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1 molecule CD28 is essential for activation of helper T cells.
2 d T cells, especially in the TH17 lineage of helper T cells.
3 he development of IL-17-producing pathogenic helper T cells.
4 or typically expressed by the TH17 subset of helper T cells.
5 -)Sirpalpha(+) DCs induced the TH1 subset of helper T cells.
6 ity to differentiate into the TH17 subset of helper T cells.
7 chanism did not appear to be shared by mouse helper T cells.
8 in controlling the proallergic generation of helper T cells.
9 ferentiation into the TH2 and TH9 subsets of helper T cells.
10 phabeta(+) cytotoxic T lymphocytes or CD4(+) helper T cells.
11 ediated functional differentiation of CD4(+) helper T cells.
12 ewildering number of fates seem possible for helper T cells.
13 tion ex vivo by LN CD4(+)CXCR5(+) follicular helper T cells.
14 on of inducible T(reg) cells into follicular helper T cells.
15 hich occurs almost exclusively in follicular helper T cells.
16 the differentiation of the T(H)17 subset of helper T cells.
17 being activated and in the function of these helper T cells.
18 hat can fine-tune the plasticity and fate of helper T cells.
19 augmented the response by activating CD4(+) helper T cells.
20 ification, differentiation and commitment of helper T cells.
21 mportant regulator of the differentiation of helper T cells.
22 nature cytokines secreted by IL-17-producing helper T cells.
23 es, especially those of the T(H)17 subset of helper T cells.
24 ne profile favoring the generation of Type 1 helper T cells.
25 e network controlling the differentiation of helper T cells.
26 4, which allowed stable expression of Cd4 in helper T cells.
27 ter B cell support by PG-specific follicular helper T cells.
28 tokine produced by regulatory T-cells and by helper T-cells.
29 uggesting a large pool of S. aureus-reactive helper T-cells.
30 ncreases proliferation of cytotoxic, but not helper, T cells.
31 autoimmune diseases through differentiating helper T cell 1 (TH1) and maintaining TH17 responses.
32 F-alpha ratio and suppressed proinflammatory helper T cell 1 (Th1) cytokine expression by autologous
33 wn-regulated pathogenic pro-inflammatory and helper T cell 1 (Th1) responses and up-regulated benefic
34 IV) disease progression is associated with a helper T cell 1 (Th1) to helper T cell 2 (Th2) cytokine
35 rmine whether blockade of the interleukin 23-helper T cell 17 (IL-23-TH17) pathway with ustekinumab r
37 n particular, nicotine is found to promote a helper T cell 2 adaptive immunologic response within T c
38 FIV employs a distinct strategy to target helper T cells; a high affinity interaction with CD134 (
41 tipeptide vaccine (6MHP), designed to induce helper T cells against melanocytic and cancer-testis ant
43 ecular interactions at the interface between helper T cells and antigen-presenting B cells govern the
45 ir differentiation into the T(H)17 subset of helper T cells and colitogenic potential, in a manner de
47 hyperactive response of the T(H)17 subset of helper T cells and developed spontaneous IL-22-dependent
48 mechanisms that regulate the T(H)9 subset of helper T cells and diseases mediated by T(H)9 cells rema
49 regulatory T cells and the T(H)17 subset of helper T cells and diverted CD4(+)Foxp3(-) T cells to a
50 function, amplified the number of follicular helper T cells and germinal-center B cells and plasmabla
51 rs and functionality of LCMV-specific CD4(+) helper T cells and impaired antiviral CD8(+) T-cell resp
52 is produced by cells of the T(H)17 subset of helper T cells and other leukocytes, not only enhances p
53 ed genes, increased the number of follicular helper T cells and plasmablasts in the spleen, and led t
54 ffector cells of the TH1 and TH17 subsets of helper T cells and the development of experimental autoi
55 ed differentiation into the T(H)17 subset of helper T cells and therefore represents a factor that ca
56 is essential for the formation of follicular helper T cells and thus GCs, although whether IRF4 plays
57 ene expression specific to the TH2 subset of helper T cells and was important for the migration of TH
58 ting immune activation was assessed based on helper T-cell and regulatory T-cell activation in mice.
59 mediated by CD4(+)CXCR5(+)PD-1(+) follicular helper T cells, and can suppress inflammation in autoimm
60 renal allograft rejection induced by memory helper T cells, and CD8 T cell depletion at the time of
61 regulatory T cells (Treg), exhausted CD4(+) helper T cells, and myeloid-derived suppressor cells (MD
62 acilitated antigen-specific interaction with helper T cells, and promoted antibody affinity maturatio
63 he generation of antigen-specific follicular helper T cells, antigen-specific GC B cells, and high-af
69 TH17 cells (interleukin-17 (IL-17)-producing helper T cells) are highly proinflammatory cells that ar
70 unctional antibody responses, via follicular helper T cells, as well as on the roles of CD4(+) T cell
71 ity complex (MHC) class II-restricted CD4(+) helper T cells but are also a common feature of MHC clas
72 class II complexes and defective priming of helper T cells but not of cytotoxic T lymphocyte (CTL) r
73 bility (MHC) class II complexes to stimulate helper T cells, but the genetic and regulatory basis for
76 ls (CD3(+)), cytotoxic T cells (CD8(+)), and helper T cells (CD4(+)) in vessels of idiopathic PAH lun
78 ggerated airway eosinophilia, release type 2 helper T cell cytokines and exhibit airway hyper-respons
80 findings demonstrate that individual type 17 helper T-cell cytokines can have proinflammatory or anti
84 fibroblasts resulted in impaired follicular helper T cell differentiation and, consequently, in redu
86 se results demonstrate that miR-29 regulates helper T cell differentiation by repressing multiple tar
87 ondary complications and a skewed follicular helper T-cell differentiation in defined monogenic immun
89 d, Nlrp10(-/-) mice had a profound defect in helper T-cell-driven immune responses to a diverse array
90 iRNA down-regulation promotes acquisition of helper T cell effector functions by relaxing the repress
91 ller cells (consisting of cytotoxic T cells, helper T cells, effector B cells, and natural killer cel
92 ht zone phenotype (site of Ag and follicular helper T cell encounter) express much higher levels of G
93 xpressed at functionally relevant amounts in helper T cells, Eomes was abundant in miRNA-deficient ce
97 opment of innate-like T-cells and follicular helper T-cells, events that are known to require strong/
101 ility of this idea to the T(H)2 cell, T(H)17 helper T cell, follicular helper T cell (T(FH) cell) and
104 ter understanding of the mechanisms by which helper T cells function in the natural history of cholan
109 (Tfh) cells comprise an important subset of helper T cells; however, their relationship with other h
110 mock-infected AMs or LMVECs and analyzed for helper T cell (i.e., Treg, Th17, Th1, and Th2) marker ex
112 anti-fungal responses of the TH17 subset of helper T cells in controlling infection with Candida alb
113 ut the differentiation of pathogenic type 17 helper T cells in experimental autoimmune uveoretinitis
114 that endogenous cells of the TH17 subset of helper T cells in lymphoid organs of naive mice 'prefere
115 ion, mature B cells interact with follicular helper T cells in specialized structures called germinal
118 ine deaminase, and IL-21(+)PD1(+) follicular helper T cells in tLTs together with CD138(+) plasma cel
119 for proper differentiation of types 1 and 2 helper T cells in vivo by restraining the expression and
120 r better showed greater maximum effector and helper T-cell increases, elevated antiviral and alloreac
124 that drive the differentiation of human CD4+ helper T cells into TFH cells remain largely undefined.
126 induced expression of FcgammaRIIIa on CD4(+) helper T-cells is an important finding since these recep
127 g cells) and the inflammatory TH17 subset of helper T cells leads to the development of autoimmune an
130 by key transcription factors, including the helper T cell master regulator ThPOK, which suppresses t
131 ts targeting mechanisms involving CD4 type 1 helper T cells may provide more effective, better tolera
132 ell (Treg) subset that suppresses follicular helper T cell-mediated B cell responses in the germinal
133 essive interferon-gamma that directly limits helper T cell-mediated support of humoral immunity and d
136 ry T cells and lymph node-derived follicular helper T cells of patients with CVID compared with those
137 nd of coreceptors through which signals from helper T cells or pathogen-associated molecular patterns
138 e differentiation and function of follicular helper T cells or that of other helper T cell subsets.
139 on (P = 0.007) and CD25 expression on CD4(+) helper T cells (P = 0.0003) in the activated cord blood
142 family in the determination of the effector helper T cell phenotype that naive CD4(+) T cells adopt
143 pt predominantly type 1 helper or follicular helper T cell phenotypes in response to bacterial or vir
146 trates that CD28 persistence is required for helper T cell polarization in response to infection, des
148 intenance and/or expansion of the follicular helper T cell population, although it was dispensable fo
149 nalysis we define an alpha4 nAChR expressing helper T-cell population (alpha4(+)CD3(+)CD4(+)) and sho
150 F(+))-producing cells and contain follicular helper T-cell populations not only in the spleen and dra
151 sulted in the post-thymic termination of the helper T cell program and the functional differentiation
152 itory circuit that stabilizes the follicular helper T cell program at least in part through the contr
153 generation of an autoreactive TH17 subset of helper T cells, prominently associated with autoimmune d
155 rs experienced significant downregulation of helper T-cell-related (T(H)1, T(H)17, and T(H)22) mRNA e
159 the proteins contribute most strongly to the helper T cell response, highlight specific weaknesses of
160 mice developed an exaggerated type 1 and 17 helper T-cell response, characterized by natural killer
163 so required to elicit proinflammatory CD4(+) helper T cell responses to infection and mucosal vaccina
167 iew the current status of the flexibility of helper T-cell responses in relation to their genetic reg
168 ese data suggest that pDCs facilitate CD4(+) helper T-cell responses to persistent viruses independen
169 mmunodeficiency viruses (FIV and HIV) target helper T cells selectively, and in doing so they induce
170 our findings suggest that the TH9 subset of helper T cells serves an important role in driving ulcer
172 what do terms like 'lineage commitment' and helper T-cell 'specification' mean in the early 21st cen
173 renal allograft rejection induced by memory helper T cells starting at day 4 after transplantation.
175 elper T cells (TFH cells) are the prototypic helper T cell subset specialized to enable B cells to fo
176 FOXP3-positive Treg cells are a critical helper T cell subset, and dysregulation of Treg generati
177 anti-tumor effects of a unique human CD4(+) helper T-cell subset that directly recognizes the cytopl
178 differentiation into at least four distinct helper T cell subsets after recognition of foreign antig
179 ve phenotypes that mirror those of polarized helper T cell subsets in their expression of core transc
182 e Notch family direct the differentiation of helper T cell subsets, but their influence on regulatory
187 ously defined 'master regulators' for CD4(+) helper T-cell subsets are also shared by ILC subsets.
188 t and functional divergence of the different helper T-cell subsets as well as in regulatory T cells.
192 an important regulator of other specialized helper T-cell subsets within germinal centers, pre-germi
193 lammatory diseases thought to be mediated by helper T-cell subtypes 1 and 2 (TH1 and TH2), respective
194 nteresting results include CSF enrichment of helper T cells (subtypes TH1 and TH17) and regulatory T
195 ntiated more readily into cytokine-producing helper T cells, suggesting that activation-induced miRNA
196 T(H)2 cell, T(H)17 helper T cell, follicular helper T cell (T(FH) cell) and induced regulatory T cell
197 lper type 1 cell (T(H)1 cell) and follicular helper T cell (T(FH) cell) gene-expression profile, resp
199 d T(reg) cell-mediated suppression of type 1 helper T cell (T(H)1 cell) responses and protected again
204 paralleled by the accumulation of follicular helper T cells (T(FH) cells) is linked to mutation of th
208 cells suppressed CD4 T cells and follicular helper T cells (T(FH)) in a perforin-dependent manner du
209 the expansion of antigen-specific follicular helper T cells (T(fh)), compared to vaccinations with so
210 CD4(+) interleukin 17 (IL-17)-producing helper T cells (T(H)17 cells) are instrumental in the im
212 s (T(H)2 cells) and interleukin 17-producing helper T cells (T(H)17 cells) but not of T helper type 1
217 Given their functional relatedness to type 2 helper T cells (T(H)2 cells), we explored whether Gfi1 a
218 ent of interleukin 4 (IL-4)-producing type 2 helper T cells (T(H)2 cells), which suggests that T(H)2
219 , patients with IMNM exhibit a strong type 1 helper T cell (T1)/classically activated macrophage M1 r
220 tches, such TH17 cells acquired a follicular helper T cell (TFH cell) phenotype and induced the devel
222 atory T cells (TFR cells) inhibit follicular helper T cell (TFH cell)-mediated antibody production.
231 g the developmental mechanisms of follicular helper T cells (TFH cells) in humans is relevant to the
232 Aberrant population expansion of follicular helper T cells (TFH cells) occurs in patients with lupus
234 cy virus (HIV), which persists in follicular helper T cells (TFH cells), and Epstein-Barr virus (EBV)
238 is is dependent on CD4(+)CXCR5(+) follicular helper T cells (TFH) and inhibited by CD4(+)CXCR5(+)Foxp
240 by the more recent definition of follicular helper T cells (Tfh) as the key T cell subset in B cell
241 In follicular lymphoma (FL), follicular helper T cells (TFH) have been depicted as one of the ma
245 ssion also expanded the number of follicular helper T cells (TFHs) in a cell-intrinsic and Ag-specifi
246 the normal balance of pneumococcal-specific helper T cell (Th) 1/Th17 immunity to colonization, resu
247 -based vaccine formulation enhances systemic helper T cells TH1 and TH2 serum antibody and cytotoxic
248 Treg cell stability to repression of type 1 helper T cell (TH1 cell) and follicular helper T cell (T
249 between groups were observed for the type 1 helper T cell (TH1)-associated chemokines CXCL9 and CXCL
250 rosis factor-alpha; decreased types 1 and 17 helper T cells (Th1 and Th17, respectively); and increas
251 uding Slc2a1, Slc2a3, Pkm and Hk2, in type 1 helper T cells (TH1 cells) exposed to low concentrations
252 r the signaling pathways of type 1, 2 and 17 helper T cells (TH1, TH2 and TH17), JAK-STAT, interferon
253 naling, induces the expression of the type 1 helper T-cell (Th1) cytokine, interferon gamma, and supp
254 negative Borrelia cultures, and the type 17 helper T cell (TH17)-associated cytokine interleukin 23
256 ntiation of interleukin 17 (IL-17)-producing helper T cells (TH17 cells) and follicular helper T cell
258 tion of interleukin (IL)-17-producing CD4(+) helper T cells (TH17 cells) has a pivotal role in autoim
259 mediated by interleukin 17 (IL-17)-producing helper T cells (TH17 cells) in the peripheral immune and
261 recently discovered interleukin-17 producing helper T cells (Th17), which are fundamental for anti-mi
262 A-regulated pathways that control the type 2 helper T cell (TH2 cell) responses that drive pathogenic
263 bl deficiency skews CD4(+) T cells to type 2 helper T cell (Th2) differentiation, and c-Abl(-/-) mice
267 ate lymphoid cells (ILC2s) and CD4(+) type 2 helper T cells (TH2 cells) are defined by their similar
268 p 2 innate lymphoid cells (ILC2s) and type 2 helper T cells (Th2 cells) are the primary source of int
269 interleukin-33 (IL-33), which induces type-2 helper T cells (Th2 cells) at the site of infection to p
272 with increased levels of eotaxins and type 2 helper T-cell (Th2) cytokines as disease progressed and
273 re prespecified according to baseline type 2 helper T-cell (Th2) status (assessed on the basis of tot
275 by dupilumab of these key drivers of type 2 helper T-cell (Th2)-mediated inflammation could help in
276 the differentiation of CD4(+) IL-9-producing helper T cells (TH9 cells) remain incompletely understoo
277 y which a B cell is optimally activated by a helper T cell that responds to the same, or physically a
279 ility complex (MHC) class II-selected CD4(+) helper T cells that expressed CD8-lineage genes such as
280 dependent skin inflammation driven by CD4(+) helper T cells that produced the cytokines IL-17 and IL-
282 ate that they are not equivalent for CD4(+) 'helper' T cells, the principal orchestrators of adaptive
283 atory disease driven by the T(H)17 subset of helper T cells through molecular mechanisms that remain
284 ulates differentiation of the TH17 subset of helper T cells, thymic T cell development and lymph-node
285 coordinates signals derived from innate and helper T cells to control the production of a regulatory
286 The discovery of the specification of CD4(+) helper T cells to discrete effector 'lineages' represent
287 the expression of genes in the TH2 subset of helper T cells to enhancer occupancy by the BATF-IRF4 tr
290 L-5 circumsporozoite protein (CSP) ratios, a helper T cell type 2 cytokine, correlated with higher od
292 t mRNA level ratio, consistent with a type 2 helper T-cell-type inflammatory response, and subacute f
294 292, enhancing T-cell activation, in NSTEMI helper T cells versus SA and controls (each, p < 0.001),
295 toimmunity and regarded as "extrafollicular" helper T cells, were rare throughout the response, despi
296 ibodies require help from other lymphocytes (helper T cells) which recognize small peptides derived f
297 F) gene (Batf(-/-)) lack TH17 and follicular helper T cells, which demonstrates that Batf is a transc
298 ls and CD4(+) Th cells, including follicular helper T cells, which resulted in high titers of anti-nu
299 103(+) DC subsets induced the TH17 subset of helper T cells, while CD103(-)Sirpalpha(+) DCs induced t
300 thogen containment to the differentiation of helper T cells, yet the cues that position cells in this
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