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1 olled by signaling pathways initiated by the T cell antigen receptor.
2 step for T cell activation triggered by the T cell antigen receptor.
3 of the ligands recognized by the gammadelta T cell antigen receptor.
4 le entry and responses to stimulation of the T cell antigen receptor.
5 pon weak recognition of self-antigens by the T cell antigen receptor.
6 ion of CD4+ T cells after stimulation of the T cell antigen receptor.
7 ignaling including that originating from the T cell antigen receptor.
8 Treg cells separable from signaling via the T cell antigen receptor.
9 s that are activated after engagement of the T cell antigen receptor.
10 ation and effector functions mediated by the T-cell antigen receptor.
11 te development is shaped by signals from the T-cell antigen receptor.
12 ns in signalling complexes downstream of the T-cell antigen receptor.
13 g on the cellular mechanisms driven by B and T cell antigen receptors.
14 t evident in the enormous diversity of B and T cell antigen receptors.
15 gens, which bind to CD1 proteins and contact T cell antigen receptors.
16 ntigens) on the surface of other cells using T cell antigen receptors.
17 les, peptides presented by HLA molecules and T-cell antigen receptors.
18 (J(alpha)) segments in the gene encoding the T cell antigen receptor alpha-chain (Tcra) and had a pro
20 luding genes that activate expression of the T-cell antigen receptor alpha chain (TCR-alpha) in devel
21 double-negative thymocytes positive for the T cell antigen receptor alphabeta subtype (TCRalphabeta)
23 ed a role for the Akt kinase in coupling the T cell antigen receptor and CD28 to NF-kappaB activation
24 the six-chain assembly intermediate between T cell antigen receptor and the CD3delta epsilon and CD3
25 a is a critical mediator of signaling by the T cell antigen receptor and the principal costimulatory
26 lls is controlled by tonic signaling through T cell antigen receptors and common gamma chain cytokine
28 ing the balance of persistent stimulation of T-cell antigen receptors and specific CD2-induced co-sti
29 tigen-specific responses, such as CD4, CD28, T-cell antigen receptor, and class I and class II major
30 CD4 T cells from old mice incubated on anti-T cell antigen receptor antibodies with transforming gro
35 crodissection, transcriptional profiling and T-cell antigen receptor beta-chain (TCRbeta) genotyping
36 ors shaping their variable repertoire of the T-cell antigen receptor beta-chain, in addition to novel
37 ence for a fundamentally different basis for T cell antigen receptor-beta (Tcrb) allelic exclusion.
38 productive rearrangement of segments of the T cell antigen receptor-beta gene (Tcrb) and formation o
39 ifs to tyrosine kinases and may regulate the T-cell antigen receptor biological activities for this c
40 d these cells can be activated through their T cell antigen receptors by microbial lipid antigens.
41 he TM domains thus shows similarities to the T cell antigen receptor-CD3 complex, in particular to th
42 with human T-lymphotropic virus type 1; (ii) T cell antigen receptor clonotype repertoires; and (iii)
47 that HAA inhibits NF-kappaB activation upon T cell antigen receptor engagement by specifically targe
49 e findings indicate that the affinity of the T cell antigen receptor for self antigen drives the diff
50 types require activation of NF-kappaB by the T cell antigen receptor for their generation, and the Nf
51 daptive immunity are the immunoglobulins and T-cell antigen receptors found in jawed vertebrates.
53 y, it was shown that Vitamin D modulates the T cell antigen receptor, further demonstrating that Vita
56 of the immunological synapse sequesters the T cell antigen receptor in a location where it cannot in
57 r differences in the binding strength of the T cell antigen receptor in the antigen-specific mechanis
59 oteolysis is therefore essential for optimal T cell antigen receptor-induced activation of NF-kappaB
61 ity complex class II and the most restricted T cell antigen receptor junctional diversity 'preferenti
66 in CD4(+) T cells, prior activation via the T cell antigen receptor limits IL-6's control of STAT1 i
68 apses are initiated by signaling in discrete T cell antigen receptor microclusters and are important
70 dent spreading only after stimulation of the T-cell antigen receptor or the integrin alpha4beta1.
71 igh expression in thymocytes between the pre-T cell antigen receptor (pre-TCR) and positive-selection
75 than did Foxp3(lo) T(reg)P cells, and had a T cell antigen receptor repertoire and transcriptome dis
77 (TEC) is essential for generating a diverse T cell antigen receptor repertoire tolerant to self-anti
80 lerant CD4+ and CD8+ populations with normal T-cell antigen receptor repertoires, cytokine secretion
81 mechanisms in vitro after activation via the T cell antigen receptor, resulting in antigen-independen
83 ck binding region of SLP-76 is essential for T cell antigen receptor signaling and normal T cell deve
85 recently reported that YopH acutely inhibits T cell antigen receptor signaling by dephosphorylating t
89 hymocyte positive selection by enhancing the T cell antigen receptor signaling response to low-affini
90 ed the tumor suppressor KLF4 'downstream' of T cell antigen receptor signaling to induce cell cycle a
91 , a cytoplasmic tyrosine kinase required for T cell antigen receptor signaling, is controlled by a re
97 ls) following suboptimal stimulation via the T cell antigen receptor (TCR) (induced T(reg) cells (iT(
98 nstream responses of T lymphocytes following T cell antigen receptor (TCR) activation are mediated by
100 lations further differed in their use of the T cell antigen receptor (TCR) alpha-chain variable regio
103 from naive precursors when signals from the T cell antigen receptor (TCR) and certain cytokine recep
104 ia acted in synergy with stimulation via the T cell antigen receptor (TCR) and coreceptor CD28 to acc
107 ) T cells lost the signaling activity of the T cell antigen receptor (TCR) and expressed a protein co
108 molecules associated with activation of the T cell antigen receptor (TCR) and of immunological-check
109 ceptor modulates the interaction between the T cell antigen receptor (TCR) and peptide-major histocom
110 The expression of Myc is regulated by the T cell antigen receptor (TCR) and pro-inflammatory cytok
111 ted directly with the signal strength of the T cell antigen receptor (TCR) and required the corecepto
112 own as protein kinase B, is activated by the T cell antigen receptor (TCR) and the cytokine interleuk
113 igh ITAM multiplicity) in the complex of the T cell antigen receptor (TCR) and the invariant signalin
114 We found that clonotypes expressing the T cell antigen receptor (TCR) beta-chain variable region
115 phosphatase PTPN22 limited signaling via the T cell antigen receptor (TCR) by weak agonists and self
116 Variable strengths of signaling via the T cell antigen receptor (TCR) can produce divergent outc
117 function correlates with genomically encoded T cell antigen receptor (TCR) chains, which suggests tha
120 we analyzed the spatio-temporal dynamics of T cell antigen receptor (TCR) complexes and linker for a
123 complex (MHC) proteins are recognized by the T cell antigen receptor (TCR) dictates the homeostasis o
128 types generally show simplified patterns of T cell antigen receptor (TCR) expression, rapid effector
131 31 was strongly induced by activation of the T cell antigen receptor (TCR) in a pathway involving cal
132 roscopy to study complexes downstream of the T cell antigen receptor (TCR) in single-molecule detail
133 interleukin 17 (IL-17), but the role of the T cell antigen receptor (TCR) in this developmental proc
134 The delivery of signals from the activated T cell antigen receptor (TCR) inside the cell relies on
139 The kinetic proofreading model can explain T cell antigen receptor (TCR) ligand discrimination; how
140 s) requires interleukin 2 (IL-2) and agonist T cell antigen receptor (TCR) ligands and is controlled
142 ing T cells, coreceptor choice is matched to T cell antigen receptor (TCR) MHC specificity during pos
143 RF) microscopy showed that signaling via the T cell antigen receptor (TCR) occurred during synapse tr
144 selection, which requires recognition by the T cell antigen receptor (TCR) of complexes of self pepti
148 ls) characterized by either a semi-invariant T cell antigen receptor (TCR) repertoire (type I NKT cel
149 er T cells (iNKT cells) express a restricted T cell antigen receptor (TCR) repertoire and they respon
151 ngle-cell RNA sequencing and high-throughput T cell antigen receptor (TCR) sequencing to characterize
153 actors and cell-intrinsic factors related to T cell antigen receptor (TCR) signal quantity and qualit
154 ning the nature of molecules involved in the T cell antigen receptor (TCR) signal transduction networ
155 le deficiencies in thymic development and in T cell antigen receptor (TCR) signal transduction, in PT
156 found that calcineurin was recruited to the T cell antigen receptor (TCR) signaling complex, where i
157 ytes transition through a stage during which T cell antigen receptor (TCR) signaling controls CD4-ver
159 f CD8(+) T cells in the thymus requires that T cell antigen receptor (TCR) signaling end in time for
161 genotype at CTLA4 is associated with altered T cell antigen receptor (TCR) signaling in naive and/or
162 to immunity and requires a limited degree of T cell antigen receptor (TCR) signaling in response to s
164 lf-reactivity, with a particular emphasis on T cell antigen receptor (TCR) signaling thresholds.
165 the Carma1-Bcl10-MALT1 (CBM) complex couples T cell antigen receptor (TCR) signaling to IkappaB kinas
166 e catalytic activity of Zap70 is crucial for T cell antigen receptor (TCR) signaling, but the quantit
167 and WASP-interacting-protein (WIP) regulate T cell antigen receptor (TCR) signaling, but their role
168 To investigate how Csk activity regulates T cell antigen receptor (TCR) signaling, we utilized a m
178 y sensor of thresholds for signaling via the T cell antigen receptor (TCR) that was essential for T c
180 Classically, signal transduction from the T cell antigen receptor (TCR) to ERK is thought to be re
181 owever, the mechanisms that allow the clonal T cell antigen receptor (TCR) to functionally engage mul
182 p1A and Foxp1D induced by stimulation of the T cell antigen receptor (TCR) to inhibit the generation
183 and the tyrosine phosphatase CD45 underpins T cell antigen receptor (TCR) triggering, but how such s
185 isplayed enhanced proximal signaling via the T cell antigen receptor (TCR) without an effect on the a
188 transduction by immunoreceptors such as the T cell antigen receptor (TCR), B cell antigen receptor (
189 press an evolutionarily conserved, invariant T cell antigen receptor (TCR), but the forces that drive
190 cating THEMIS in signaling downstream of the T cell antigen receptor (TCR), but the mechanistic under
192 When T cells encounter antigens via the T cell antigen receptor (TCR), information about the qua
195 in T cells in response to engagement of the T cell antigen receptor (TCR), which induced expression
198 lated from tissues of Ctla4(-/-) mice showed T cell antigen receptor (TCR)-dependent accumulation in
203 chanistically, we demonstrate a link between T cell antigen receptor (TCR)-induced asymmetric express
204 e-operated Ca(2+) channel and contributed to T cell antigen receptor (TCR)-induced Ca(2+) influx, TCR
205 ular signaling molecule that is required for T cell antigen receptor (TCR)-induced cytokine synthesis
206 d immunodeficiency syndrome due to defective T cell antigen receptor (TCR)-induced NF-kappaB signalin
207 cell-activating NKG2D-DAP10 complex and the T cell antigen receptor (TCR)-invariant signaling protei
208 -forming subunit Ca(v)1.4 and attenuation of T cell antigen receptor (TCR)-mediated global Ca(2+) ent
210 Analysis of 11 crystal structures of MAIT T cell antigen receptor (TCR)-MR1-AML ternary complexes,
212 re, we have adopted a procedure developed in T cell antigen receptor (TCR)-transgenic mice to convert
225 In mice that express a transgene for the 2C T cell antigen-receptor (TCR) and lack a recombinase-act
226 blocked effector T-cell proliferation after T cell-antigen receptor (TCR) engagement, but had no sig
231 organization of CD4, and its relationship to T-cell antigen receptor (TCR) and the active form of Src
238 lts in aberrant activation of NF-kappaB upon T-cell antigen receptor (TCR) ligation, which is mediate
239 e use phage display to isolate and enhance a T-cell antigen receptor (TCR) originating from a CTL lin
243 f RNA-seq for assessing T-cell clonality and T-cell antigen receptor (TCR) repertoire of the neoplast
247 toire requires appropriate interpretation of T-cell antigen receptor (TCR) signals by CD4(+ ) CD8(+)
250 We demonstrate that upon ligation of the T-cell antigen receptor (TCR), the TCR associates with a
251 ls that develop in these mice have defective T-cell antigen receptor (TCR)-induced calcium flux but e
255 ires are biased toward particular gammadelta T cell antigen receptors (TCRs) according to location.
256 responses are driven by interactions between T cell antigen receptors (TCRs) and complexes of peptide
257 e responses, T cells harboring high-affinity T cell antigen receptors (TCRs) are preferentially expan
258 t of innate CD8(+) T cells that have diverse T cell antigen receptors (TCRs) but have a memory phenot
261 quence of intrathymic selection during which T cell antigen receptors (TCRs) expressed by immature th
262 und molecules are subsequently recognized by T cell antigen receptors (TCRs) expressed on the surface
265 question is whether an altered repertoire of T cell antigen receptors (TCRs) is associated with such
266 II-restricted self antigens by autoreactive T cell antigen receptors (TCRs) is established, but how
269 liferation of naive T lymphocytes expressing T cell antigen receptors (TCRs) specific for foreign pep
270 ll features, including variable sequences of T cell antigen receptors (TCRs) that confer antigen spec
271 the virus activated T cells expressing dual T cell antigen receptors (TCRs) that were able to recogn
273 e-positive (DP)) thymocytes are signaled via T cell antigen receptors (TCRs) to undergo positive sele
275 ve selection is based on the interactions of T cell antigen receptors (TCRs) with self peptide-major
276 respond rapidly to stress despite expressing T cell antigen receptors (TCRs), a hallmark of adaptive
282 We observed that colonic T(reg) cells used T-cell antigen receptors (TCRs) different from those use
283 clones is diverse and contains cells bearing T-cell antigen receptors (TCRs) that differ in their aff
286 checkpoint inhibition, mAbs, and engineered T-cell antigen receptors, the incidence and pattern of m
287 rates generate a diverse repertoire of B and T cell antigen receptors through the rearrangement of im
288 s that mediate inside-out signaling from the T cell antigen receptor to integrins, giving rise to inc
291 recognition of beta-GlcCer by the invariant T cell antigen receptor translates innate danger signals
292 show that T cell activation mediated by the T cell antigen receptor translocates plasma membrane S1P
293 (LAT) is a critical signaling hub connecting T cell antigen receptor triggering to downstream T cell
294 onors display altered alpha3135-145-specific T-cell antigen receptor usage, HLA-DR15-alpha3135-145 te
295 T cells, enriched for self antigen-specific T cell antigen receptors, was also present in healthy ho
297 solvent-exposed and therefore accessible to T-cell antigen receptors were predicted to be immunogeni
298 nhanced responses to weak stimulation of the T cell antigen receptor, when transferred into lymphopen
299 Phorbol esters or the engagement of the T cell antigen receptor, which activate PKC and the expr
300 n important class of immune receptors (e.g., T-cell antigen receptors) whose ligands are anchored to