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1 genetic alteration of Ag-experienced memory CD8 T cells.
2 ted to the activation of IFN-gamma-producing CD8 T cells.
3 cing plasma cells, and activation of CD4 and CD8 T cells.
4 of the ECM and an increased infiltration of CD8+ T cells.
5 ectively mediated by virus-specific CD4+ and CD8+ T cells.
6 n injected GBMs and an increase in IFNgamma+ CD8+ T cells.
7 e regulatory mechanisms mediated by CD4+ and CD8+ T cells.
8 companied by increased tumor infiltration of CD8(+) T cells.
9 antigen presentation and recruit innate-like CD8(+) T cells.
10 because of dampened activation of cytotoxic CD8(+) T cells.
11 supports residence of hypertension-specific CD8(+) T cells.
12 ated with the abundance of effector HLA-DR(+)CD8(+) T cells.
13 tes, with a particular focus on NK cells and CD8(+) T cells.
14 CR signaling in senescent-like CD27(-)CD28(-)CD8(+) T cells.
15 cytokine production in allogeneic CD4(+) and CD8(+) T cells.
16 apoptosis in Fcgr2b(+), but not Fcgr2b(-/-), CD8(+) T cells.
17 ect tumors in high proportions, dependent on CD8(+) T cells.
18 o CD4(+) T cells, whilst Granzyme B/TIA-1 to CD8(+) T cells.
19 inase domain to mediate mTORC1 activation in CD8(+) T cells.
20 cells, which improves anti-tumor efficacy of CD8(+) T cells.
21 mitochondrial-biogenesis in activated mouse CD8(+) T cells.
22 -restricted peptides targeted by circulating CD8(+) T cells.
23 abeta repertoire diversity of virus-specific CD8(+) T cells.
24 st cancer patients, also increases cytotoxic CD8(+) T cells.
25 agnitude of NFAT1 activation in single mouse CD8(+) T cells.
26 presenting cells relate to the activation of CD8(+) T-cells.
28 merging as a central player in physiology of CD8(+) T cells, acting as a barrier to prevent premature
29 ame effect on memory responses by CD4(+) and CD8(+) T cells activated after transplantation has not b
30 neural and adipose cells and how it promotes CD8 T cell activation, as well as epithelial repair.
31 Neutrophilia and higher levels of CD4 and CD8 T-cell activation were found in CDC patients as well
32 n type I and III responses, early CD4(+) and CD8(+) T cell activation, and counterregulation by the c
34 lear cells revealed an increase in activated CD8+ T cells after CYD-TDV vaccination, a phenomenon tha
35 threshold and a conceptually simple model of CD8(+) T cell Ag recognition, in which Ag dose and affin
36 1c(+) APCs are critical for early priming of CD8 T cells against the immunodominant TMEV peptide VP2(
37 d bladder tumor elimination requires CD4 and CD8 T cells, although augmentation or inhibition of bact
38 reveals prominent interactions of exhausted CD8 + T-cells and PD-L1 + macrophages and PD-L1 + tumor
39 d Akt-dependent nuclear trafficking in mouse CD8 T cells and augmented the expression of canonical Fo
40 o1) was largely excluded from the nucleus of CD8 T cells and failed to transactivate these genes.
42 ted in an increased number of central memory CD8(+) T cells and diabetes protection by central memory
43 n processing and priming for both CD4(+) and CD8(+) T cells and of the direct orchestration of their
44 al unique molecular signatures of protective CD8(+) T cells and pave the way for T-cell-based immunot
45 ablation of Dot1L resulted in loss of naive CD8(+) T cells and premature differentiation toward a me
47 , led to exhaustion of anti-male tetramer(+) CD8(+) T cells and subsequently the acceptance of skin g
48 e therapy, CRTH2-expressing ILC2, CD4(+) and CD8(+) T cells and Treg cells showed attenuated response
49 an anergic T-bet(-)IFN-gamma(-) phenotype in CD8(+) T cells and was equally suppressive compared to P
50 acteristics comparable to influenza-specific CD8(+) T cells and were detectable in SARS-CoV-2 convale
51 adverse outcome was correlated with elevated CD8+ T cell and reduced granulocytic cell proportions.
52 sed 5-hydroxymethylcytosine (5hmC) levels of CD8+ T cells and enhanced their cytotoxic activity in a
53 icantly increase the population of cytotoxic CD8+ T cells and simultaneously decrease the population
54 planation is that coordinated CD4(+) T cell, CD8(+) T cell, and antibody responses are protective, bu
55 d to license the cytotoxic activity of tumor CD8(+) T cells, and in their absence, T cells did not ly
60 pre-existing and induced SARS-CoV-2-specific CD8(+) T cells, applying peptide-loaded major histocompa
62 epletion studies revealed that both cDC1 and CD8(+) T cells are required for tumor regression followi
63 text optimal for generating antigen-specific CD8 T cells, as they have natural tropism for dendritic
65 r rationale for renewed efforts to develop a CD8(+) T cell-based HIV vaccine in conjunction with B ce
66 reductionist system, in which primary human CD8(+) T cell blasts are stimulated by recombinant pepti
69 restore cancer- and virus-induced exhausted CD8(+) T cells, by enhancing the quality and survival of
71 evidence that cellular immunity mediated by CD8(+) T cells can sustain long-term disease-free and tr
72 imilar rapid, early response in EM and TEMRA CD8(+) T cells, CD16 engagement resulted in selective ac
73 ets of gamma-delta T cells (CD3(+)TCRgd(+)), CD8(+) T cells (CD3(+)CD8(+)CD161(+)PD1(+)), and memory
75 substantial population of 'memory-phenotype' CD8(+) T cells (CD8-MP cells) that exhibit hallmarks of
76 In an HIV-1 latency model using autologous CD8(+) T cell clones as biosensors of antigen presentati
77 n from abacavir/abacavir analogue-responsive CD8(+) T-cell clones was measured using IFN-gamma ELIspo
80 indings demonstrate that STAT1 signaling and CD8 T cells concomitantly act to mitigate MuPyV-encephal
81 that CD8(+) T cells express all 19 Wnts and CD8(+) T cell-conditioned medium (CM) induced canonical
82 ific T cell receptors (TCRs) transduced into CD8+ T cells conferred antileukemic activity in vitro.
83 of memory CD4(+) T cells were reduced, while CD8(+) T cells consisted predominately of expanded diffe
84 36 or M36, exhibit greater susceptibility to CD8 T cell control than mutants lacking the set of immun
85 d from several mumps cases, and MuV-specific CD8+ T cells could be identified by peptide/dextramer st
87 A class I autoantigen epitopes implicated in CD8 T cell (CTL)-mediated beta-cell destruction in type
88 that the histone deacetylase HDAC3 inhibits CD8 T cell cytotoxicity early during activation and is r
89 NOD-LNSC significantly reduced G9Calpha(-/-)CD8(+) T-cell cytotoxicity and dendritic cell-induced pr
91 ased, naive B cells increased, and senescent CD8 T cells decreased (human cells); effects were genera
92 ith patients with low SDom and low CD3(+) or CD8(+) T-cell density (P = 0.002 and P = 0.03, respectiv
93 ients with both high SDom and high CD3(+) or CD8(+) T-cell density had markedly improved disease-spec
94 FTY720 and BAF312 caused a profound CD4+ and CD8+ T cell depletion in blood and lungs but only treatm
95 ng chronic infection generated new antiviral CD8 T cells, despite sustained virus replication in the
96 oxic marker expression by mucosal CD4(+) and CD8(+) T cells differed according to the mucosal compart
100 Here, we discuss recent insights into memory CD8(+) T cell differentiation and exhaustion and the ass
103 inal intraepithelial CD8(+) T-cell lines, or CD8(+) T cells directly isolated from intestinal biopsie
107 ly expressed on highly functional ganglionic CD8(+) T cells during acute and latent HSV-1 infection.
109 lly, TCR signal strength is able to regulate CD8(+) T cell effector cytokine R production independent
110 athway in which exhausted or "dysfunctional" CD8+ T cells enhance cellular adhesiveness to maintain t
118 e terminally differentiated dysfunctional UC CD8(+) T cells expressing IL-26, which attenuate acute c
119 There was no increase in tumor infiltrating CD8+ T cells expressing "exhaustion" markers, yet oHSV i
120 vels return to near baseline, LSD1-deficient CD8 T cells failed to remethylate the Pdcd1 locus to the
121 ver, by mapping the long-term development of CD8(+) T cell families derived from single naive precurs
122 and is required for persistence of activated CD8 T cells following resolution of an acute infection.
123 Zr-IAB22M2C, a radiolabeled minibody against CD8+ T cells, for targeted imaging of CD8+ T cells in pa
125 ailable transcriptomes and DNA methylomes of CD8(+) T cells from 3 adult patient cohorts with and wit
126 how restricted growth of B16-F10 tumors, and CD8(+) T cells from these mice express less PD-1 and TOX
130 , we found that Tim-3 (often associated with CD8(+) T cell functional exhaustion) is not upregulated
132 ceptor 2 (TGFBR2) in CD4(+) T cells, but not CD8(+) T cells, halts cancer progression as a result of
134 ve transfer of ex vivo expanded CMV-specific CD8+ T cells has provided proof-of-concept that immunoth
138 hus, immunomodulatory therapies that improve CD8(+) T cell immune surveillance and clearance of CHIKV
140 for dendritic cells, preeminent inducers of CD8 T cell immunity; elicit Th1-promoting inflammation;
145 tion of highly differentiated virus-specific CD8(+) T cells in an Ag-dependent manner, a phenomenon k
146 here is a protective role for central memory CD8(+) T cells in autoimmune diabetes and that this prot
147 compiled an unbiased atlas of human colonic CD8(+) T cells in health and ulcerative colitis (UC) usi
150 , we have uncovered the diverse landscape of CD8(+) T cells in psoriatic and healthy skin, including
152 ntly expands the proportion of proliferating CD8(+) T cells in the tumor with enhanced cytolytic pote
154 of susceptibility/severity; (2) RSV-specific CD8+ T cells in bronchoalveolar lavage fluid preinfectio
158 t oHSV infection led to a reduction in PD-1+ CD8+ T cells in injected GBMs and an increase in IFNgamm
161 igen, R848, and PUUC increased percentage of CD8+ T-cells in the lungs, percentage of antigen-specifi
162 rete lineages of intestinal antigen-specific CD8(+) T cells, including a Blimp1(hi)Id3(lo) tissue-res
163 Immunohistochemistry confirmed enhanced CD8(+) T cell infiltration and accumulation by R848-TSLs
164 urden and neoantigen load) and the degree of CD8(+) T cell infiltration were not associated with clin
166 uiescent phenotype and promoted intratumoral CD8(+) T-cell infiltration, overcoming the exclusion eff
171 e PD-1/PD-L1 pathway reinvigorates exhausted CD8(+) T cells, it fails to restore T cell repertoire di
174 timulated primary intestinal intraepithelial CD8(+) T-cell lines, or CD8(+) T cells directly isolated
177 Treatment-induced changes in intratumoral CD8(+) T cells may represent a biomarker to identify pat
182 hat are essential for cross-presentation and CD8 T cell-mediated immunity against intracellular patho
188 cination directly correlates with downstream CD8(+) T cell memory and protective immunity against inf
189 us, aberrant activation and dysregulation of CD8+ T cells occur in patients with severe COVID-19 dise
191 these pDCexos primed naive antigen-specific CD8 T cells only in the presence of bystander cDCs, simi
192 adoptive transfer of virus-specific effector CD8(+) T cells or immunization with a vaccine that induc
194 s dual system of peptide generation enhances CD8(+) T cell participation in diversifying both antigen
195 Regenerative stem cell-like memory (T(SCM)) CD8(+) T cells persist longer and produce stronger effec
196 sure created an environment that altered the CD8+ T cell phenotype, for example expression of regulat
200 lungs, with a depleted and exhausted CD4 and CD8 T-cell population that resides within a heavily hype
201 early effects on the phenotype of the total CD8 T-cell population were apparent only in HLA-B*57-neg
202 uction in mean tumor volume, increase in the CD8 T-cell population, and immune activated gene signali
203 thus possible to visualize antigen-specific CD8(+) T-cell populations in vivo, which may serve progn
204 show accumulation of activated ZIKV-specific CD8(+) T cells primed by recombinant L. monocytogenes is
205 vaccine that induces virus-specific effector CD8(+) T cells prior to infection enhanced the clearance
206 at all antileishmanial drugs inhibit CD4 and CD8 T cell proliferation at the doses that are not relat
210 currently understood to focus on deflecting CD8 T cell recognition of infected cells by disrupting a
211 , we investigated whether naive MBP-specific CD8+ T cells recruited to the CNS during CD4+ T cell-ini
212 Congruently, gene editing of LAYN in human CD8+ T cells reduced direct tumor cell killing ex vivo.
214 ar TCRs were identified in EBV(RPP)-specific CD8(+) T cell repertoires across multiple HLA-B7(+) indi
215 In conclusion, we show that MEKi leads to CD8(+) T cell reprogramming into T(SCM) that acts as a r
218 n of the CNS is cleared in C57BL/6 mice by a CD8 T cell response restricted by the MHC class I molecu
219 ss of H-2D(b) on CD11c(+) APCs mitigates the CD8 T cell response, preventing early viral clearance an
220 vast sequence diversity, the ability of the CD8 T-cell response to recognize several variants of a s
222 c versus acute viral infections and identify CD8 T cell responses and downstream anorexia as driver m
223 vaccination had higher baseline MA-specific CD8 T cell responses but no evidence for improved functi
226 uence of HLA-B*57:01 on the deterioration of CD8 T-cell responses during HIV infection in the absence
228 HLA-B*57:01-restricted, HIV epitope-specific CD8 T-cell responses showed beneficial functional patter
229 compared HLA-B*57:01-restricted HIV-specific CD8 T-cell responses to responses restricted by other HL
231 oss-reactive and induced SARS-CoV-2-specific CD8(+) T cell responses as potentially important determi
232 pre-existing and induced SARS-CoV-2-specific CD8(+) T cell responses during the natural course of SAR
233 ore, we demonstrated that SYIPSAEKI-specific CD8(+) T cell responses elicited by viral-vectored CSP-e
234 ibitors are effective in restoring exhausted CD8(+) T cell responses in persistent viral infections o
235 arge but transient boost of the SIV-specific CD8(+) T cell responses occurred in IL-2-DT-treated RMs.
237 n the light of 'protective' or 'detrimental' CD8(+) T cell responses which are restricted by the host
238 4) and D614G mutant(2) SARS-CoV-2 as well as CD8(+) T cell responses, and protects against SARS-CoV-2
243 ction-elicited influenza-specific CD4(+) and CD8(+) T-cell responses were measured using flow cytomet
244 Here we demonstrate that contraction of lung CD8+ T cell responses after influenza infection is conte
248 ) model, Tregs are known to inhibit effector CD8+ T-cell responses and contribute to virus persistenc
250 ce of STAT1 signaling, however, depletion of CD8 T cells resulted in lytic infection of the choroid p
251 in vitro activation of both mouse and human CD8(+) T cells resulted in an increased number of centra
253 teomics analysis on cytokine-producing fixed CD8(+) T cells revealed that IL-2(+) cells produce helpe
255 scriptome, phenotype, and function of memory CD8(+) T cells, sharing the same HSV-1 epitope-specifici
258 ddition, treatment expanded a CXCR3+PD1-/low CD8 T-cell subset with the ability to secrete cytokines.
259 nd their association with antiviral effector CD8+ T cell subsets were also characterized in lung infi
260 rging data indicate that SARS-CoV-2-specific CD8(+) T cells targeting different viral proteins are de
261 s, NKT, MAIT, TCR-gammadelta, Monocytes, and CD8 + T-cells that are related to both gene activation a
262 ganglia (TG) is influenced by virus-specific CD8(+) T cells that infiltrate the ganglia at the onset
263 rus-specific T cells comprised both CD4+ and CD8+ T cells that expressed markers for central memory a
264 Contrary to the established role of CD69 on CD8 T cells, the functions of CD103 and CD49a on this po
265 umour cells disrupt methionine metabolism in CD8(+) T cells, thereby lowering intracellular levels of
266 onferred this compromised metabolic state to CD8(+) T cells, thereby paralyzing their effector functi
268 c potential is restored, thereby sensitizing CD8 T cells to DEX-induced apoptosis in vitro and signif
269 ore antigen-specific multifunctional CD4 and CD8 T cells to the lung parenchyma prior to challenge an
270 adapts the CRISPR/Cas9 technology for memory CD8 T cells to undertake gene editing in vivo, for the f
271 Cs induced proliferation of naive CD4(+) and CD8(+) T cells to a larger extent than B. burgdorferi.
273 is contemporized with egress of CD69+/CD103+ CD8+ T cells to the draining mediastinal LN via the lymp
274 antigen-specific progeny of individual naive CD8+ T cells to the T effector (TEFF), T circulating mem
275 , B, and NK cells and exhibited a skewing of CD8+ T cells toward a terminally differentiated/senescen
276 ces an influx of stem-like Tcf1(+) Slamf6(+) CD8(+) T cells, triggers regression not only of primary,
279 ors expressing HBV Ags engender HBV-specific CD8(+) T cells unconventionally restricted by MHC class
281 up has demonstrated that CNS myelin-specific CD8 T cells unexpectedly harbor immune regulatory capaci
282 nstrate this by functionally altering memory CD8 T cells using CRISPR/Cas9-mediated targeted gene dis
283 geted mutations can be introduced into naive CD8(+) T cells using CRISPR-based homology-directed repa
285 lthough some Ags were detected by CD4(+) and CD8(+) T cells, VME1 was mainly recognized by CD4(+) T c
286 cells were reduced, while the proportion of CD8(+) T cells was significantly increased in both tumor
288 interventional study, BKPyV-specific CD4 and CD8 T cells were measured in 32 of 36 viremic pediatric
291 had fewer neutrophils, while their cytotoxic CD8(+) T cells were activated, reflected as higher HLA-D
292 pecific poly-functional/cytotoxic CD4(+) and CD8(+) T cells were detected with the IL-4R antagonist a
293 en, and bone marrow, as well as expansion of CD8 T cells, which has been observed in CD4-depleted hum
294 nt resulted in selective activation of TEMRA CD8(+) T cells, which mediated antibody-dependent cytoto
295 arget cell killing by freshly isolated human CD8(+) T cells, which represent a challenging but valuab
296 iated with cerebrovascular engagement of CD3+CD8+ T cells, which is exacerbated by HIV coinfection.
297 XCR3 is upregulated in the expanded synovial CD8 T cells, while two CXCR3 ligands, CXCL9 and CXCL10,
301 , IL-17, and IL-22 cytokine levels in CD4(+)/CD8(+) T cells, with inducible costimulator molecule and