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1 ISTA (V-domain Ig-containing Suppressor of T cell Activation).
2 Th1 cell polarization and cytotoxic CD8(+) T cell activation.
3 played allergen on VLPs failed to cause mast cell activation.
4 iperacillin and the threshold required for T cell activation.
5 rticularly those that depend on Ag-induced T cell activation.
6 CR stimulation and is required for optimal T cell activation.
7 nucleotide synthesis or nucleotide-dependent cell activation.
8 its role as a novel regulator of naive CD4 T-cell activation.
9 it MYD88/p100 signaling as a regulator for B-cell activation.
10 e effects of TGF-beta on IL-33-mediated mast cell activation.
11 perate and thus enhance the sensitivity of T cell activation.
12 ucuronidase heparanase that increase upon NK cell activation.
13 show how the mutations function to improve T-cell activation.
14 1 even when stimulated by antigen-specific T cell activation.
15 ew insights into antigen properties and MAIT cell activation.
16 to how physiological cues may influence stem cell activation.
17 contribute to the endogenous pathway of iNKT cell activation.
18 e role of DNA methylation in regulating mast cell activation.
19 on (DR) as the results of hepatic progenitor cell activation.
20 lter immune effector cell numbers or myeloid cell activation.
21 itical NKp30 ligand B7-H6 thus inhibiting NK cell activation.
22 CD8+ T cells, and CD4/CD8 ratio) and CD4+ T-cell activation.
23 ustion by regulating Pdcd1 expression upon T cell activation.
24 w downstream events can ultimately lead to T cell activation.
25 cterial infections by controlling effector T cell activation.
26 rabinose residues, decreased the extent of B cell activation.
27 attempted limitation of pathogenic CD8(+) T-cell activation.
28 propose plays a crucial role in regulating T cell activation.
29 clinical disease and signs of chronic immune cell activation.
30 tumor microenvironment promotes malignant B cell activation.
31 ) is required for gastric colonization and T-cell activation.
32 ants with stronger suppression of in vitro T cell activation.
33 l d 1 displayed on VLPs fails to induce mast cell activation.
34 s production of reactive oxygen species upon cell activation.
35 esenting cells (APCs) and induce alphabeta T-cell activation.
36 fector cell differentiation by controlling B cell activation.
37 costimulation similarly increased human iNKT cell activation.
38 mobilization and to the attenuation of mast cell activation.
39 nt antigens, leading to systemic and local T cell activation.
40 nization properties diminishes pAg-induced T cell activation.
41 effect of CXCL4 in modulating DC-mediated T cell activation.
42 cross-present capsid antigen during CD8(+) T-cell activation.
43 nd kinase activity are induced upon CD4(+) T cell activation.
44 that can clinically inhibit Vgamma9Vdelta2 T cell activation.
45 ma) against EBV-infected cells, enhancing NK cell activation.
46 CD80 and CD86), is a negative regulator of T-cell activation.
47 , where it rapidly disassociated following T-cell activation.
48 ) on TCR-ligand interaction and subsequent T cell activation.
49 eton in regulating force generation during T-cell activation.
50 ng, costimulatory pathways are involved in T cell activation.
51 13 production in lung tissue, as well as TH2 cell activation.
52 ional programs that are a hallmark of immune cell activation.
53 degranulation, IVIG attenuated post-ICH mast cell activation.
54 igins induced cytokine production and immune cell activation.
55 fluorescence in situ hybridization during T-cell activation.
56 ructure has been shown to be important for T cell activation.
57 and NFAT translocation, a measure of full T-cell activation.
58 nt of pAg sensing that ultimately leads to T cell activation.
59 l guanosine triphosphate protein linked to T-cell activation.
60 fall in oxygen levels might initiate Type I cell activation.
61 promote hyperplasia, fibrosis, and vascular cell activation.
62 on regulatory or effector T cells reduces T cell activation.
64 enhanced inflammation, stronger endothelial cell activation, a more disturbed vascular integrity, an
65 However, although NKp65 utilizes Syk for NK cell activation, a physical association of Syk with the
68 yndrome, which is characterized by massive T cell activation and a predominant Th1 profile of cytokin
70 ght to determine the mechanisms that drive B cell activation and antibody production during chronic a
71 mulates the CD27 pathway, which results in T-cell activation and antitumor activity in tumor models.
72 eased B regulatory cell [Breg] counts, and B cell activation and apoptosis) is specifically associate
74 stigated their role in alloantigen-induced T cell activation and asked whether their absence might im
76 significantly increased tumor-infiltrating T-cell activation and cytotoxicity and decreased the frequ
77 apidly decreased liver inflammation and MAIT cell activation and cytotoxicity, and increased the MAIT
79 ostimulatory interactions are required for T cell activation and development of an effective immune r
80 BAFF, IL-2, and IL-21 induce memory and DN B cell activation and differentiation has implications for
81 naling and metabolic pathways critical for T-cell activation and differentiation into Th1 and Th17 su
85 le for cyclin-dependent kinase 5 (Cdk5) in T-cell activation and effector function, but the contribut
86 +) T regulatory (Treg) cells suppress immune cell activation and establish normal immune homeostasis.
88 ng in adoptively transferred CTLs enhances T cell activation and IFN-gamma production in vitro, leadi
89 pha production, resulting in superior immune cell activation and increased immunotherapeutic properti
96 cytokine that potently promotes endothelial cell activation and pathological angiogenesis in our pre
97 tein) chromatin regulator is controlled by B cell activation and potentiates steady-state and postimm
98 or autophagy in the regulation of microglial cell activation and pro-inflammatory molecule secretion,
99 f Mer in dendritic cells promotes enhanced T cell activation and proinflammatory cytokine production.
100 pensate for the lack of Cdc42 in TLR-induced cell activation and proliferation, so the two proteins p
103 nflammatory mediators leading to mononuclear cell activation and recruitment could underlie the abnor
106 rbon receptor (AhR) is highly induced upon B cell activation and serves a critical role in regulating
107 -derived macrophages were able to suppress T-cell activation and showed restored antimycobacterial ac
108 t use iPS cell factors and thus differs from cell activation and signaling-directed (CASD) reprogramm
111 cts with FcmuR on B cells to support early B cell activation and the development of long-lived humora
113 ubtilis EPS can be used to broadly inhibit T cell activation and, thus, control T cell-mediated immun
116 development of lymphadenopathy and CD4(+) T cell activation, and autoimmunity that mainly targeted s
118 te expression profiles during drug-induced T cell activation, and expression of each receptor was enh
119 instructed TNFalpha expression, endothelial cell activation, and intratumoral T-cell infiltration.
121 lipoproteins and phospholipids, endothelial cell activation, and macrophage infiltration/activation
122 gamma response, CD16-mediated natural killer cell activation, and monocyte/macrophage activation.
124 nge by 84% to 90%, as well as diarrhea, mast cell activation, and TH2 cytokine responses and serum al
125 induced hypertension, vascular injury, and T-cell activation; and gammadelta T cells are associated w
126 with biased capacity for CD4(+) and CD8(+) T cell activation are asymmetrically distributed in lymph
127 s has illustrated that important facets of T-cell activation are controlled at the level of translati
128 l receptor (TCR) triggering and subsequent T-cell activation are essential for the adaptive immune re
129 endent ILC2 expansion, and IL-33-driven mast cell activation are necessary for induction of type 2 im
131 Whereas metabolic changes occurring during T cell activation are well characterized, the metabolic de
132 o inhibit the unintentional Vgamma9Vdelta2 T cell activation as a consequence of aminobisphosphonate
133 tion genes, which correlated (r=0.78) with T-cell activation as measured by CD8-positive expression.
134 deal molecule to improve early pathways of B cell activation, as it links innate and adaptive immunit
135 hat lymphostatin is likely to act early in T cell activation, as stimulation of T cells with concanav
137 y kinase Lck sets a critical threshold for T cell activation because it phosphorylates the TCR comple
139 he molecular mechanisms for hepatic stellate-cell activation by HCV-infected hepatocytes are underexp
140 of 76 kDa (SLP-76) plays a crucial role in T cell activation by linking antigen receptor (T cell rece
141 b1) restrains PD-1 expression induced upon T cell activation by recruiting a nucleosome remodeling de
142 e investigated a mechanism for suppressing T cell activation by stimulating a natural inhibitory rece
144 y a new role for T cell TRAF3 in promoting T cell activation, by regulating localization and function
145 ere are conditions in which Vgamma9Vdelta2 T cell activation can be considered inappropriate for the
146 ytotoxicity response from a polyfunctional T cell activation caused hepatotoxicity and the rapid indu
147 We undertook translatome analysis of CD8 T-cell activation, combining polysome profiling and microa
148 several genes involved in TCR signaling and cell activation, confirming its role as a novel regulato
149 ) cells specifically inhibited TH1 and CD8 T cell activation consistent with their co-localization wi
150 that titrating PD-1 expression during CD8 T cell activation could have important ramifications in va
151 r the rFlaA:Betv1 conjugate and analyzed for cell activation, cytokine secretion, and metabolic state
152 to the RBC cell surface strongly inhibited B cell activation, cytokine secretion, and proliferation.
153 We demonstrated that while ICH induced mast cell activation/degranulation, IVIG attenuated post-ICH
154 ndothelial cell capillarization and stellate cell activation demonstrates allograft injury in proximi
155 , and pathogenic infections can all affect T cell activation, differentiation, and the kinetics of gr
158 nt knowledge about the various types of mast cell activation disorders, their treatment, and areas of
160 n about their capacity to influence CD4(+) T-cell activation during a primary or secondary response t
161 insight into the mechanisms underlying CD8 T cell activation during infection, which may be useful in
163 reochemical and energetic influences on MAIT cell activation, enabling design of a water stable synth
166 tedly, however, we observed increased immune cell activation following administration of PapMV to com
167 which the pericardial AT coordinates immune cell activation, granulopoiesis, and outcome after MI.
169 M-resistant BALB/c mice leads to amplified T cell activation, higher serum gamma interferon (IFN-gamm
170 are required for antigen receptor-mediated T-cell activation, how T-cells feedback to APCs to sustain
172 holangiocytes promoted quiescent mesenchymal cell activation in a platelet-derived growth factor (PDG
173 The cell surface receptor CD6 regulates T cell activation in both activating and inhibitory manner
174 lopment, and significantly increased granule cell activation in both control and chronically epilepti
175 allergy is associated with IgE-mediated mast cell activation in conjunctival tissue leading to the re
176 xpression is reduced during hepatic stellate cell activation in culture and in a mouse model of alcoh
177 red the capability of Fel d 1 to induce mast cell activation in its free form versus displayed on VLP
179 suppressed expression of markers of stellate cell activation in livers of mice fed a diet rich in tra
180 he specific neoantigen qualities promoting T-cell activation in long-term survivors, we discovered th
184 e I interferon (IFN) for natural killer (NK) cell activation in response to viral infection is known,
185 s have suggested that it also inhibits glial cell activation in rodents, and may alter opioid-mediate
186 says, and the variant was found to silence T-cell activation in seven of the eight blood donors who r
188 in nonatopic, nonallergic adults was muted T-cell activation in the peripheral blood and inflammatory
193 MSDC-0602 directly reduced hepatic stellate cell activation in vitro, and MSDC-0602 treatment or hep
197 beta-dependent Treg-cell suppression of mast cell activation, in the absence of modulation of T- or B
198 haracterized by tissue eosinophilia and mast cell activation, including abundant production of prosta
199 with an hCD22 ligand were shown to prevent B cell activation, increase cell death, and induce toleran
201 at concentrations that triggered similar NK cell activation, indicating that cell-associated gp350(+
202 patocyte MPC2 deletion also limited stellate cell activation indirectly by affecting secretion of exo
203 In secondary lymphoid organs, Ag-driven B cell activation induces terminal maturation and Ig isoty
205 ts the importance of monitoring peripheral T cell activation inhibitor-mitochondrial expression, LBP
206 Peripheral and intragraft expressions of T cell activation inhibitor-mitochondrial were stable in l
208 h optimal stroma permeabilization and immune cell activation is able to markedly increase therapy res
213 er of differentiation 1 (CD1) proteins for T cell activation is susceptible to lipophilic environment
214 1 (MR1) participation, is required for MAIT cell activation; iv) MAIT cell responses to SEB can occu
216 First, peripheral blood CD4(+) and CD8(+) T-cell activation levels initially decreased in M- partici
217 ant target proteins UL83 or UL123, and the T-cell activation marker interferon-gamma (IFN-gamma).
218 romatic flow cytometry was used to analyze T-cell activation markers (CD107, CD154, interleukin-2 [IL
221 eceptors, antimicrobial peptides, monocytoid cell activation markers, and numerous genes annotated as
222 d anticoagulation, fibrinolysis, endothelial cell activation, matricellular protein release, and tiss
223 adducts accompanied by evidence of stellate cell activation, matrix remodeling, and fibrosis (P < 0.
224 r organization, and changes in LADs during T-cell activation may provide an important additional mode
225 ids on the cell surface and thereby regulate cell activation, migration, adhesion, and signaling.
226 tibody production, cytokine secretion, and T-cell activation; moreover, B cell misregulation is impli
227 e expression, fragmented mitochondria, glial cell activation, muscle atrophy, weight loss, and reduce
228 ite maraviroc prophylaxis showed increased T-cell activation, naive T-cell skewing, and elevated seru
229 ng with 12 signatures tracking CD8 and CD4 T-cell activation, natural killer cells, and IFN activatio
230 perturbation promoted downstream endothelial cell activation, neutrophil accumulation, endothelial ce
236 l VACV intranasal challenge, or defects of T cell activation or T cell homing to the site of inoculat
237 s a prominent role for the CD16-dependent NK cell activation pathway in the complex array of factors
239 d eosinophilic airway inflammation and a TH2 cell activation phenotype that was not different from th
242 T cell activation profiles, the extent of B cell activation prior to ART did not correlate with HIV
245 e show that type I IFNs support robust CD8 T cell activation (proliferation and IFN-gamma and granzym
246 c cells in vivo and in vitro, IVM impaired T-cell activation, proliferation, and cytokine production
247 stimulation of ILC2s with NMU induced rapid cell activation, proliferation, and secretion of the typ
249 ylated CD6 cytoplasmic Y662 residue during T cell activation, providing an activating signal to T cel
251 FcgammaRIIB-mediated inhibition of effector cell activation requires direct ligation to an activatin
253 totic signaling pathways, the noncytotoxic T cell activation showed extended proliferative, metabolic
254 nate proinflammatory response or increased T cell activation/skewing display a more impaired behavior
256 h depression of serum markers of the myeloid cell activation, such as CCL5, CCL11, and C-X-C motif ch
257 over-representation of genes relevant for T cell activation, such as CD40L, IRAK1, IRAK2, STAT1, and
258 way, or the loss of negative regulators of T cell activation, such as the E3 ubiquitin ligase Cbl-b,
261 g clonal mast cell disorder (monoclonal mast cell activation syndrome or systemic mastocytosis) and t
264 flammatory cytokines, and evidence of innate cell activation that included neutrophil extracellular t
265 reg cell TCR repertoire led to marked immune cell activation, tissue inflammation, and an ultimately
266 ses while maintaining low levels of CD4(+) T-cell activation to avoid the generation of target cells
267 and morphological events occurring during T-cell activation to model force generation and to reveal
268 d levels of serum tryptase, a marker of mast-cell activation, to a greater extent than did placebo (d
269 ion of CD22 ligands in RBCs should abolish B cell activation toward its cognate Ag on the surface of
270 ensitive to apoptosis but also accelerated T cell activation under phorbol 12-myristate 13-acetate/io
272 ese cells, including several mediators of NK cell activation (VAV3 and LYN) and a large array of NK r
273 hat IVIG will attenuate the ICH-induced mast cell activation via FcgammaRIIB/SHIP1 pathway, resulting
274 ies to expand myeloma-specific T cells and T-cell activation via PD-1/PD-L1 blockade are currently be
275 hat during homeostasis, FRCs also suppress T cell activation via producing high level of prostaglandi
277 V-domain Immunoglobulin Suppressor of T cell Activation (VISTA) is an inhibitory immune-checkpoi
282 dal endothelial cell activation and stellate cell activation was increased in patients with non-HLA a
288 signatures of innate immunity and dendritic cell activation were highly associated with protection i
290 molecule that suppresses CD4(+) and CD8(+) T cell activation when expressed on antigen-presenting cel
291 Recently, they have been implicated in T cell activation, where small numbers of antigenic recept
292 gonism also increased markers of endothelial cell activation, which was partially reduced by genetic
293 , senescence, fibrosis, and hepatic stellate cell activation, which were reduced in Hdc(-/-) HFD mice
295 nderlying mechanisms by which MIA leads to T cell activation with increased IL-17a in the maternal ci
296 Cytoplasmic RNA granules are formed upon cell activation with mitogens, including stress granules
297 itive signaling modalities that control mast cell activation, with an emphasis on novel FcepsilonRI r
299 t PD-L1 may result from the high degree of T-cell activation within the highly immunogenic milieu of
300 g and balancing the requirement for cortical cell activation without uncontrolled cell proliferation.
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