, we detected alterations in MAIT cells, including increased production of granzyme B
209 velopment of mucosal-associated invariant T (MAIT) cells is dependent upon the class Ib molecule MHC-
210 cteristic of mucosal-associated invariant T (MAIT) cells is the expression of TRAV1-2(+) T cell recep
211 s and human immunodeficiency virus patients, MAIT cells isolated from HBV patients are not deleted bu
212 Moreover, TCR-independent activation of MAIT cells leads to a reduction of HCV replication in vi
213 mation, regulated TCR-mediated activation of MAIT cells, licensing them to dramatically increase Th1
214 ents, we show that the most active synthetic MAIT cell ligand displays the same functional avidity fo
215 d human MR1 tetramers loaded with the potent MAIT cell ligand, reduced 6-hydroxymethyl-8-D-ribityllum
216 r, these results show that most, if not all, MAIT cell ligands found in Escherichia coli are related
217 a show systemically decreased frequencies of MAIT cells likely attributable to enhanced turnover in S
219 AIT cells and DCs and demonstrate that human MAIT cells mature monocyte-derived and primary DCs in an
223 cells and CD8 cells, but most potently from MAIT cells (median IFN-gamma-positive frequencies, 2.9,
225 ricted mucosal associated invariant T cells (MAIT cells), MHC class Ib-reactive T cells, and gammadel
230 , however, the cognate recognition of MR1 by MAIT cells on the infected MPhi was found to play only a
232 ory T cells, mucosal-associated invariant T (MAIT) cells, other T-cell subsets, and granulocyte media
233 d to wild-type (WT) mice, demonstrating that MAIT cells play a unique role among innate lymphocytes i
237 y, distribution, and clonotypic structure of MAIT cell populations in the peripheral blood, liver, me
240 ction, we show here that purified polyclonal MAIT cells potently inhibit intracellular bacterial grow
241 or gammat (RORgammat), whereas RORgammat(lo) MAIT cells predominantly express T-bet and produce IFN-g
245 e iValpha19 transgenic and Vbeta6 transgenic MAIT cell progenitors requires MHC-related 1-expressing
248 bacterial and synthetic compounds activating MAIT cells, providing the capacity to modulate MAIT cell
251 of MR1-Ag tetramers that specifically stain MAIT cells, recognition by the MAIT TCR, and our emergin
255 ogeneity were apparent across the functional MAIT cell repertoire as a whole, especially for TCRbeta
256 R1-restricted mucosa-associated invariant T (MAIT) cells represent a large antimicrobial T-cell subse
257 1-restricted mucosal-associated invariant T (MAIT) cells represent a subpopulation of alphabeta T cel
258 T cells and mucosal-associated invariant T (MAIT) cells represent peculiar T-lymphocyte subpopulatio
261 ylococcal enterotoxin B (SEB); ii) the human MAIT cell response to SEB is rapid and far greater in ma
264 n, is required for MAIT cell activation; iv) MAIT cell responses to SEB can occur in a T cell recepto
265 nstrate considerable functional diversity of MAIT cell responses, as well as that MR1-restricted MAIT
267 were deficient in MR1, and therefore lacked MAIT cells, revealed a loss of gut integrity and increas
268 of MR1-deficient (MR1(-/-)) mice, which lack MAIT cells, revealed defects in early mucosal cytokine p
269 this inhibitory activity was dependent upon MAIT cell selection by MR1, secretion of gamma interfero
272 s been suggested through the analysis of the MAIT cell TCR repertoire in humans and differential reac
273 exist in cord blood, from which a prominent MAIT cell (TCR Valpha7.2(+)) population emerges post-nat
274 from normal mice more closely resemble human MAIT cells than previously appreciated, and this provide
279 ial-independent, cross-species reactivity of MAIT cells to define the molecular basis of MAIT-TCR/MR1
283 Notably, whereas the function of residual MAIT cells was at least partly restored by effective ant
284 checkpoint that generated mature functional MAIT cells was controlled by multiple factors, including
293 s were as frequent, but granzyme B-producing MAIT cells were more frequent upon stimulation with Esch
297 tly lower frequencies of IFN-gamma-producing MAIT cells were seen, whereas there were no differences
299 results underscore an important property of MAIT cells, which can be of translational relevance to r
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