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1 ent points of intervention for modifying the T cell response.
2 althy blood donors with a predominantly CD4+ T cell response.
3 Cs) that mediated immune escape by impairing T cell response.
4 of aggregates on DCs and consequently on the T cell response.
5 gens and challenging mice at the peak of the T cell response.
6 tibility complex (MHC) class I-primed CD8(+) T cell response.
7 le for the induction of a virus-specific CD8 T cell response.
8 physical restoration of the antigen-specific T cell response.
9 f antigen-specific models to interrogate the T cell response.
10 sponds to immunosuppression of an Ag-induced T cell response.
11 ng of the antigenic landscape of the overall T cell response.
12 ificantly higher EBOV-specific CD8+ and CD4+ T-cell response.
13 and subsequent hyperactivation of the CD8(+) T-cell response.
14 turation and subsequently reduced allogeneic T-cell response.
15 ing orientations and the ability to induce a T-cell response.
16 nate immune responses and adaptive cytotoxic T cell responses.
17 elayed kinetics and induce suboptimal CD8(+) T cell responses.
18 inducing potent cytotoxic CD4(+) and CD8(+) T cell responses.
19 key determinant of Ag specificity in CD8(+) T cell responses.
20 ponsive macrophage population, and activated T cell responses.
21 ith induction of neutralizing antibodies and T cell responses.
22 enerating potent tumor antigen-specific CD8+ T cell responses.
23 to human T helper type 1 (Th1) and cytotoxic T cell responses.
24 ostimulatory molecules that promote improved T cell responses.
25 rm targeting CD169(+) DCs to drive antitumor T cell responses.
26 opes in vaccine cells which activate de novo T cell responses.
27 e frequency of Ebola GP-specific CD4 and CD8 T cell responses.
28 of circulating Tregs and reduced anti-donor T cell responses.
29 eveal the mechanisms by which PD-1 regulates T cell responses.
30 al inhibitory receptor that limits excessive T cell responses.
31 dritic cells can enhance induction of Ab and T cell responses.
32 l features involved in the generation of CD8 T cell responses.
33 y promoting rather than terminating effector T cell responses.
34 ) T cell responses predominating over CD8(+) T cell responses.
35 igs combined high Ab titers and strong local T cell responses.
36 oles in both naive T cell priming and memory T cell responses.
37 enabled us to closely monitor and quantitate T cell responses.
38 icrobiome shifts and enhanced intestinal CD8 T cell responses.
39 elicit broadly protective CD4(+) and CD8(+) T cell responses.
40 n is associated with enhanced HIV-1-specific T cell responses.
41 cells and the induction of protective CD8(+) T cell responses.
42 can be attributed to defective Th1 and CD8+ T cell responses.
43 cination approach to activate tumor-specific T cell responses.
44 lope V2 loop and of envelope-specific CD4(+) T cell responses.
45 in the elicitation of antibody and cytotoxic T cell responses.
46 Ankara vector to induce HBV-specific B- and T-cell responses.
47 responses and low or undetectable Th2 or CD8 T-cell responses.
48 characterized by poor LASV-specific effector T-cell responses.
49 ster of differentiation 8-positive (CD8(+) ) T-cell responses.
50 cytokine staining to measure HIV-1-specific T-cell responses.
51 virus and poor Lassa virus-specific effector T-cell responses.
52 C, therefore, induce qualitatively different T-cell responses.
53 ciated with a significant increase in CD4(+) T-cell responses.
54 on of innate immune factors, antibodies, and T-cell responses.
55 broad induction of FSP-specific CD8 and CD4 T-cell responses.
56 mucosal and systemic antibodies and systemic T-cell responses.
57 we demonstrate that contraction of lung CD8+ T cell responses after influenza infection is contempori
58 , we observed a dominant polyfunctional CD8+ T-cell response after natural mumps virus (MuV) infectio
59 infected study participants in terms of CD4+ T-cell responses after anti-CD3 stimulation (P = .19) al
60 in-Barr virus and influenza virus can elicit T cell responses against abnormally expressed cellular a
61 ied role of these PARPs in the modulation of T cell responses against AT-3-induced breast tumors.
63 iming and effector phases, provokes systemic T cell responses against dominant and subdominant neoant
65 e parasites can induce protective memory CD8 T cell responses against liver-stage malaria; however, w
66 munospot (ELISPOT) assay to characterize the T cell responses against peptide pools derived from the
67 cine was safe and elicited mutation-specific T cell responses against predicted neoepitopes not detec
68 humoral responses, it blunted type 1 CD4(+) T cell responses against the SIV envelope protein and fa
72 ofunctional and polyfunctional CD4+ and CD8+ T-cell responses against influenza A/H1N1, A/H3N2, and B
75 strate that cross-reactivity at the level of T cell responses among different flaviviruses is very li
76 Therefore, the magnitude of the antitumor T cell response and the corresponding downstream IFN-gam
78 o the longevity of beta cell-specific CD8(+) T cell responses and document the use of this methylatio
79 rsus acute viral infections and identify CD8 T cell responses and downstream anorexia as driver mecha
80 ine vector is not likely to generate optimal T cell responses and might thus impair vaccine performan
81 hemokines involved in generation of effector T cell responses and migration of inflammatory cells to
82 d antigen presentation, enhanced anti-tumour T cell responses and reduced tumour growth in syngeneic
83 depletion also impaired allospecific memory T cell responses and thereby enhanced donor hematopoieti
84 ed that chronic inflammation interferes with T-cell response and macrophage function and is also detr
86 ur findings indicate that poor LASV-specific T-cell responses and activation of nonspecific T cells w
87 epitopes with the potential for stimulating T-cell responses and B-cell antibodies against LASV and
88 llomavirus (HPV) E6-specific and E7-specific T-cell responses and cervical lesion regression in patie
89 el, Tregs are known to inhibit effector CD8+ T-cell responses and contribute to virus persistence.
91 s of tumour cells induced systemic cytotoxic T-cell responses and immunological memory associated wit
92 nduced type 1 helper T-cell (Th1)-biased CD4 T-cell responses and low or undetectable Th2 or CD8 T-ce
94 r, the effects of chronic viral infection on T-cell responses and vaccination against highly pathogen
95 peptides were shown to activate this type of T cell response, and four out of these contain class I a
96 temic and mucosal immunoglobulin A (IgA) and T cell responses, and almost entirely prevents SARS-CoV-
97 ory receptor expression, HBV-specific CD4(+) T cell responses, and augmentation by checkpoint blockad
98 eptor programmed cell death 1 (PD1) inhibits T cell responses, and blockade of this interaction has p
99 echanistically, alphaCD40/ICB primed durable T cell responses, and efficacy required DCs and host exp
100 D614G mutant(2) SARS-CoV-2 as well as CD8(+) T cell responses, and protects against SARS-CoV-2 infect
101 thy young adults that VZV-specific B and CD4 T cell responses are detectable in bone marrow (BM) and
108 ctive and induced SARS-CoV-2-specific CD8(+) T cell responses as potentially important determinants o
109 ines induces strong type 1 CD4(+) and CD8(+) T cell responses, as well as long-lived plasma and memor
110 ion of MHC-II and CD86, and induced a memory T-cell response, attenuating tumor onset and growth afte
111 imited cross-reactivity for both CD4 and CD8 T cell responses between flaviviruses and have implicati
112 sed to measure the frequency of EBV-specific T-cell responses between groups following stimulation wi
115 cination had higher baseline MA-specific CD8 T cell responses but no evidence for improved functional
116 the main targets of the Lassa virus-specific T cell responses, but, to date, only a few T cell epitop
120 nctional capacity of peptide-specific CD4(+) T-cell responses characterized after vaccination, are co
121 rsely associated with H3.3K27M-reactive CD8+ T cell responses.CONCLUSIONAdministration of the H3.3K27
122 we established that epitope-specific CD8(+) T cell responses contribute to parasite killing followin
126 om immunotherapy results from an exaggerated T-cell response directed against normal tissue, resultin
127 or inhibition of bacterial antigen-specific T cell responses does not alter the efficacy of BCG-indu
128 ken together, TBE vaccination induced CD4(+) T cell responses dominated by IL-2 and TNF production to
130 d interventions enhanced SIV-specific CD8(+) T cell responses during ART or viral control after ART i
132 sting and induced SARS-CoV-2-specific CD8(+) T cell responses during the natural course of SARS-CoV-2
133 e of HLA-B*57:01 on the deterioration of CD8 T-cell responses during HIV infection in the absence of
134 demonstrated that SYIPSAEKI-specific CD8(+) T cell responses elicited by viral-vectored CSP-expressi
136 al vaccine therapies that could mount robust T cell responses, enhance tumor killing, and provide cli
139 which HCV infection modulates donor-specific T cell responses following LT and the influence of HCV e
140 n only, implying the importance of cytotoxic T-cell responses for the former and CD4(+) T-cell helper
142 gs with INO-4800 we measure antigen-specific T cell responses, functional antibodies which neutralize
143 Our results illustrate the heterogeneity of T cell responses, furthering our understanding of inflam
145 metabolic pathways that underly normal human T cell responses have taught us that there is still much
148 CD4(+) Th1 responses predominate over CD8(+) T cell responses, have a more inflammatory profile, and
149 vides crucial co-stimulatory signals for CD4 T cell responses, however the precise cellular interacti
150 consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tum
151 nclude IT CMP-001 induces a robust antitumor T cell response in an anti-Qbeta Ab-dependent manner and
152 een previously demonstrated to induce CD8(+) T cell response in Chagas' disease patients, or bind HLA
153 endogenous hepatitis B virus (HBV)-specific T cell response in CHB patients have demonstrated little
154 l epitopes induced a robust antiviral CD4(+) T cell response in the cornea that was associated with p
155 d proteome-wide profiling of HPV-16-specific T cell responses in a cohort of 66 patients with HPV-ass
156 found three novel peptides that induced CD8 T cell responses in at least two Mamu-A1*001-positive an
157 antially more antigen-responsive CD4 and CD8 T cell responses in blood, spleen, bronchoalveolar lavag
159 ent cross-reactive and induced memory CD8(+) T cell responses in cross-sectionally analyzed individua
160 e study of endogenous antigen-specific naive T cell responses in disease and infection, but has been
161 nalysis further suggests a role for specific T cell responses in hereditary versus idiopathic CP path
163 ntification of dominant Lassa virus-specific T cell responses in Lassa fever survivors and vaccinated
167 a and discuss strategies to directly augment T cell responses in parallel with myeloid cell- and micr
168 reclinical models and can improve anticancer T cell responses in patients with advanced cancers.
169 are effective in restoring exhausted CD8(+) T cell responses in persistent viral infections or tumor
173 document increased HIV-1 Gag-specific CD8(+) T cell responses in the peripheral blood of all nine stu
174 phenotypic landscape of SARS-CoV-2-specific T cell responses in unexposed individuals, exposed famil
175 pes describe here are expected to elicit CD8 T cell responses in up to 87% of the population and coul
176 clearance does not improve HBV-specific CD8+ T cell responses in vivo and may have important implicat
177 influenza-specific TFH-cell (CXCR5+CD57+CD4+ T cell) responses in children, and to a lesser extent in
179 haracteristics of the peanut-specific CD4(+) T-cell response in peanut-allergic patients that correla
180 We investigated EBOV-specific CD8+ and CD4+ T-cell responses in 37 Sierra Leonean EBOV disease survi
187 of specificity and dynamics of RSV-specific T-cell responses in the target organ, allowing the preci
188 etion implicates Yap as a mediator of global T-cell responses in the tumor microenvironment and as a
189 for the optimal induction of de novo CD8(+) T-cell responses, in contrast to adjuvants that operate
190 M1 (MVA-NP+M1) to activate M1-specific CD8+ T-cell response, including TRM cells, in nasopharynx-ass
191 MVA-NP+M1 elicits a substantial M1-specific T-cell response, including TRM cells, in nasopharynx-ass
194 ction, a highly frequent class I allele, the T cell response is dominated by an epitope spanning resi
195 lass I molecules, the latent-specific CD8(+) T cell response is focused on epitopes derived from the
197 gulation of the MHC class II-mediated CD4(+) T cell response is understudied in endogenous MHC class
199 esponsive host gene expression, HIV-specific T cell responses, low-level HIV viremia, rca-RNA, and th
204 and allows for robust endogenous CD8 and CD4 T cell responses on neoantigen induction in peripheral t
206 ncreases in pathogen-specific functional CD4 T-cell responses on ART, and early decreases in lung fun
209 In the ChAdOx1 nCoV-19 group, spike-specific T-cell responses peaked on day 14 (median 856 spot-formi
210 ptide pools in most individuals, with CD4(+) T cell responses predominating over CD8(+) T cell respon
211 f H-2D(b) on CD11c(+) APCs mitigates the CD8 T cell response, preventing early viral clearance and im
213 s able to activate tumor neoantigen-specific T cell responses, providing a potent, individual tumor-s
214 he fourth vaccination) and Env-specific CD4+ T-cell response rates after the third and fourth vaccina
217 antiviral responses and SARS-CoV-2-specific T cell responses remained similar between the two groups
221 (+)TNFalpha(+) and IFNgamma(+) IL2(+) CD4(+) T cell responses respectively, in comparison to 33% and
222 the CNS is cleared in C57BL/6 mice by a CD8 T cell response restricted by the MHC class I molecule H
224 ulture assay was also used to analyze memory T cell responses.RESULTSWe found responses to the spike
225 between them, polyfunctional gE-specific CD4 T-cell responses, safety, and confirmed HZ cases were as
226 pic model of TCR signaling in which multiple T cell responses share a common rate-limiting threshold
228 B*57:01-restricted, HIV epitope-specific CD8 T-cell responses showed beneficial functional patterns a
229 teps are involved to elicit extensive memory T cell response: stimulation of naive T cells with robus
230 dly directed and functionally replete memory T cell responses, suggesting that natural exposure or in
232 results in a CXCR5+ CCR7+ Tfh/central memory T cell response that persists well after parasite cleara
233 CSP has been shown to induce robust CD8(+) T cell responses that are capable of eliminating develop
234 ation, and functionality of RHV-specific CD8 T cell responses that are essential for protection again
236 idence of complement activation and a robust T cell response, the patient developed persistent SARS-C
237 We set out to characterize the human CD4(+) T cell response throughout primary TBE immunization.
239 ovide the first glimpse of the overall human T cell response to HPV in a clinical setting and offer g
242 tion also reported Notch signaling in CD8(+) T cell responses to dendritic cell immunization, Listeri
243 We likewise consider that potent, nonclonal T cell responses to microbial superantigens may reflect
244 ger a bystander effect leading to additional T cell responses to nonviral tumor-associated antigens t
245 rance prevents autoimmunity, but also limits T cell responses to potentially immunodominant tumor epi
246 ) T cells, and improved regulation of CD4(+) T cell responses to proinsulin at 9 months of age, as co
249 studies have highlighted various aspects of T cell responses to SARS-CoV-2 infection that are starti
253 then focused on HCoV-NL63 and detected broad T cell responses to the spike protein and identified 22
255 y infected with CL13 mounted a strong CD8(+) T-cell response to ECTV-Delta036 and survived without si
257 t sequence diversity, the ability of the CD8 T-cell response to recognize several variants of a singl
261 type 1 diabetes is characterized by effector T-cell responses to pancreatic beta-cell-derived peptide
262 thers with T1D had reduced cord blood CD4(+) T-cell responses to proinsulin and insulin, a reduction
263 ared HLA-B*57:01-restricted HIV-specific CD8 T-cell responses to responses restricted by other HLA cl
264 nt to develop vaccines that can also mediate T-cell responses to SARS-CoV-2 to limit severity of infe
267 ates of hospitalization and decreased memory T-cell responses to tetanus vaccine were associated with
269 ings enhance our understanding of the CD8(+) T cell response toward a common EBV determinant in HLA-B
274 asis, the ability of VISTA to restrain naive T cell responses was lost under inflammatory conditions.
280 ndent cohorts showed that alpha-syn-specific T cell responses were highest shortly after diagnosis of
281 e novo neoantigen-specific CD4(+) and CD8(+) T cell responses were observed post-vaccination in all o
282 breadth and overall strength of HPV-specific T cell responses were significantly higher before the co
289 licited influenza-specific CD4(+) and CD8(+) T-cell responses were measured using flow cytometry and
291 L25 enhanced splenic and vaginal Ag-specific T cell responses whereas CCL28 increased the levels of s
292 ed a high titer of neutralizing Abs but poor T cell responses, whereas Aer induced powerful respirato
293 ight of 'protective' or 'detrimental' CD8(+) T cell responses which are restricted by the host HLA cl
295 ive range, multifunctional CD8(+) and CD4(+) T cell responses with S protein-specific killing activit
296 e tested for their effect on the size of the T cell response, with a>=50% loss defined as an escape m
297 CD2 downregulation may attenuate antitumor T cell responses, with implications for checkpoint immun
298 ads to the development of a strong anti-ZIKV T-cell response without eliciting significant anti-ZIKV
299 A-B*52:01-restricted p24 Gag-specific CD8(+) T-cell response without incurring a significant loss to
300 magglutinin (HA) protein resulted in anti-HA T-cell responses without the development of significant