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1 of the antigenic landscape of the overall T cell response.
2 t points of intervention for modifying the T cell response.
3 icantly higher EBOV-specific CD8+ and CD4+ T-cell response.
4 thy blood donors with a predominantly CD4+ T cell response.
5 ) that mediated immune escape by impairing T cell response.
6 aggregates on DCs and consequently on the T cell response.
7 ns and challenging mice at the peak of the T cell response.
8 g orientations and the ability to induce a T-cell response.
9 onds to immunosuppression of an Ag-induced T cell response.
10 ions that are normally restrained by a T(H)1 cell response.
11 te immune responses and adaptive cytotoxic T cell responses.
12 an be attributed to defective Th1 and CD8+ T cell responses.
13 nation approach to activate tumor-specific T cell responses.
14 ignaling is required for optimal adaptive NK cell responses.
15 nkara vector to induce HBV-specific B- and T-cell responses.
16 pe V2 loop and of envelope-specific CD4(+) T cell responses.
17 actively suppressing de novo alloreactive B cell responses.
18 the elicitation of antibody and cytotoxic T cell responses.
19 feration, bacterial cell physiology and host cell responses.
20 ayed kinetics and induce suboptimal CD8(+) T cell responses.
21 nducing potent cytotoxic CD4(+) and CD8(+) T cell responses.
22 ey determinant of Ag specificity in CD8(+) T cell responses.
23 n and dysregulated T follicular helper and B cell responses.
24 nsive macrophage population, and activated T cell responses.
25 sponses and low or undetectable Th2 or CD8 T-cell responses.
26 o co-evolution between the virus and human B cell responses.
27 h induction of neutralizing antibodies and T cell responses.
28 erating potent tumor antigen-specific CD8+ T cell responses.
29 human T helper type 1 (Th1) and cytotoxic T cell responses.
30 timulatory molecules that promote improved T cell responses.
31 targeting CD169(+) DCs to drive antitumor T cell responses.
32 aracterized by poor LASV-specific effector T-cell responses.
33 ation of memory B cell and long-lived plasma cell responses.
34 es in vaccine cells which activate de novo T cell responses.
35 frequency of Ebola GP-specific CD4 and CD8 T cell responses.
36 f circulating Tregs and reduced anti-donor T cell responses.
37 er of differentiation 8-positive (CD8(+) ) T-cell responses.
38 eal the mechanisms by which PD-1 regulates T cell responses.
39 t which BAFF-producing cells contribute to B cell responses.
40 robiome shifts and enhanced intestinal CD8 T cell responses.
41 abled us to closely monitor and quantitate T cell responses.
42 licit broadly protective CD4(+) and CD8(+) T cell responses.
43 is associated with enhanced HIV-1-specific T cell responses.
44 lls and the induction of protective CD8(+) T cell responses.
45 road induction of FSP-specific CD8 and CD4 T-cell responses.
46 d "classical" low-dimensional hexagonal grid cell responses.
47 cosal and systemic antibodies and systemic T-cell responses.
48 lar metabolism is essential for effective NK cells responses.
49 anscriptional control, facilitate optimal NK cells responses.
50 nter-individual differences in T helper (Th) cell responses affect susceptibility to infectious, alle
51 fected study participants in terms of CD4+ T-cell responses after anti-CD3 stimulation (P = .19) alth
52 demonstrate that contraction of lung CD8+ T cell responses after influenza infection is contemporize
53 ynamics and specificity of germinal centre B cell responses after influenza vaccination in humans.
55 -Barr virus and influenza virus can elicit T cell responses against abnormally expressed cellular ant
58 ing and effector phases, provokes systemic T cell responses against dominant and subdominant neoantig
60 unctional and polyfunctional CD4+ and CD8+ T-cell responses against influenza A/H1N1, A/H3N2, and B.
63 nospot (ELISPOT) assay to characterize the T cell responses against peptide pools derived from the sp
64 ne was safe and elicited mutation-specific T cell responses against predicted neoepitopes not detecte
66 umoral responses, it blunted type 1 CD4(+) T cell responses against the SIV envelope protein and fail
67 oxia, clonal stem cell selection, and immune cell response, all of which have been recently shown to
68 that chronic inflammation interferes with T-cell response and macrophage function and is also detrim
71 findings indicate that poor LASV-specific T-cell responses and activation of nonspecific T cells wit
72 pitopes with the potential for stimulating T-cell responses and B-cell antibodies against LASV and al
73 ntigen valency has multifaceted effects on B cell responses and can dictate affinity thresholds and c
76 the longevity of beta cell-specific CD8(+) T cell responses and document the use of this methylation-
77 us acute viral infections and identify CD8 T cell responses and downstream anorexia as driver mechani
78 of tumour cells induced systemic cytotoxic T-cell responses and immunological memory associated with
79 uced type 1 helper T-cell (Th1)-biased CD4 T-cell responses and low or undetectable Th2 or CD8 T-cell
80 mokines involved in generation of effector T cell responses and migration of inflammatory cells to th
82 antigen presentation, enhanced anti-tumour T cell responses and reduced tumour growth in syngeneic ho
83 thin lymph nodes, we observed augmented GC B cell responses and the promotion of T(h)1 gene expressio
84 epletion also impaired allospecific memory T cell responses and thereby enhanced donor hematopoietic
85 the effects of chronic viral infection on T-cell responses and vaccination against highly pathogenic
86 ptides were shown to activate this type of T cell response, and four out of these contain class I and
87 alivary IgA concentrations and tonsillar TFH-cell responses, and a positive correlation between tonsi
88 mic and mucosal immunoglobulin A (IgA) and T cell responses, and almost entirely prevents SARS-CoV-2
89 y receptor expression, HBV-specific CD4(+) T cell responses, and augmentation by checkpoint blockade.
90 tor programmed cell death 1 (PD1) inhibits T cell responses, and blockade of this interaction has pro
91 hanistically, alphaCD40/ICB primed durable T cell responses, and efficacy required DCs and host expre
92 14G mutant(2) SARS-CoV-2 as well as CD8(+) T cell responses, and protects against SARS-CoV-2 infectio
93 s that revealed large differences in cell-by-cell responses, and, more interestingly, between alleles
94 t age-associated defects in the cDC2 and Tfh cell response are not irreversible and can be enhanced t
95 y young adults that VZV-specific B and CD4 T cell responses are detectable in bone marrow (BM) and bl
102 Chen et al. revealed that initial CD4+ T cell responses are similar during early infection and th
103 ive and induced SARS-CoV-2-specific CD8(+) T cell responses as potentially important determinants of
105 n of MHC-II and CD86, and induced a memory T-cell response, attenuating tumor onset and growth after
106 ited cross-reactivity for both CD4 and CD8 T cell responses between flaviviruses and have implication
107 d to measure the frequency of EBV-specific T-cell responses between groups following stimulation with
108 assay to investigate a wide array of single-cell responses (beyond ROS) upon exposure to different t
111 nation had higher baseline MA-specific CD8 T cell responses but no evidence for improved functional r
112 hifted the translation component of Purkinje cell responses, but did not affect the tilt component.
113 ting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC
114 e main targets of the Lassa virus-specific T cell responses, but, to date, only a few T cell epitopes
115 extrinsic downregulation of the antiviral NK cell response by adrenergic neuroendocrine signals.
116 at ACh can modulate population-level granule cell responses by altering the ratios of excitation and
119 e of these fundamental factors that affect B cell responses can inform current vaccine design efforts
122 tional capacity of peptide-specific CD4(+) T-cell responses characterized after vaccination, are comp
124 ely associated with H3.3K27M-reactive CD8+ T cell responses.CONCLUSIONAdministration of the H3.3K27M-
127 r inhibition of bacterial antigen-specific T cell responses does not alter the efficacy of BCG-induce
129 interventions enhanced SIV-specific CD8(+) T cell responses during ART or viral control after ART int
130 gests that dysfunctional natural killer (NK) cell responses during hepatitis C virus (HCV) infection
131 of HLA-B*57:01 on the deterioration of CD8 T-cell responses during HIV infection in the absence of an
132 ing and induced SARS-CoV-2-specific CD8(+) T cell responses during the natural course of SARS-CoV-2 i
133 emonstrated that SYIPSAEKI-specific CD8(+) T cell responses elicited by viral-vectored CSP-expressing
134 vaccine therapies that could mount robust T cell responses, enhance tumor killing, and provide clini
137 ich HCV infection modulates donor-specific T cell responses following LT and the influence of HCV era
138 only, implying the importance of cytotoxic T-cell responses for the former and CD4(+) T-cell helper r
140 s well as antigen-specific CD8+ T-cell and B-cell responses from peripheral blood mononuclear cells u
141 with INO-4800 we measure antigen-specific T cell responses, functional antibodies which neutralize t
142 ur results illustrate the heterogeneity of T cell responses, furthering our understanding of inflamma
143 Foxp3-Cre Ptenfl/fl mice with augmented Tfr cell responses had markedly higher levels of peanut-spec
147 tabolic pathways that underly normal human T cell responses have taught us that there is still much t
148 4(+) Th1 responses predominate over CD8(+) T cell responses, have a more inflammatory profile, and ha
149 des crucial co-stimulatory signals for CD4 T cell responses, however the precise cellular interaction
150 ught to discover what underpins the poor Tfh cell response in ageing and whether it is possible to co
154 s required in T cells for a protective T(H)2 cell response in mice infected with the helminth Heligmo
155 racteristics of the peanut-specific CD4(+) T-cell response in peanut-allergic patients that correlate
156 epitopes induced a robust antiviral CD4(+) T cell response in the cornea that was associated with pro
157 e investigated EBOV-specific CD8+ and CD4+ T-cell responses in 37 Sierra Leonean EBOV disease survivo
158 ound three novel peptides that induced CD8 T cell responses in at least two Mamu-A1*001-positive anim
159 tially more antigen-responsive CD4 and CD8 T cell responses in blood, spleen, bronchoalveolar lavage
161 lysis further suggests a role for specific T cell responses in hereditary versus idiopathic CP pathog
162 ART significantly reduced HIV-specific T-cell responses in HIV controllers but did not adversely
163 xpression and roles as checkpoints in immune cell responses in human diseases such as cancer, asthma,
166 ification of dominant Lassa virus-specific T cell responses in Lassa fever survivors and vaccinated i
167 th infections are known to influence T and B cell responses in latent tuberculosis infection (LTBI).
172 re effective in restoring exhausted CD8(+) T cell responses in persistent viral infections or tumors.
175 sufficient for the induction of acute T(H)2-cell responses in the lungs that is independent of dendr
177 f specificity and dynamics of RSV-specific T-cell responses in the target organ, allowing the precise
178 ion implicates Yap as a mediator of global T-cell responses in the tumor microenvironment and as a ne
179 aches aimed at resolving detrimental myeloid cell responses in tissues, including those occurring in
180 henotypic landscape of SARS-CoV-2-specific T cell responses in unexposed individuals, exposed family
181 VA-NP+M1 elicits a substantial M1-specific T-cell response, including TRM cells, in nasopharynx-assoc
184 strate that the CoV-2-specific CD4+ T helper cell response is directed against all 3 proteins with co
185 ion, a highly frequent class I allele, the T cell response is dominated by an epitope spanning residu
190 ponsive host gene expression, HIV-specific T cell responses, low-level HIV viremia, rca-RNA, and the
191 e important information relating to normal B cell responses, malignant B cell expansion, and generic
195 Prior to immunotherapy, mite-induced Th-cell response networks involved multiple discrete co-exp
198 reases in pathogen-specific functional CD4 T-cell responses on ART, and early decreases in lung funct
202 the ChAdOx1 nCoV-19 group, spike-specific T-cell responses peaked on day 14 (median 856 spot-forming
203 H-2D(b) on CD11c(+) APCs mitigates the CD8 T cell response, preventing early viral clearance and immu
205 We profiled genome-wide allergen-induced Th-cell responses prospectively during 24 months subcutaneo
206 able to activate tumor neoantigen-specific T cell responses, providing a potent, individual tumor-spe
208 ntiviral responses and SARS-CoV-2-specific T cell responses remained similar between the two groups.
212 )TNFalpha(+) and IFNgamma(+) IL2(+) CD4(+) T cell responses respectively, in comparison to 33% and 13
213 he CNS is cleared in C57BL/6 mice by a CD8 T cell response restricted by the MHC class I molecule H-2
215 ture assay was also used to analyze memory T cell responses.RESULTSWe found responses to the spike pr
216 tween them, polyfunctional gE-specific CD4 T-cell responses, safety, and confirmed HZ cases were asse
217 c model of TCR signaling in which multiple T cell responses share a common rate-limiting threshold an
218 Current immunotherapies involving CD8+ T cell responses show remarkable promise, but their effica
220 57:01-restricted, HIV epitope-specific CD8 T-cell responses showed beneficial functional patterns and
221 y directed and functionally replete memory T cell responses, suggesting that natural exposure or infe
223 sults in a CXCR5+ CCR7+ Tfh/central memory T cell response that persists well after parasite clearanc
224 CSP has been shown to induce robust CD8(+) T cell responses that are capable of eliminating developin
226 phagy is recognized as one component of host cell responses that has an essential role in innate and
228 We performed detailed characterization of B cell responses through high-dimensional flow cytometry t
229 idin (SA-PDL1) that inhibited the T effector cell response to alloantigens and converted T convention
232 ide the first glimpse of the overall human T cell response to HPV in a clinical setting and offer gro
233 l function, but the complexities of the stem cell response to increases in damaged or aggregated prot
236 sequence diversity, the ability of the CD8 T-cell response to recognize several variants of a single
241 play partially redundant roles to restrain B cell responses to antigen in the absence of co-stimulati
243 on also reported Notch signaling in CD8(+) T cell responses to dendritic cell immunization, Listeria
244 s of M.tb infection and BCG vaccination on B cell responses to heterologous pathogen recall antigens.
245 r a bystander effect leading to additional T cell responses to nonviral tumor-associated antigens thr
246 performed high-throughput analysis of single-cell responses to odor blends using Swept Confocally Ali
247 pe 1 diabetes is characterized by effector T-cell responses to pancreatic beta-cell-derived peptides
248 Epitope density has a profound impact on B cell responses to particulate Ags, the molecular mechani
250 nce prevents autoimmunity, but also limits T cell responses to potentially immunodominant tumor epito
251 ers with T1D had reduced cord blood CD4(+) T-cell responses to proinsulin and insulin, a reduction in
252 T cells, and improved regulation of CD4(+) T cell responses to proinsulin at 9 months of age, as comp
254 ed HLA-B*57:01-restricted HIV-specific CD8 T-cell responses to responses restricted by other HLA clas
256 tudies have highlighted various aspects of T cell responses to SARS-CoV-2 infection that are starting
257 to develop vaccines that can also mediate T-cell responses to SARS-CoV-2 to limit severity of infect
261 es of hospitalization and decreased memory T-cell responses to tetanus vaccine were associated with H
262 en focused on HCoV-NL63 and detected broad T cell responses to the spike protein and identified 22 ta
263 ling alterations that could influence cancer cell responses to the tumor mechanical microenvironment
266 etabolomics and genetics to characterize the cells' response to acute glucose depletion and identify
271 es to wild-type mice, suggesting that this B cell response was independent of cognate T cell help.
273 is, the ability of VISTA to restrain naive T cell responses was lost under inflammatory conditions.
281 ent cohorts showed that alpha-syn-specific T cell responses were highest shortly after diagnosis of m
283 cited influenza-specific CD4(+) and CD8(+) T-cell responses were measured using flow cytometry and in
284 novo neoantigen-specific CD4(+) and CD8(+) T cell responses were observed post-vaccination in all of
285 eadth and overall strength of HPV-specific T cell responses were significantly higher before the comm
287 5 enhanced splenic and vaginal Ag-specific T cell responses whereas CCL28 increased the levels of spe
288 ts in the medOB decreased the reticulospinal cell responses whereas the D2 receptor antagonist raclop
289 a high titer of neutralizing Abs but poor T cell responses, whereas Aer induced powerful respiratory
290 ht of 'protective' or 'detrimental' CD8(+) T cell responses which are restricted by the host HLA clas
291 from a single construct to achieve enhanced cell response while maintaining cellular heterogeneity d
292 chanisms through which NHERF1 modulates mast cell responses will lend insights into the development o
293 e range, multifunctional CD8(+) and CD4(+) T cell responses with S protein-specific killing activity
294 tested for their effect on the size of the T cell response, with a>=50% loss defined as an escape mut
295 CD2 downregulation may attenuate antitumor T cell responses, with implications for checkpoint immunot
297 -valency antigens induced smaller effector B cell responses, with preferential recruitment of high-af
298 s to the development of a strong anti-ZIKV T-cell response without eliciting significant anti-ZIKV an
299 B*52:01-restricted p24 Gag-specific CD8(+) T-cell response without incurring a significant loss to vi
300 ble of dissecting physiologically relevant B cell responses without the use of an engineered BCR.