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1 nds to mucosal-associated invariant T cells (MAIT cells).
2 (lL)-12 + IL-18 as compared with circulating MAIT cells.
3 ly MR1A can present mycobacterial antigen to MAIT cells.
4 the first transcriptomic analysis of murine MAIT cells.
5 more accurately in CD8(+) than CD4(-)CD8(-) MAIT cells.
6 ng indispensable for TNF-alpha production by MAIT cells.
7 cytokine expression (IFNgamma, TNF) by human MAIT cells.
8 ompounds, that either inhibited or activated MAIT cells.
9 eactivity in a discrete subset of TRAV1-2(+) MAIT cells.
10 exacerbations and is a plausible target for MAIT cells.
11 ts that control the generation of functional MAIT cells.
12 on of MR1 Ags as well as into the biology of MAIT cells.
13 geneous and largely distinct from TRAV1-2(+) MAIT cells.
14 nds from Mycobacterium tuberculosis (Mtb) to MAIT cells.
15 phoidal Salmonella enterica strains activate MAIT cells.
16 entation of exogenous metabolite antigens to MAIT cells.
17 ted liver cirrhosis, and focus especially on MAIT cells.
18 d the capacity of monocytic APC to stimulate MAIT cells.
19 T) cells and mucosal-associated invariant T (MAIT) cells.
20 to activate mucosal-associated invariant T (MAIT) cells.
21 tabolites to Mucosal-Associated Invariant T (MAIT) cells.
22 In the rabbit, which has very few NKT and no MAIT cells, a previously unrecognized iTRA was identifie
27 apy rapidly decreased liver inflammation and MAIT cell activation and cytotoxicity, and increased the
29 asal MAIT cell priming in mice induces early MAIT cell activation and expansion after M. tuberculosis
30 ugh MAIT cell priming significantly enhanced MAIT cell activation and expansion early after M. tuberc
33 ment with interferon-alpha leads to specific MAIT cell activation in vivo in parallel with an enhance
36 ribityl chain of the AML strongly influences MAIT cell activation potency through dynamic compensator
38 l stereochemical and energetic influences on MAIT cell activation, enabling design of a water stable
42 otein 1 (MR1) participation, is required for MAIT cell activation; iv) MAIT cell responses to SEB can
44 ses of blood mucosal associated invariant T (MAIT) cells against in vitro stimulation with pneumococc
47 cilitates evasion from immune recognition by MAIT cells and contributes to the invasive pathogenesis
48 sms dictating the interactions between human MAIT cells and DCs and demonstrate that human MAIT cells
52 iNKT) cells, mucosal-associated invariant T (MAIT) cells, and gammadelta T cells, maintain a poised e
59 and velpatasvir, we found that intrahepatic MAIT cells are activated by monocyte-derived cytokines a
63 with age in humans, our understanding of how MAIT cells are altered during different phases across th
64 tibility complex (MHC)-related 1-restrictied MAIT cells are detected at similar levels with tetramers
66 for the first time that: i) mouse and human MAIT cells are hyperresponsive to SAgs, typified by stap
69 MHC-restricted T cells, blood frequencies of MAIT cells are poor correlates of TB disease but may pla
70 argely contributed by IL-12 and IL-18; v) as MAIT cells are primed by SAgs, they also begin to develo
71 avin metabolite antigens have suggested that MAIT cells are relatively homogeneous and uniform in res
73 in this study reveal for the first time that MAIT cells are systemically depleted in an AIDS virus in
80 human blood, mucosal-associated invariant T (MAIT) cells are abundant T cells that recognize antigens
97 er T (iNKT) and mucosal-associated innate T (MAIT) cells, are a heterogeneous T lymphocyte population
98 in the absence of TCR ligation, identifying MAIT cells as innate sentinels in inflammatory environme
99 cells, called mucosa-associated invariant T (MAIT) cells, as the most powerful source of pro-inflamma
101 y, the data suggest that activation of blood MAIT cells by innate inflammatory cytokines is a major m
105 brosis had significantly elevated numbers of MAIT cells compared with either nonfibrotic samples from
106 Escherichia coli-specific responses in aged MAIT cells compared with their young adult counterparts
107 receptor alpha (TCRalpha) repertoire in the MAIT cell compartment without redistribution to other an
110 the intrinsic metabolic pathways controlling MAIT cell cytokine production and highlight mTORC1 as an
115 n studies indicate that blood frequencies of MAIT cells, defined by cell surface markers, decline dur
121 early after M. tuberculosis challenge, these MAIT cells did not restrict M. tuberculosis bacterial lo
126 is uncoupled from the hallmark depletion of MAIT cells during HIV infection; and 2) the lack of PTM
127 and characteristics develop progressively in MAIT cells during infection, in parallel with TCR repert
130 rize the key molecular mechanisms that drive MAIT cell effector functions and to identify those which
133 during HIV infection; and 2) the lack of PTM MAIT cell enrichment at the gut mucosa may prevent deple
134 ting M. tuberculosis growth, suggesting that MAIT cell enrichment in the lung is not sufficient to co
137 an macaques, several studies have shown that MAIT cell frequencies actually decrease in peripheral bl
141 tivation and cytotoxicity, and increased the MAIT cell frequency among intra-hepatic but not blood T
152 indings establish a novel mechanism by which MAIT cells function to promote both innate and adaptive
153 cumulating evidence, however, indicates that MAIT cell functions are inducible by cytokine stimuli in
157 that is important in antimicrobial defense, MAIT cells have immune-modulatory functions that could e
161 ion profiles and clonal expansion in iNKT or MAIT cells, highly expanded conventional CD8(+) T cells
162 bsiella pneumoniae and Escherichia coli; vi) MAIT cell hyperactivation and anergy co-utilize a signal
164 een iNKT and mucosal-associated invariant T (MAIT) cells, illustrating a common core developmental pr
165 NTHi constitutes a target for pulmonary MAIT-cell immune responses, which are significantly impa
167 es of a T cell antigen receptor (TCR) from a MAIT cell in complex with MR1 bound to the non-stimulato
170 ls, but they had higher percentages of CD38+ MAIT cells in blood, which declined on entecavir treatme
173 ation and the loss/dysfunction of peripheral MAIT cells in HIV infection is well described, MAIT cell
177 f human MR1, forms MR1 tetramers that detect MAIT cells in human PBMCs, and stimulates cytokine expre
181 IT cells in HIV infection is well described, MAIT cells in nonhuman primate models are poorly charact
184 PTM)-specific MR1 tetramer and characterized MAIT cells in serial samples from naive and SIV- or simi
185 e novo riboflavin synthesis, and the role of MAIT cells in STSS has therefore so far been overlooked.
186 of chronic inflammation, the contribution of MAIT cells in such scenarios needs to be determined.
187 findings indicate that human tissue-resident MAIT cells in the kidney may contribute to the fibrotic
188 inverse correlation between the frequency of MAIT cells in the liver and histologically determined le
189 ata provide evidence for a cytotoxic role of MAIT cells in the lung and highlight important differenc
192 Together our data highlight the role of MAIT cells in the maintenance of gut integrity and the c
195 the human life span, we show that naive-like MAIT cells in umbilical cord blood switch to a central/e
196 stingly, BCG-induced IFN-gamma expression by MAIT cells in vitro was mediated by the innate cytokines
198 tic (NOD) strain, we detected alterations in MAIT cells, including increased production of granzyme B
201 cteristic of mucosal-associated invariant T (MAIT) cells is the expression of TRAV1-2(+) T cell recep
202 s and human immunodeficiency virus patients, MAIT cells isolated from HBV patients are not deleted bu
203 of in vitro experiments, we demonstrate that MAIT cells isolated from obese adults display defective
205 a show systemically decreased frequencies of MAIT cells likely attributable to enhanced turnover in S
207 we identify a new inflammatory mechanism in MAIT cells linking the DR3/TL1A axis with amplification
209 AIT cells and DCs and demonstrate that human MAIT cells mature monocyte-derived and primary DCs in an
212 cells and CD8 cells, but most potently from MAIT cells (median IFN-gamma-positive frequencies, 2.9,
213 study we investigated the interplay between MAIT cell-mediated antibacterial effector functions and
217 the CD69 activation marker on blood iNKT and MAIT cells of COVID-19 patients on admission was predict
225 y, distribution, and clonotypic structure of MAIT cell populations in the peripheral blood, liver, me
232 n priming and aerosol infection, and testing MAIT cell priming in nitric oxide synthase 2 (NOS2)-defi
239 typhoidal invasive disease in Africa, escape MAIT cell recognition through overexpression of ribB Thi
244 yme B(+) and gamma interferon (IFN-gamma)(+) MAIT cells relative to that in uninfected P2C/5-OP-RU-tr
245 velopment of mucosal-associated invariant T (MAIT) cells relies on a specific temporal window, after
246 mpaired phenotype in circulation, peritoneal MAIT cells remain abundant, activated, and highly functi
251 ylococcal enterotoxin B (SEB); ii) the human MAIT cell response to SEB is rapid and far greater in ma
255 ly higher polyfunctionality and magnitude of MAIT cell responses involving a range of effector functi
256 conducted a comprehensive analysis of human MAIT cell responses to GAS, aiming to understand the con
257 n, is required for MAIT cell activation; iv) MAIT cell responses to SEB can occur in a T cell recepto
260 cine-induced Abs enhanced Ag presentation to MAIT cells, resulting in more potent effector responses.
262 were deficient in MR1, and therefore lacked MAIT cells, revealed a loss of gut integrity and increas
263 -specific alpha-CD3, alpha-CD28 stimulation, MAIT cells showed a greater capacity to secrete cytokine
268 s, and mucosal-associated invariant T cells (MAIT cells) that are restricted to the MHC-related prote
269 enotype and transcriptional profile of human MAIT cells, they exhibited uniquely low expression of th
274 ation by IgG opsonization allows innate-like MAIT cells to mount a faster, stronger, and qualitativel
280 checkpoint that generated mature functional MAIT cells was controlled by multiple factors, including
286 s were as frequent, but granzyme B-producing MAIT cells were more frequent upon stimulation with Esch
291 ngs from prior studies, frequencies of blood MAIT cells were similar among patients with TB disease a
292 results underscore an important property of MAIT cells, which can be of translational relevance to r
293 ession by phenotypic (CD8(+)CD26(+)CD161(+)) MAIT cells, which constituted the majority (75%) of BCG-
294 ood frequencies of BCG-reactive IFN-gamma(+) MAIT cells, which returned to baseline frequencies a yea
295 etween defined members of the microbiota and MAIT cells, which sequentially controls both tissue-impr
296 tabolites to mucosal associated invariant T (MAIT) cells, which are characterized, in part, by the TR
297 dysfunction, mucosal-associated invariant T (MAIT) cells, which have the capacity to respond to bacte
298 The full-length isoform, MR1A, can activate MAIT cells, while the function of the isoforms, MR1B and
300 There is significant interest in targeting MAIT cells with immunostimulatory agents to enhance immu