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1 onses by presenting HLA-epitope complexes to naive T cells.
2 become a cell superbly adapted to activating naive T cells.
3 a(2+) stores that were sensitive to NAADP in naive T cells.
4 nd increased memory T cells while decreasing naive T cells.
5 ant peptides and derived preferentially from naive T cells.
6 ase UBR5, which suppressed DUBA abundance in naive T cells.
7 y of mature DCs produced IL-12 and activated naive T cells.
8 allenge to maintain the functions unique for naive T cells.
9 icipate in the immune response as peripheral naive T cells.
10 s that were indistinguishable from wild-type naive T cells.
11 ted in cocultures with heterologous neonatal naive T cells.
12 e specialized APCs with the ability to prime naive T cells.
13 ssion of CD45RA is generally associated with naive T cells.
14 elta-like ligand 4 (DLL4) amplify priming of naive T cells.
15 g link between Wnt signaling and survival of naive T cells.
16 Cs) since they are also able to prime/induce naive T cells.
17 N TCM cells in similar numbers from the same naive T cells.
18 hrough life via homeostatic proliferation of naive T cells.
19 ls, and IL-6 can induce low-level cycling of naive T cells.
20 otein tyrosine phosphatases as compared with naive T cells.
21 ional maturation to become long-lived mature naive T cells.
22 LNs, despite still resulting in the loss of naive T cells.
23 kappaB activity is shared by mouse and human naive T cells.
24 igen levels that activate these functions in naive T cells.
25 cell counts, but was related to a decline in naive T cells.
26 mory T cells and classical Th22 subsets from naive T cells.
27 Ags linked to the activating PAMP and prime naive T cells.
28 y induction of Treg properties in cocultured naive T cells.
29 erial infection to present Ag information to naive T cells.
30 ls of protein expression in Mettl3-deficient naive T cells.
31 degradation and thereby support survival of naive T cells.
32 SE = 0.59 +/- 0.21, p = .006), but not with naive T cells.
33 tile cell with a limited ability to activate naive T cells.
34 functional, and metabolic differentiation of naive T cells.
35 n the generation of Ca(2+) signals in murine naive T cells.
36 d in the final maturation of thymocytes into naive T cells.
37 rt survival and homeostatic proliferation of naive T cells.
38 mbrane domains, known as protein islands, on naive T cells.
39 des where they present processed antigens to naive T-cells.
42 zation is associated with T cell priming, as naive T cells activated in vitro were fully capable of p
48 dies have shown that hRSV infection prevents naive T-cell activation by antigen-presenting cells, the
49 t to measure the drug-specific activation of naive T cells after perturbation of PD-L1/2/PD-1 binding
51 Aging is associated with a gradual loss of naive T cells and a reciprocal increase in the proportio
52 s uncover a Fas-mediated interaction between naive T cells and antigen-experienced T cells that drive
54 ary lymphoid organs recruit large numbers of naive T cells and harbor lymphocyte subsets with opposin
55 on pathway predominantly controls priming of naive T cells and hence generation of adaptive memory ce
56 s can inhibit Th17 cell differentiation from naive T cells and IL-17 production in established Th17 c
57 esponders had higher percentages of baseline naive T cells and lower percentages of terminally differ
58 n-educated" DCs stimulated the activation of naive T cells and polarized a subset of these cells into
60 d specific to activated effector T cells, as naive T cells and regulatory T cells did not require lep
61 y APCs that effectively activate Ag-specific naive T cells and restore the responsiveness of anergic
62 in effector T cells as in their counterpart naive T cells and seemed to be equally important for the
63 e in response to lower doses of antigen than naive T cells and with reduced requirements for co-stimu
64 ith higher vs. lower CCR5 levels (memory vs. naive T cells) and in memory T cells with higher vs. low
65 transitional B cells, CD56(bright) NK cells, naive T cells, and accumulation of terminally differenti
66 high proportion of relatively HIV resistant naive T cells, and an unparalleled capacity to regenerat
68 utoimmune hemolytic anemia, the reduction in naive T cells, and poor Ab responses to vaccine in sever
69 +) T cells and includes only memory T cells; naive T cells are excluded to limit the potential for al
72 e periphery, the majority of HDAC3-deficient naive T cells are recent thymic emigrants, indicating a
74 e knockdown with RNAi is challenging because naive T cells are refractory to transduction with viral
76 ed, depleting FAP(+) FRCs causes the loss of naive T cells, B cells, and dendritic cells from LNs, an
77 es against pathogens, such that viability of naive T cells before antigen encounter is critical to pr
79 evelopment of mature, antigen-inexperienced (naive) T cells begins in the thymus and continues after
80 kingly, they had a substantial deficiency in naive T cells but an over-representation of senescent ef
83 ogether with Egr2 and 3, T-bet is induced in naive T cells by Ag stimulation, but Egr2 and 3 expressi
85 SOCE directs the metabolic reprogramming of naive T cells by regulating the expression of glucose tr
88 he biology of CD4 T cells is complex because naive T cells can differentiate into various subpopulati
89 exhaustion of the proliferative capacity of naive T cells causes a sharp decline of their effective
90 sleep greater than 8 hours), epigenetic age, naive T cell (CD8+CD45RA+CCR7+), and late differentiated
94 after the age of approximately 60 y because naive T cells collectively approach replicative senescen
96 ght on functional differentiation within the naive T cell compartment and the importance of the thymu
97 fe resulted in functional restoration of the naive T cell compartment, implicating the thymus as havi
98 nfected DCs from CD8alpha(-/-) mice, with WT naive T cells contributed to an increase in PD-1 express
100 ly distinct from their more mature but still naive T cell counterparts, because they exhibit dampened
107 t of potential new therapeutics, centered on naive T-cell depletion, interleukin-17/21 inhibition, ki
108 and the causative auto-IgM cross-reacts with naive T cells despite the lack of glycan change on T cel
109 In hosts with a replete T cell compartment, naive T cells died rapidly in the absence of Zap70 expre
111 We now understand that cGVHD is initiated by naive T cells, differentiating predominantly within high
112 RORgammat, GATA3 and others is essential for naive T cell differentiation into effector T cells.
113 s a positive regulator that is essential for naive T-cell differentiation and in vivo T-cell response
114 pectedly found that EGR2 promotes peripheral naive T-cell differentiation, with delayed T-cell recept
121 olled, and dependent on the context in which naive T cells encounter antigen, can either result in fu
122 s a growing body of evidence that the use of naive T cells enhances the efficacy of adoptive T cell t
124 secondary lymphoid environment that impaired naive T cell entry and access to key survival factors.
125 8(+) T cells, reduction in the proportion of naive T cells, evidence of T cell exhaustion and senesce
126 CRTg mice; that is, old VM, but not old true naive, T cells exhibited blunted TCR-mediated, but not I
127 irst, a small population of epitope-specific naive T cells expands by several orders of magnitude.
129 go positive selection and differentiate into naive T cells expressing a highly diverse self-MHC-restr
131 nse to IL-7 signalling in order to reprogram naive T cells for proliferation and differentiation.
132 ted loci and show the advantage of utilizing naive T cells for understanding autoimmune diseases.
134 able to find a correlation between specific naive T cell frequency and peptide solvent accessibility
138 an naive T cells, the selective depletion of naive T cells from allografts might constitute a way of
139 study shows that clinical-grade depletion of naive T cells from an allograft through the use of magne
140 yed T-cell receptor-induced proliferation in naive T cells from Egr2 conditional knockout (CKO) mice
146 b(+)CD16(+) neutrophils, and CD4(+)CD45RA(+) naive T cells from the same 125 healthy individuals.
147 response to acute viral infection, activated naive T cells give rise to effector T cells that clear t
154 Salsa6f during T cell receptor activation in naive T cells, helper Th17 T cells and regulatory T cell
155 t this molecule is an important regulator of naive T cell homeostasis and it has been linked to immun
158 reatment with IL-7/mAb complexes can restore naive T cell homeostatic proliferation in aged mice.
161 e frequency of the corresponding Ag-specific naive T cells in A2(+) and A2(-) individuals, as well as
166 are present on antigen-presenting cells and naive T cells in the AT, are known to mediate the crosst
167 ll motility suggested that the activation of naive T cells in the lymph node occurs in distinct phase
168 populations are maintained by production of naive T cells in the thymus, clonal expansion of activat
169 ipheral T-cell pool depends on production of naive T cells in the thymus; however, delivery of progen
170 s for the chemokine system in the priming of naive T cells, in cell fate decisions such as effector a
171 and resulted in a linked contraction of all naive T cells, including CD31(+)/CD4(+) putative thymic
173 c reticular cells support the maintenance of naive T cells, induce Ag-specific tolerance, and restric
175 or blockade prevented differentiation of the naive T cells into antigen-specific IL-22-secreting cell
177 tions with TGF-beta to promote conversion of naive T cells into Foxp3(+) regulatory T cells and, ther
180 e found that MR regulates differentiation of naive T cells into T-helper type 17 (Th17) effector cell
185 Apc-deficient T cells, we found that loss of naive T cells is due to T cell intrinsic dysregulation o
187 ma, indicating that the continual priming of naive T cells is not required for vitiligo or its associ
188 ason for the pulse of IFN-gamma synthesis by naive T cells is uncertain, but the lack of antiviral im
189 Although memory cells are the progeny of naive T cells, it is unclear that all naive cells from a
190 mmune-related effector gene promoters within naive T cells lacked the permissive H3K4me3 modification
191 in vivo partially restored the abundance of naive T cells, largely 'rescued' the in vitro T cell def
192 products-mediated epigenetic modification of naive T cells leading to p38 MAPK-dependent chromatin de
193 unction of the memory differentiation state (naive T cells < central memory T cells < effector memory
194 + effector memory T cells that reexpress the naive T cell marker CD45RA have many characteristics of
197 EBV-related T-cell expansions do not impair naive T-cell numbers or maintenance of protective respon
198 the coreceptor from CCR5 to CXCR4 to infect naive T cells or adapting to the use of low levels of CD
200 ut not long sleep, was associated with fewer naive T cells (p < .005) and neither was related to late
201 is, where IL-6R expression was suppressed in naive T cells, paralleled by a significant reduction of
202 ion, antigen presentation, and activation of naive T cells, pathogenesis lessons that may be informat
204 tenance of immunotherapy-specific memory and naive T-cell phenotypes as early as 3 mo into immunother
205 rmed that the Treg-DC-mediated skewed CD4(+) naive T cell polarization resulted from decreased IL-12
206 nt novel evidence that Treg-DC skewed CD4(+) naive T cell polarization toward a regulatory phenotype
207 mory T cell populations showed that even the naive T cell pool contained self-reactive T cell precurs
209 n of LIP ensures the generation of a diverse naive T cell pool in lymphopenic neonates that is mandat
210 pendent on thymic output, but in adults, the naive T cell pool is primarily maintained by peripheral
212 strongest support for a model in which both naive T-cell pools contain kinetically distinct subpopul
217 N TCM cell clones were derived from a common naive T cell precursor after skin immunization, generati
219 ingle positively selecting ligand influences naive T cell precursor frequency remains undefined.
220 e-related defects--drastic reduction in true naive T cell precursors and impaired proliferative capac
221 ucing T cells can differentiate from CCR6(+) naive T cell precursors in the presence of IL-2, IL-1bet
222 udies investigate the possible phenomenon of naive T cell priming in hosts with melanoma-initiated, s
224 LR-2 costimulation also dramatically reduced naive T cell production of the immunosuppressive cytokin
226 at autoimmune melanocyte destruction induces naive T cell proliferation in skin-draining lymph nodes,
227 is predicts that, without an increase in the naive T cell proliferation rate, this decline will occur
229 lling maintains the mitochondrial content of naive T cells, providing cells with the energy to contin
231 About half of the patients had less than 10% naive T cells, reduced/absent T-cell proliferation, and
239 ymic degeneration is associated with loss of naive T cells, restriction of peripheral T-cell diversit
240 s a low number of nucleated cells and mostly naive T cells, resulting in prolonged time to engraftmen
241 antibodies directed at both erythrocytes and naive T cells, revealing a possible mechanistic link bet
242 ow that, compared with more mature but still naive T cells, RTEs are impaired in their ability to per
245 phylaxis showed increased T-cell activation, naive T-cell skewing, and elevated serum CXCL9 and CXCL1
248 n preclinical models, the use of a purified, naive T cell subset enhances persistence and antitumor i
249 only CD8alpha(+) DCs were able to stimulate naive T cells, suggesting that this DC subset cross-pres
250 in vivo differentiation landscapes of human naive T cells, supporting the notion that progenies of s
252 sgammac suppressed IL-7 signaling to impair naive T cell survival during homeostasis and exacerbated
254 ergo an additional maturation step to mature naive T cells that circulate through secondary lymphoid
255 rants [RTEs]) are functionally distinct from naive T cells that have completed postthymic maturation.
256 mune responses require a large repertoire of naive T cells that migrate throughout the body, rapidly
260 alloreactivity is mainly derived from human naive T cells, the selective depletion of naive T cells
261 ections are due to diminished recruitment of naive T cells through infection-induced decreases in che
262 a hallmark of which is the profound loss of naive T cells (TN) associated with decline in thymic out
266 s of plasmacytoid dendritic cells (pDCs) and naive T cells (Tns) in BM allografts were independently
268 ditioned medium of treated keratinocytes and naive T cells to disclose the molecular details that reg
269 PD-1H in mice blocks the differentiation of naive T cells to Foxp3(+) inducible Treg cells (iTreg) w
270 ipients had diminished ability compared with naive T cells to increase donor chimerism when transferr
271 e of T cell-intrinsic CD18 in trafficking of naive T cells to secondary lymphoid organs and in Ag-dep
272 n an increase in the intrinsic reactivity of naive T cells to self-antigens, it did not cause spontan
274 on is required for efficient polarization of naive T cells to Th1 effector cells in vitro, as well as
275 -subunit (CD127), enabling responsiveness of naive T cells to the prosurvival effects of IL-7 and all
277 rocess, allowing differentiation of neonatal naive T cells toward IFN-gamma-producing TH1 cells.
279 Enhancer deletion skewed polarization of naive T cells towards a pro-inflammatory T helper (TH17)
280 equired for normal T-cell development or for naive T-cell trafficking to lymph nodes and spleen.
281 by a progressive harmonization of memory and naive T cell traits, is broadly amenable to experimental
283 depletion in naive CD4(+) T-cells, although naive T-cell turnover was relatively unaffected by eithe
284 butes to the recruitment of CD4(+) CD45RA(+) naive T cells under in vitro defined flow conditions.
285 been shown that in a lymphopenic environment naive T cells undergo expansion due, at least in part, t
287 a), and may be driven by a reduced number of naive T cells unmasking underlying memory clonality.
290 tantly, expression of beta-catenin in mature naive T cells was sufficient to drive integrin alpha4bet
291 proliferative response and reduced counts of naive T cells were observed in addition to a restricted
294 response to LPS but were unable to activate naive T cells, whereas the majority of mature DCs produc
295 mal T cell function, including reductions in naive T cells, which correlate with clinical severity.
296 persistent autoimmune-mediated depletion of naive T cells, which is induced by changes in erythrocyt
298 as in vitro during differentiation assays of naive T cells with specific inhibitor of Foxo1 or inhibi
300 exclusively regulates homeostasis of mature naive T cells without affecting thymocytes and/or recent
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