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1                                              T cell-specific deletion of talin in Tln1(fl/fl)Cd4(Cre)
2                                              T cells isolated from TAC-treated hearts show enhanced p
3 178.8 nA/mug mL(-1), A = 92.9 nA/mug mL(-1), T = 1.4 nA/mug mL(-1), and C = 15.1 9 nA/mug mL(-1)), lo
4 w limit of detection (G, A = 0.5 mug mL(-1); T, C = 1.0 mug mL(-1)), and high selectivity in the pres
5             ShRNA knockdown of La in HEK 293 T cells increased Sendai virus infection efficiency, dec
6                                    In-bore 3-T MR-guided prostate biopsy was performed in 134 targets
7          Results Relaxivities in serum (0.94 T at room temperature) of Fe-tCDTA (r1 = 2.2 mmol(-1) .
8 a peripheral element of the RNA that forms a T-loop module and a subset of nucleotides in the cobalam
9         Combined immunodeficiency (CID) is a T-cell defect frequently presenting with recurrent infec
10                                    THEMIS, a T cell-specific protein with high expression in CD4(+)CD
11  pathways to generate mutations at G-C and A-T base pairs, respectively.
12      The Ag specificities of these activated T cells were determined by a novel CD154 T cell epitope
13  activity has been correlated with activated T-cell recognition of neoantigens, which are tumour-spec
14                                Additionally, T-bet-deficient Treg cells lacked expression of the Th1-
15 ed from PD-1(+) TILs can be used in adoptive T-cell therapy (ACT).
16  Efforts to improve the efficacy of adoptive T-cell therapies and immune checkpoint therapies in myel
17 1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/t
18 icantly associated with childhood adversity (T = 2.3; P = .03).
19   A common variant (rs1619661; coded allele: T) significantly modified the QT-PM10 association (p=2.1
20 l cells to recruit and activate alloreactive T cells.
21                    We revealed that altering T-cell receptor stimulation influenced recruitment of mR
22 IS is essential for the development of B and T lymphocytes.
23 ed in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, suggesting mTORC1 signal
24          Levels of interleukin 23 (IL23) and T-helper (Th) 17 cell pathway molecules are increased in
25  the ability to suppress lymphadenopathy and T helper cell type 2 activation.
26  (possibly including tissue macrophages) and T and B lymphocytes in the presence of detectable inflam
27 were successful in the induction of NAbs and T cell responses in guinea pigs.
28 has a crucial role in positive selection and T cell development.
29 itizing cytokines and promotion of antitumor T cell responses.
30 to proliferation, is common in newly arising T cells (so-called "recent thymic emigrants") in adults,
31                     This phenotype, known as T cell exhaustion, occurs during chronic infections caus
32                         Trichosporon asahii (T. asahii) has emerged as a dangerous pathogen that caus
33 change bias field (HEX) started to appear at T 40 K and its value increased by decreasing the tempera
34  the dominant dissipation pathways occurs at T 110 K with relatively larger contributions from phon
35 CARs are designed with elements that augment T cell persistence and activity.
36 patients, the frequency of CD1b-autoreactive T cells was increased compared with that in healthy cont
37 in thymic negative selection of autoreactive T cells by promoting the ectopic expression of tissue-sp
38                  Thus, the dichotomy between T-like and B-like cells and the presence of dedicated ly
39              Thus, sequence homology between T cell epitopes of 2 self-proteins and a related order o
40 ted by antigen-specific interactions between T lymphocytes and dendritic cells (DCs).
41 is is an autoimmune disease characterized by T-cell infiltration in the skin that leads to fibrosis,
42 ation during hypoglycemia as demonstrated by T-wave symmetry and principal component analysis ratio c
43  not affect HIV-1 gene expression induced by T cell activation in these rCD4s.
44        Pdcd1 (PD-1) disruption augmented CAR T cell mediated killing of tumor cells in vitro and enha
45 tate safer application of effective CD19 CAR T-cell therapy.
46  the inhibitory microenvironment and how CAR T cells can be further engineered to maintain efficacy.
47 lculations using the B3LYP, CASPT2, and CCSD(T) methods all predict linear geometries for both the an
48 ted T cells were determined by a novel CD154 T cell epitope mapping assay.
49 lls (and, to a lesser extent, cardiac CD3(+) T cells) from donor mice with HF induced long-term left
50 lying dermis, predominantly composed of CD3+ T cells, scattered CD20+ B cells, and relatively few PD-
51                                          CD4 T cells can differentiate into multiple effector subsets
52                             In addition, CD4 T cells produced less interferon-gamma in response to T-
53 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as a therapeutic tar
54                     Activated and memory CD4 T cells, macrophages, and dendritic cell (DC) showed che
55                At T0, the frequencies of CD4 T cell subsets, including peripheral T follicular helper
56  Furthermore, OVA-exposed lung Ptx3(-/-) CD4 T cells exhibit an increased production of IL-17A, an ef
57 ive capacity of M. tuberculosis-specific CD4 T cells was markedly impaired in HIV-infected individual
58    Trauma-induced expansion of Th17-type CD4 T cells was seen with increased expression of interleuki
59 trauma, including induction of Th17-type CD4 T cells, reduced T-bet expression by natural killer cell
60  including CD8(+) T cells for age and CD4(+) T cells and monocytes for sex, we detected a direct effe
61 anisms leading to IL-10 expression by CD4(+) T cells are being elucidated, with several cytokines imp
62  subsets including human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49
63 phosphorylated in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, suggesting m
64 d murine wild-type and Rheb-deficient CD4(+) T cells, as well as murine CD4(+) T cells activated in t
65 capable of transforming primary human CD4(+) T cells into immortalized cell lines indistinguishable f
66 Collectively, these findings identify CD4(+) T cell subsets with properties critical for improving ca
67                     Antibody-mediated CD4(+) T-cell depletion in HF mice (starting 4 weeks after liga
68 ent CD4(+) T cells, as well as murine CD4(+) T cells activated in the presence of rapamycin, a pharma
69 s constitutively acetylated and naive CD4(+) T cells are potentiated in Th17/Treg cell differentiatio
70 tion) reduced cardiac infiltration of CD4(+) T cells and prevented progressive left ventricular dilat
71 activin-A instructs the generation of CD4(+) T cells that express the Tr1-cell-associated molecules I
72 tative restriction factors in primary CD4(+) T cells from rhesus macaques under various conditions, f
73 FN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expression of Th1 and Th2 associated tr
74  whereas B cell-deficient mice showed CD4(+) T cell loss but recovered from infection without lethali
75 The TCR repertoire of Gag293-specific CD4(+) T cells proved highly biased, with a predominant usage o
76  whereas adoptive transfer of splenic CD4(+) T cells (and, to a lesser extent, cardiac CD3(+) T cells
77 py (ART) correlated with HIV viremia, CD4(+) T-cell counts, and immune activation markers, suggesting
78 -controllers from those who experience CD4(+)T-cell decline.
79 de of Aspergillus fumigatus and ensuing CD4+ T-cell polarization are poorly characterized.
80 ed of extracellular release by infected CD4+ T cells on protein quality control and autophagy in card
81                Absolute counts and % of CD4+ T cells and Treg cells (CD4 + CD25 + FOXP3 + CD127dim/-)
82 t), with antibody-mediated depletion of CD4+ T cells.
83 tively promoted reactivation of resting CD4+ T-cell, as indicated by an increased viral transcription
84  exosomes, derived from IL-2 stimulated CD4+ T cells, effectively promoted reactivation of resting CD
85             The differentiation of naive CD8 T cells into effector cytotoxic T lymphocytes upon antig
86     We undertook translatome analysis of CD8 T-cell activation, combining polysome profiling and micr
87                           Virus-specific CD8 T cells home to the site of recurrent infection and part
88 d CCR10, are upregulated on HSV-specific CD8 T cells in blood.
89 cursor effector subset of virus-specific CD8 T cells transferred into antigen-free mice revealed that
90 ro T cell culture system, MART1-specific CD8 T cells were expanded from healthy donors using artifici
91  expressed on circulating HSV-2-specific CD8 T cells.
92 des a proof of principle that suboptimal CD8 T cell in old organisms can be optimized by manipulating
93 ntDeltadriven vectorial migration, while CD8 T cell migration across LEC was not.
94                                       CD8(+) T cell specificity depends on the recognition of MHC cla
95                                       CD8(+) T cells require sustained Ca(2+) signaling for inflammat
96 s with biased capacity for CD4(+) and CD8(+) T cell activation are asymmetrically distributed in lymp
97 e E-selectin binding among CD4(+) and CD8(+) T cells but no binding by B cells.
98 nity by regulating natural killer and CD8(+) T cells, epigenetic downregulation of HLA-E by high-risk
99 it an immune response from CD4(+) and CD8(+) T lymphocytes.
100 type 1 diabetes-relevant autoreactive CD8(+) T cells.
101                    Additionally, both CD8(+) T cells and CD8(+) dendritic cells were identified in th
102 nd reduced production of IFN-gamma by CD8(+) T cells.
103 ng human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49 recombinant chem
104 n suppress activation of diabetogenic CD8(+) T cells.
105 D57 was significantly up-regulated in CD8(+) T cells from patients with hepatitis delta.
106 and sex on gene expression, including CD8(+) T cells for age and CD4(+) T cells and monocytes for sex
107                    Indeed, absence of CD8(+) T cells prevented recovery from MRV infection and led to
108 uence analysis of T-cell receptors of CD8(+) T cells revealed the presence of H-2L(d)/AH1-specific T
109 s and steps controlling postinfection CD8(+) T cell terminal effector versus memory differentiation a
110                            Central to CD8(+) T cell-mediated immunity is the recognition of peptide-m
111 , most strikingly in the least abundant CD8+ T effector population.
112 egs and M2-like macrophages and reduces CD8+ T cells to promote lung tumor growth.
113 etection method, phenotype/genotype (B cell, T cell, Philadelphia chromosome), and EFS and OS.
114 quency of IFN-gamma secreting total T cells, T-helper and CTLs against both H1N2 and H1N1 SwIV.
115  key transcriptional determinant controlling T cell responses during transplantation.
116 e autophagic machinery in DCs in a cytotoxic T-lymphocyte-associated protein 4-dependent (CTLA4-depen
117 istetraprolin-deficient mice after cytotoxic T lymphocyte depletion, but also in WSX-1/tristetraproli
118 of naive CD8 T cells into effector cytotoxic T lymphocytes upon antigen stimulation is necessary for
119 presenting immunogenic peptides to cytotoxic T lymphocytes.
120 l reduction in the number of tumor cytotoxic T lymphocytes.
121 tober 13, 2016, 18 patients who received D + T 150/2 remained in the study (13 [24%] of 54 enrolled a
122 ially administered D who crossed over to D + T).
123  tumor cells, and mice with NFATc1-deficient T cells are defective in controlling Listeria infection.
124 nt mechanism that involves caspase-dependent T cell apoptosis and upregulation of inhibitory immune c
125             Here, we show that in developing T cells, the Bcl11b enhancer repositioned from the lamin
126  here, integrates the activities of distinct T-cell subsets and by definition is dynamic and responsi
127  equivalent between control and EVL/VASP dKO T cells upon alpha4 integrin blockade.
128  specific recognition of target dsDNA (dsDNA-T), which in turn leads to the formation of a high densi
129                             In dysfunctional T cells that have a decreased cytotoxic capacity, 4-1BB
130       Among several pathways implicated in E-T coupling, activation of voltage-gated L-type Ca(2+) ch
131                                     Effector T cell migration through tissues can enable control of i
132 (OXPHOS) for energy production, and effector T cells (Teffs) rely on glycolysis for proliferation, th
133 n and the subsequent development of effector T cell responses.
134                        Although the effector T-cell response in patients with celiac disease has been
135                            The agreement for T stage was good/substantial (k=0.790) and for N stage w
136 on-phonon and electrostatic interactions for T > 110 K and larger contributions from clamping losses
137 arger contributions from clamping losses for T < 110 K.
138  Despite emerging data indicating a role for T cells in profibrotic cardiac repair and healing after
139 levels of VSG expression in bloodstream form T. brucei.
140     We find that EZH2 deficiency in FOXP3(+) T cells results in lethal multiorgan autoimmunity.
141                                 Furthermore, T-cell diapedesis became equivalent between control and
142 he absence of a surface, FXII-R353A and FXII-T activate prekallikrein and cleave the tripeptide S-230
143 ur findings demonstrate that lung gammadelta T cells provide an early source of innate IL-17, which p
144 pe mice, and adoptive transfer of gammadelta T cells prevented sensitization.
145                                   gammadelta-T-cell-deficient mice developed profound RPE and retinal
146 m a heterozygous mutant PEX6 allele (c.2578C&gt;T [p.Arg860Trp]) was overrepresented due to allelic expr
147    Abnormal development of follicular helper T (TFH) cells can induce the GC response to self-antigen
148 eg) subset that suppresses follicular helper T cell-mediated B cell responses in the germinal center
149 the cultured ELISPOT assay detected a higher T-cell response to pp65 than to IE-1 or IE-2, whereas in
150 ated hemorrhagic shock and tissue trauma (HS/T).
151                                        Human T-cell leukemia virus type 1 (HTLV-1) is the etiological
152 and chemotaxis of previously activated human T cells to CXCL11, but not CXCL10 or CXCL12.
153 and positive selection of conventional human T cells from all sources of HSPCs.
154 es induced by naive and in vivo-primed human T helper 2 cells.
155 (SCID) is characterized by severely impaired T-cell development and is fatal without treatment.
156 nclear how RICD sensitivity is calibrated in T cells derived from different individuals or subsets.
157                                   Defects in T cell receptor (TCR) repertoire are proposed to predisp
158 f interferon-gamma (IFN-gamma) expression in T cells and to generate pathogenic TH17 cells in vivo.
159 al that IFN-gamma induces CD70 expression in T cells, and CD70 limits T cell expansion via a regulato
160 ression of the transcription factor Foxp3 in T cells, trans-presentation of IL-6 by DC-bound IL-6Ralp
161 ling, costimulatory pathways are involved in T cell activation.
162 n-2 inducible T cell kinase (Itk) results in T cell immunodeficiency in mice and humans.
163 timulates the CD27 pathway, which results in T-cell activation and antitumor activity in tumor models
164 igands and receptors play important roles in T-cell co-stimulation and co-inhibition.
165                Our novel findings, including T-tubule dilatation and disorganization, associated with
166 nique subset of innate-like CD1d-independent T cells.
167 1-cell-associated molecules IL-10, inducible T-Cell costimulator (ICOS), lymphocyte activation gene 3
168 he Tec family kinase Interleukin-2 inducible T cell kinase (Itk) results in T cell immunodeficiency i
169 also demonstrate that a norovirus can infect T cells, a previously unrecognized target, in vitro.
170 ge reduction (QS in V1-V3) and inferolateral T-wave inversion.
171 d that a discrete proportion of infiltrating T cells and B cells underwent proliferation within the p
172 current helminth infection potently inhibits T cell immunity; however, whether helminthes prevent T c
173 f food allergies in offspring by instructing T reg formation via neonatal Fc receptor (FcRn)-mediated
174 ce-associated PKs provides new insights into T. brucei-host interaction and reveals novel potential p
175                 Mucosal-associated invariant T (MAIT) cells are a recently discovered, innate-like su
176 eases with increasing water content, and its T g decreases correspondingly.
177 n receptor (TCR) expressed by natural killer T cells (NKT cells) and the antigen-presenting molecule
178 udy is to explore the role of natural killer T cells in impaired liver regeneration.
179 ugh a sT domain that also inhibits MCV large T oncoprotein turnover.
180  CD70 expression in T cells, and CD70 limits T cell expansion via a regulatory T cell-independent mec
181 ophages is one pathway that suppresses local T cell proliferation.
182 lation of infiltrated MAC387(+) macrophages, T cells, dendritic cells (DCs), and residential macropha
183 were detected in the blubber of 4 adult male T. truncatus.
184  engraftment (TME), the presence of maternal T cells in peripheral blood before transplantation, is d
185                                     The MEF8 T-DNA insertion (mef8) line exhibited reduced editing at
186 ncy of Pf-specific polyfunctional CD4 memory T cells was associated with protection.
187 n resting naive, central and effector memory T cells using ChIP-Seq and found that unlike the naive c
188 elements of the cytokine genes in the memory T cells are marked by activating histone modifications e
189                   The gene coding for middle T antigen (MT) is the murine polyomavirus oncogene most
190                Although polyoma virus middle T-driven tumors showed altered primary and metastatic pr
191 scription assays demonstrated that the minor T allele variation at rs604723 increased the activity of
192 radionuclides, such as manganese-52 ((52)Mn, T(1/2)=5.6days), allow the imaging of this biodistributi
193                  The immune system can mount T cell responses against tumors; however, the antigen sp
194 ated" DCs stimulated the activation of naive T cells and polarized a subset of these cells into CD4+C
195 f antigens by dendritic cells (DCs) to naive T lymphocytes.
196     IFN-gamma-primed MCs guide activation of T cells by Staphylococcus aureus superantigen and, when
197 o found that rmIFN induces the activation of T, B, and NK cells and exhibits antiviral, antiprolifera
198                         Sequence analysis of T-cell receptors of CD8(+) T cells revealed the presence
199  Furthermore, antibody-mediated depletion of T cells prevented nasopharyngeal infection by S. pyogene
200 RNA expression profiling data from hearts of T. cruzi infected mice.
201                      After identification of T cell epitope-containing parts on each of the 3 parenta
202 ant element to support the implementation of T cruzi screening programmes at primary health centres i
203                      Selective inhibition of T-channels and global deletion of CaV 3.1 channels compl
204 gical processes leading to the initiation of T helper 1 (TH1) immunity against dietary gluten and cel
205 bited a faster development and maturation of T cells.
206                              Mouse models of T. cruzi infection have been used to study heart damage
207 le in the flagellar assembly and motility of T. denticola.
208 l rates result in near-optimal production of T cells that are capable of surviving selection and reco
209 that critically links cellular properties of T-type Ca(2+) channels to their physiological roles.
210 ly shown to be involved in the regulation of T cell proliferation and function.
211 a recently discovered, innate-like subset of T cells with cytotoxic function, the role of which in lu
212  genes and pathways, and stage or subtype of T-ALL.
213                         Adoptive transfer of T cells engineered to express a hepatitis B virus-specif
214 nse rates have been reported with the use of T cells modified by chimeric antigen receptor (CAR) that
215 at Ca(2+) entry exerts a feedback control on T-type channel activity, by modulating the channel avail
216 lonisation increased aphid phloem feeding on T. monococcum MDR037 and MDR045, colonisation also incre
217 MR assignments, and JM mutants (ST(296)AA or T(304)A) investigated, confirm that the backbone amide o
218                 Unlike B cell depletion, pan-T cell aplasia is prohibitively toxic.
219  purified immune subsets including human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK
220 ce expression and rescues, at least in part, T follicular helper numbers and the abnormal Ab producti
221 esponses in preclinical models, particularly T cell responses, remain sparse.
222                                   Pathogenic T cells in individuals with rheumatoid arthritis (RA) in
223 cytes prior to treatment or among peripheral T cells after treatment would be associated with effecti
224  of CD4 T cell subsets, including peripheral T follicular helper (pTfh) cells, which provide help to
225         Interleukin (IL)-13 is a pleiotropic T helper type 2 cytokine frequently associated with asth
226 nt epitopes for gluten-specific CD4-positive T cells.
227  stimulate, and the complemented PF-positive T. denticola strain restored the activation.
228 few PD-1+ (programmed cell death 1-positive) T cells, an immunophenotypic pattern also observed in ot
229 mmunity; however, whether helminthes prevent T cell priming or skew clonal recruitment and effector d
230   Immunization with low doses of gp96 primes T helper type 1 (Th1) immune responses, whereas high-dos
231 se (ROCK)2 downregulates the proinflammatory T cell response while increasing the regulatory arm of t
232                               The protective T allele at rs7178051 was also associated with reduced A
233                              While quiescent T cells use oxidative phosphorylation (OXPHOS) for energ
234 ansferred polyclonal cancer antigen-reactive T cells deficient in the regulator diacylglycerol kinase
235  induction of Th17-type CD4 T cells, reduced T-bet expression by natural killer cells, and expansion
236      The transcribed ultraconserved regions (T-UCRs) encode long non-coding RNAs implicated in human
237      The cell surface receptor CD6 regulates T cell activation in both activating and inhibitory mann
238 D70 limits T cell expansion via a regulatory T cell-independent mechanism that involves caspase-depen
239 primes responses characterized by regulatory T (Treg) cells and immunosuppression.
240 ed that soluble CD137 produced by regulatory T cells contributed to their autoimmune-suppressive func
241 T (TFR) cells are a newly defined regulatory T cell (Treg) subset that suppresses follicular helper T
242                        Follicular regulatory T (TFR) cells are a newly defined regulatory T cell (Tre
243  these cells into CD4+CD25+FoxP3+ regulatory T cells (Tregs).
244 imulatory molecules such as ICOS, regulatory T cells and by compounds such as nicotine.
245 ivation of host immunosuppressive regulatory T (Treg) cells.
246 n well characterized, the role of regulatory T (Treg) cells in the loss of tolerance to gluten remain
247 he distinct metabolic features of regulatory T cells (Tregs) are less well established.
248 lets and suggest that therapeutic regulatory T cells directly or indirectly regulate their influx by
249                              When regulatory T cells (2 x 106/mouse) were intravenously administered
250                    Blockade of ICOSL rescues T cell ICOS surface expression and rescues, at least in
251 tic cells and macrophages as well as resting T-cells, SAMHD1 blocks HIV-1 infection through this dNTP
252                                   In resting T cells cholesterol keeps TCRs in the resting conformati
253 ibitory receptor blockade partially reversed T cell unresponsiveness.
254 elevated in carriers of the GABRA6 rs3219151 T allele with several independent markers and predictors
255       5) Finally, SERCA2a 971-990-sensitized T cells were able to transfer disease to naive recipient
256 itor of mTORC1, we were able to identify six T-bet phosphorylation sites.
257         Merkel cell polyomavirus (MCV) small T (sT) oncoprotein induces centrosome overduplication, a
258 te infection pp65-, IE-1-, and IE-2-specific T cells were detected at comparable levels.
259 evealed the presence of H-2L(d)/AH1-specific T cells and an expansion of sequence diversity in treate
260 oint therapies target tumor antigen-specific T cells, but less is known about their effects on natura
261               Determination of HCMV-specific T cells by cultured ELISPOT, in pregnant women with prim
262 ights into the nature of neoantigen-specific T cells and the effects of checkpoint blockade immunothe
263 escribe the appearance of transgene-specific T-cell responses in two subjects that were part of the p
264  a hepatitis B virus-specific (HBV-specific) T cell receptor (TCR) may supplement HBV-specific immune
265 sms whereby HIV infection impedes successful T cell-mediated control of M. tuberculosis have not been
266 Fibroblasts possess the capacity to suppress T cell responses, although the molecular mechanisms of t
267 hat exhibits a glass-transition temperature (T g ) and a rubbery plateau.
268 )alpha4beta7(high) subsets enhanced Th1/Th17 T cell generation and accumulation in the intestine, and
269                         Here, we report that T cells activated in such a context are mainly IFN-gamma
270                  Recent studies suggest that T reg cells can participate in tissue repair in a manner
271                  The interaction between the T cell antigen receptor (TCR) expressed by natural kille
272            This study aimed to determine the T-cell response to Phl p 12 in profilin-sensitized patie
273 sion of MYC signaling and an increase in the T cell chemoattractant CCL5.
274         Conversion of pyruvate to CO2 in the T. brucei bloodstream form provides new support for the
275  functional studies define landscapes of the T cell proteome and phosphoproteome and reveal signaling
276                    Detailed knowledge of the T cell response may further contribute to the identifica
277 ghlight the need for further analysis of the T cells involved in insulitis to elucidate their role in
278                     An induced switch of the T reg cell TCR repertoire to a random repertoire also pr
279 and alternating phenylene (P) and thiophene (T) units as PTP and TPT.
280 erein, we exhibit that CD26 identifies three T helper subsets with distinct immunological properties
281 ciated with Wnt-responsive enhancers through T cell factors (TCF) and kept silent by Groucho/TLE co-r
282 itude and frequency of Ca(2+) influx through T-type and L-type Ca(2+) channels.
283             Mitochondrial flux from ASMCs to T cells was partially FGF2b and FGFR1 dependent.
284 vent of pAg sensing that ultimately leads to T cell activation.
285  disease, chronic immune activation leads to T-cell exhaustion.
286              We postulate that resistance to T-DM1 occurs through multiple mechanisms, one of which i
287 roduced less interferon-gamma in response to T-cell stimulation.
288 d the frequency of IFN-gamma secreting total T cells, T-helper and CTLs against both H1N2 and H1N1 Sw
289 -carotenoid triplet-triplet energy transfer (T-TET) is slow, in the tens of nanoseconds range, wherea
290 ield-induced metamagnetic phase transitions (T N = 58 K) and high spontaneous polarization ( 63.3 mu
291 kade (ICB) therapies can unleash anti-tumour T-cell responses.
292                                    Wild-type T. denticola and the purified PF triggered activation of
293 nd -independent activation of Vgamma9Vdelta2 T cells and, importantly, strongly reduced the productio
294                              In our in vitro T cell culture system, MART1-specific CD8 T cells were e
295 eads in the inner chamber produced ET-1 when T cells were activated with antigen or anti-CD3 antibody
296 fter ischemia, little is known about whether T cells directly impact cardiac fibroblasts (CFBs) to pr
297 search, we also assessed the extent to which T's effects on aggressive behavior would depend on varia
298 n elevated mutation load in combination with T cell clonal dominance among intratumoral lymphocytes p
299 ility of using rapamycin in conjunction with T cell-activating agents in HIV-1 cure strategies.
300 educed PDW was significantly correlated with T stage, N stage, TNM stage, and histological type of th

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