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1 tions with CD4(+) follicular helper T cells (TFH cells).
2 se development of follicular helper T cells (TFH cells).
3 a cell type with properties of both Treg and TFH cells.
4 tigen uptake and antigen presentation to the Tfh cells.
5 irements for their differentiation: Th17 and Tfh cells.
6 ated interference increased the frequency of TFH cells.
7 ndependent method to identify Ag-specific GC Tfh cells.
8 in the expansion and function of pathogenic TFH cells.
9 ethod identified 85-fold more Ag-specific GC Tfh cells.
10 receptors to form Th1-, Th2-, and Th17-like Tfh cells.
11 iR-155 exhibited decreases in GC B cells and Tfh cells.
12 elated to an effect on PD-L1(hi) B cells and Tfh cells.
13 by impaired differentiation and function of Tfh cells.
14 differentiation in the presence of residual Tfh cells.
15 s are germinal center-homing CXCR5(+)Bcl6(+) Tfh cells.
16 s that regulate the differentiation of human TFH cells.
17 mportant for the function and homeostasis of Tfh cells.
18 the presence of IL-12 and IL-21 to generate TFH cells.
19 ut-homing alpha4beta7 integrin expression on Tfh cells.
20 -1 included TFR cells in their definition of TFH cells.
21 ulating Tfr cells, leading to suppression of Tfh cells.
22 ncreased recruitment of T follicular helper (TFH) cells.
23 pment and maturation of T follicular helper (Tfh) cells.
24 ukin-4 (IL-4)-committed T follicular helper (Tfh) cells.
25 per 17 (Th17) cells and T follicular helper (Tfh) cells.
26 in germinal center (GC) T follicular helper (Tfh) cells.
27 ion and accumulation of T follicular helper (TFH) cells.
28 .8% after therapy), and decreased numbers of Tfh cells (12% +/- 1.3% before therapy vs 8% +/- 0.9% af
29 sting interactions with T follicular helper (Tfh) cells, a process that depends on antigen uptake and
30 rominently expressed on T follicular helper (TFH) cells, a specialized CD4(+) T cell subset that orch
31 surement of Ag-specific T follicular helper (TFH) cell activity in rhesus macaques has not previously
32 T-bet and STAT4 are coexpressed with Bcl6 in Tfh cells after acute viral infection, with a temporal d
35 cells into systemic sites, boosted systemic Tfh cell and auto-antibody responses that exacerbated ar
39 ells modulated IL-21 receptor expressions on TFH cells and B cells, and their suppressive activities
40 ells induced a distinct suppressive state in TFH cells and B cells, in which effector transcriptional
42 ion had phenotypic or functional features of Tfh cells and contribute to the production of HCV-specif
45 deficiency induces excessive development of TFH cells and GC responses in a T-cell-intrinsic manner.
47 gamma(KO) mice induced higher proportions of TFH cells and germinal center (GC) B cells following imm
50 ates the ontogeny and homeostasis of B6.Sle1 TFH cells and influences the function of TFH cells durin
51 ndicate that T-bet is expressed with Bcl6 in Tfh cells and is required alongside STAT4 to coordinate
52 ETV5 expression is derepressed in Cic null TFH cells and knockdown of Etv5 suppresses the enhanced
53 ells or CD25 in dendritic cells have reduced Tfh cells and mount defective T-cell-dependent plasma ce
54 characteristics of both follicular and blood Tfh cells and of the IL-21/IL-21R system in the context
55 evidenced by reduced expression of CD40L on Tfh cells and reduced B cell proliferation in treated mi
56 ith acute HCV infection expressed markers of Tfh cells and secreted interleukin 21 in response to HCV
57 e observed the development of IL-4-producing TFH cells and TH2 cells in draining lymph nodes after ai
58 onally, and functionally similar to lymphoid Tfh cells and that such HIV-specific Tfh cells were incr
60 ifficulty of quantifying antigen-specific GC Tfh cells and the difficulty of tracking GC in human and
63 uency of total and SIV Env-specific IL-21(+) TFH cells and total germinal center B cells, the size an
65 te interactions between T follicular helper (Tfh) cells and B cells are essential for promoting prote
66 induced higher rates of T follicular helper (Tfh) cells and germinal center (GC) B cells from drainin
67 to the hypothesis that T follicular helper (Tfh) cells and germinal centers (GC) play a critical rol
71 y T cells that suppress T follicular helper (Tfh) cells and the generation of high affinity antibody-
72 f CXCR5 expression by B follicular helper T (Tfh) cells and the subsequent discovery of their depende
73 which persists in follicular helper T cells (TFH cells), and Epstein-Barr virus (EBV), which persists
74 owed more robust Id2 expression than that of TFH cells, and depletion of Id2 via RNA-mediated interfe
75 onal and phenotypic similarities to lymphoid Tfh cells, and hence representing peripheral Tfh (pTfh)
76 e highly dependent on the activity of CD4(+) Tfh cells, and may be constrained by host tolerance cont
77 s share some phenotypic characteristics with TFH cells, and studies that showed that TFH cells are hi
78 s the diversity among IL-21 producing CD4(+) Tfh cells, and the interrelationship between the intesti
81 ly, our results indicate that IL-4-producing Tfh cells are central orchestrators of the type 2 immune
83 ions has been challenging, as Ag-specific GC Tfh cells are difficult to identify by conventional intr
85 with TFH cells, and studies that showed that TFH cells are highly permissive to HIV-1 included TFR ce
87 ummary, AIM demonstrates that Ag-specific GC Tfh cells are intrinsically stingy producers of cytokine
97 evidence suggests that T follicular helper (Tfh) cells are the primary producer of IL-4 in the react
99 dence on BCL6 that led to the recognition of Tfh cells as an independent helper subset and accelerate
100 work identified PD-1(+) follicular helper T (Tfh) cells as an important cellular compartment for vira
103 for differentiation of T follicular helper (TFH) cells, but not TH1 effectors, elicited by viral inf
104 Altogether, mTOR acts as a central node in Tfh cells by linking immune signals to anabolic metaboli
105 ic germinal center (GC) T follicular helper (Tfh) cells by cytokine production has been particularly
107 Abnormal development of follicular helper T (TFH) cells can induce the GC response to self-antigens,
108 and promotes the induction of follicular Th (TFH) cells, CD4(+) T cells that support B cell affinity
109 lated to that of CD4(+) T follicular helper (TFH) cells, CD8(+) T cell memory precursors and haematop
110 Therapy inhibited excessive accumulation of Tfh cells coexpressing IL-21 and IFN-gamma, and suppress
112 ession of Aiolos was elevated in Ag-specific TFH cells compared with that observed in non-TFH effecto
113 Here we show that a proportion of human TFH cells contain dense-core granules marked by chromogr
117 dies on the mechanisms of induction of GFP(+)Tfh cells demonstrated that they required the intestinal
118 t that deficient activities might impair the TFH cell-dependent control of humoral immunity and might
119 ate cellular responses, but their control of TFH cell-dependent humoral immune responses is unknown.
120 responses during the sensitization phase or Tfh cell depletion prevented Th2 cell-mediated responses
122 duction, and autoantibodies, indicating that Tfh cell-derived IL-21 is critical for pathological B ce
126 these studies suggest that requirements for Tfh cell development change in lymphopenia-associated au
130 ions upon viral infection because of reduced Tfh cell differentiation and defective expression of pro
132 and 2 (mTORC1 and mTORC2) are essential for Tfh cell differentiation and GC reaction under steady st
133 IL-10 influences the balance between Th1 and Tfh cell differentiation and negatively regulates the de
134 LRBA deficiency reflects impaired control of TFH cell differentiation because of profoundly decreased
136 ic cells in the outer T zone further augment Tfh cell differentiation by producing membrane and solub
137 cient regulatory T cells suppressed in vitro TFH cell differentiation in a CTLA4-dependent manner.
138 nd knockdown of Etv5 suppresses the enhanced TFH cell differentiation in Cic-deficient CD4(+) T cells
142 Mechanistically, SOCE controlled Tfr and Tfh cell differentiation through NFAT-mediated IRF4, BAT
143 -6, a transcriptional repressor critical for Tfh cell differentiation, and inhibition of LFA-1 abolis
144 pression of TFH cell motility, alteration of TFH cell differentiation, reduced TFH abundance and supp
145 e, the role of miR-31 is restricted to human TFH cell differentiation, reflecting a species specifici
150 lyses included in vitro follicular helper T (TFH) cell differentiation and cTFH/naive B-cell cocultur
152 suggest that water-in-oil adjuvants promote Tfh cell-dominated responses by triggering endogenous al
153 le1 TFH cells and influences the function of TFH cells during aberrant germinal center B cell respons
154 cells were required to expand IL-4-committed Tfh cells during the sensitization phase, but did not di
156 lts define unique functions for LFA-1 in the Tfh cell effector program and suggest that integrin acti
157 n mice with viral infections, virus-specific Tfh cells expand and are required to contain the infecti
159 helper (TFH) cells, is critical as aberrant TFH cell expansion is associated with autoimmune disease
162 pted as being important for the induction of Tfh cell fate decision, other molecules may play key rol
164 quantified SIV Env-specific IL-21-producing TFH cells for the first time, to our knowledge, in a non
165 young and aged animals during infection, but TFH cells from aged mice exhibit significant differences
166 a) demonstrated a more diverse repertoire of TFH cells from female CKO mice than of those from wild-t
167 lating Tfh cells are produced by movement of Tfh cells from lymph nodes after dendritic cell contact.
169 ged environment thus impact antigen specific TFH cell function and formation, which contribute to red
171 entiation, and inhibition of LFA-1 abolished Tfh cell generation and prevented protective humoral imm
172 DCs specifically enhanced the development of Tfh cells, germinal center B cells and antibody response
174 ary lymphoid follicles, follicular helper T (TFH) cells have previously been shown to be highly permi
176 nd is required alongside STAT4 to coordinate Tfh cell IL-21 and IFN-gamma production and for promotio
179 restingly, OX40 was coexpressed with ICOS on Tfh cells in and around the GC, and ICOS-ICOSL interacti
180 c deletion of ICOS impacted the expansion of TFH cells in B6.Sle1 mice and inhibited the differentiat
182 ssay identified >10-fold more Ag-specific GC Tfh cells in HIV Env protein-immunized macaques (BG505 S
185 thors show that Def6 limits proliferation of TFH cells in mice via alteration of mTORC1 signaling and
189 lity, restricted expansion of antigen-pulsed Tfh cells in vitro, and possessed a unique gene expressi
195 o be selective for Treg, Th1, Th2, Th17, and Tfh cells, including CD194 (CCR4)(+)FOXP3(+) Treg and CD
196 Our results suggest that the SIV-specific TFH cells, initially induced by replicating adenovirus-r
197 the impact of HIV antigenemia on B cells and Tfh cell interactions warrants further exploration.
198 by driving differentiation and egress of PP Tfh cells into systemic sites, boosted systemic Tfh cell
199 fector cells, as the biological role of a GC Tfh cell is to provide help to individual B cells within
201 on, generating balanced responses of Th1 and Tfh cells is important to induce effective cell-mediated
202 CXCR5(+)PD-1(+)ICOS(+)-activated circulating Tfh cells is increased both in children with newly diagn
203 stinal helminth infection, IL-4 derived from Tfh cells is required for IgE class switching and plasma
204 The recently described T follicular helper (Tfh) cell is required for the production of high affinit
205 production of IL-21 by T follicular helper (Tfh) cells is vital in driving the germinal centre react
206 ranscription factor for T follicular helper (TFH) cells, is critical as aberrant TFH cell expansion i
207 A new T-cell subset, follicular helper T (TFH) cells, is specialized in supporting B-cell maturati
208 ed the interaction between MZB cells and pre-TFH cells, leading to PDL1-mediated suppression of TFH c
210 eukin 2 to CD4(+) T cells, thereby enhancing Tfh cell master regulator Bcl-6 in a dendritic cell-depe
214 GC B cells via cognate interaction; thus, GC Tfh cells may be stingy cytokine producers, fundamentall
217 lls, leading to PDL1-mediated suppression of TFH cell motility, alteration of TFH cell differentiatio
218 ter contact with follicular dendritic cells, Tfh cells move into the germinal centre and provide help
219 +) T cells resulted in a marked reduction in TFH cell numbers and IgE antibody levels, but type 2 cyt
222 found to be polyclonal and related to GFP(-)Tfh cells of Peyer's Patches in TCR repertoire compositi
226 ), and positive correlations with numbers of Tfh cells (P = .03) and serum levels of cryoglobulin (P
229 icacy of HIV/SIV vaccine candidates and that TFH cells play a pivotal role in aiding B cell maturatio
233 essive expansion of the T follicular helper (TFH) cell pool is associated with autoimmune disease and
234 ubsets, including similarity between Th1-Th2-Tfh cell populations and Th17 cells, as well as similari
237 (DCs) are important for T follicular helper (Tfh) cell priming, how this process is regulated in vivo
239 have impeded our understanding of the GC and Tfh-cell processes involved in bnAb generation, includin
241 Whereas Group A Streptococcus-specific GC Tfh cells produced minimal detectable cytokines by intra
252 ne assays missed 98% of Ag-specific human GC Tfh cells, reflecting the biology of these cells, which
253 riguingly, this suggests that broadening the Tfh cell repertoire by vaccination may speed up the evol
255 the Tfh cell response or the breadth of the Tfh cell repertoire markedly facilitates the evolution o
257 ce did not generate an excessive primary CD4 TFH cell response nor an enhanced alloantibody reaction.
261 a agonist pioglitazone significantly reduced TFH cell responses in female mice while pioglitazone and
263 pathogen-associated molecular patterns, the Tfh cell responses observed were dependent, in part, on
265 ine responses, impaired follicular helper T (TFH) cell responses and reduced numbers of plasma cells.
269 TORC2 in T cells exerted distinct effects on Tfh cell signature gene expression, whereas increased mT
272 viously included in the follicular helper T (TFH) cell subset, which consists of cells that are highl
273 n of humoral responses: T follicular helper (Tfh) cells support germinal center formation and provide
278 uately supported Bcl6 and ICOS expression in TFH cells, Tcf1 long isoforms remained important for sup
280 ly capturing and presenting more peptides to Tfh cells than other lineages of more specific B cells.
281 in mice, we show that OX40 was expressed on Tfh cells that accumulated at the T/B borders in the whi
283 nown to be regulated by follicular helper T (TfH) cells, the mechanism by which B cells initially see
285 peripheral blood counterparts of lymph node Tfh cells to assess the immune response and the influenc
288 find that TFR cells are more permissive than TFH cells to R5-tropic HIV-1 ex vivo TFR cells expressed
292 del, we demonstrated that Peyer's patch (PP) Tfh cells were essential for gut commensal segmented fil
294 ymphoid Tfh cells and that such HIV-specific Tfh cells were increased in RV144 trial vaccine recipien
296 y impaired formation of follicular helper T (Tfh) cells, which are essential for humoral immunity.
297 of cognate peptides to follicular helper T (Tfh) cells, which provide survival signals to the B cell
298 fic microbiota regulate T follicular helper (Tfh) cells, whose excessive responses can inflict antibo
299 he multiple correlations of SIV Env-specific TFH cells with systemic and mucosal SIV-specific B cell
300 ifying vaccine induction of HIV/SIV-specific TFH cells would greatly benefit vaccine development.
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