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1 ivity are increased in efficient cTfh2-17/GC-Tfh cells.
2 to provide static and dynamic information on Tfh cells.
3 ut-homing alpha4beta7 integrin expression on Tfh cells.
4 elated to an effect on PD-L1(hi) B cells and Tfh cells.
5 the presence of IL-12 and IL-21 to generate TFH cells.
6 -1 included TFR cells in their definition of TFH cells.
7 ulating Tfr cells, leading to suppression of Tfh cells.
8 a cell type with properties of both Treg and TFH cells.
9 tigen uptake and antigen presentation to the Tfh cells.
10 irements for their differentiation: Th17 and Tfh cells.
11 ated interference increased the frequency of TFH cells.
12 and influenced the functional properties of Tfh cells.
13 aring of CTLA-4 and more potent targeting of Tfh cells.
14 tor Bach2 as a central negative regulator of Tfh cells.
15 of public TCRbeta clonotypes in circulating Tfh cells.
16 c germinal center B cell production required Tfh cells.
17 ally and clonally similar to germinal center Tfh cells.
18 er the GCs to control/eliminate HIV-infected Tfh cells.
19 om lymph nodes into the blood as circulating Tfh cells.
20 cell follicles, where they can interact with Tfh cells.
21 in germinal center (GC) T follicular helper (Tfh) cells.
22 s, including defects in T follicular helper (Tfh) cells.
23 ion and accumulation of T follicular helper (TFH) cells.
24 nment, including CD4(+) T follicular helper (Tfh) cells.
25 ncreased recruitment of T follicular helper (TFH) cells.
26 +) T cell subset called T follicular helper (Tfh) cells.
27 ting "help" from follicular helper CD4(+) T (Tfh) cells.
28 en-specific B cells and T follicular helper (Tfh) cells.
29 rafollicular CD4(+) and follicular T helper (Tfh) cells.
30 .8% after therapy), and decreased numbers of Tfh cells (12% +/- 1.3% before therapy vs 8% +/- 0.9% af
31 sting interactions with T follicular helper (Tfh) cells, a process that depends on antigen uptake and
33 T cells did not affect T follicular helper (Tfh) cell accumulation unless IL-6R-deficient T cells we
34 T-bet and STAT4 are coexpressed with Bcl6 in Tfh cells after acute viral infection, with a temporal d
36 ells modulated IL-21 receptor expressions on TFH cells and B cells, and their suppressive activities
37 tion promotes caspase-mediated pyroptosis of Tfh cells and controls the development of pathogenic ICO
38 low numbers of activated T cells, including Tfh cells and decreased amounts of intestinal IgA and IL
41 deficiency induces excessive development of TFH cells and GC responses in a T-cell-intrinsic manner.
42 ficient in IL-13 showed decreased numbers of Tfh cells and germinal center B cells and produced signi
43 ndicate that T-bet is expressed with Bcl6 in Tfh cells and is required alongside STAT4 to coordinate
44 ETV5 expression is derepressed in Cic null TFH cells and knockdown of Etv5 suppresses the enhanced
45 mas, engages the inhibitory receptor BTLA on Tfh cells and loss of HVEM leads to exaggerated T cell h
46 required for appropriate ICOS expression in Tfh cells and provides a competitive advantage for Tfh a
47 evidenced by reduced expression of CD40L on Tfh cells and reduced B cell proliferation in treated mi
48 e observed the development of IL-4-producing TFH cells and TH2 cells in draining lymph nodes after ai
50 ifficulty of quantifying antigen-specific GC Tfh cells and the difficulty of tracking GC in human and
52 receptor restricts the expansion of aberrant Tfh cells and the generation of self-reactive antibodies
54 te interactions between T follicular helper (Tfh) cells and B cells are essential for promoting prote
55 induced higher rates of T follicular helper (Tfh) cells and germinal center (GC) B cells from drainin
57 to the hypothesis that T follicular helper (Tfh) cells and germinal centers (GC) play a critical rol
59 ive abundance of CD4(+) T follicular helper (Tfh) cells and regulatory T cells was selectively decrea
60 y T cells that suppress T follicular helper (Tfh) cells and the generation of high affinity antibody-
62 owed more robust Id2 expression than that of TFH cells, and depletion of Id2 via RNA-mediated interfe
63 e highly dependent on the activity of CD4(+) Tfh cells, and may be constrained by host tolerance cont
64 frequencies of antigen-specific GC B cells, Tfh cells, and overall antigen-specific Ab after immuniz
65 s share some phenotypic characteristics with TFH cells, and studies that showed that TFH cells are hi
66 B cells, as well as to T follicular helper (TFH) cells, and directly regulates B cells and TFH in a
68 ly, our results indicate that IL-4-producing Tfh cells are central orchestrators of the type 2 immune
71 with TFH cells, and studies that showed that TFH cells are highly permissive to HIV-1 included TFR ce
72 en together, our data suggest that, although Tfh cells are more prone to harbor viral DNA, other func
73 rsely, in central regions of GC light zones, Tfh cells are much more static, forming long-lasting con
78 ent view is that CD4(+) T follicular helper (Tfh) cells are the main subset regulating autoreactive B
79 ector T cells including follicular helper T (Tfh) cells are the major producers of TLR7-induced IFN-g
80 evidence suggests that T follicular helper (Tfh) cells are the primary producer of IL-4 in the react
82 (Tfh) differentiation and the requirement of Tfh cells as the specialized subset of CD4(+) T cells ne
83 work identified PD-1(+) follicular helper T (Tfh) cells as an important cellular compartment for vira
84 for differentiation of T follicular helper (TFH) cells, but not TH1 effectors, elicited by viral inf
85 Abnormal development of follicular helper T (TFH) cells can induce the GC response to self-antigens,
87 lated to that of CD4(+) T follicular helper (TFH) cells, CD8(+) T cell memory precursors and haematop
88 Therapy inhibited excessive accumulation of Tfh cells coexpressing IL-21 and IFN-gamma, and suppress
90 ession of Aiolos was elevated in Ag-specific TFH cells compared with that observed in non-TFH effecto
93 Here, we review current understanding of how Tfh cells contribute to the selection of GC B cells, wit
96 f tonsillar follicles and influenza-specific TFH-cell (CXCR5+CD57+CD4+ T cell) responses in children,
101 t that deficient activities might impair the TFH cell-dependent control of humoral immunity and might
102 ate cellular responses, but their control of TFH cell-dependent humoral immune responses is unknown.
104 duction, and autoantibodies, indicating that Tfh cell-derived IL-21 is critical for pathological B ce
108 upon allergen exposure play a major role in Tfh cell development, IgE Ab production, and initiation
115 LRBA deficiency reflects impaired control of TFH cell differentiation because of profoundly decreased
117 cient regulatory T cells suppressed in vitro TFH cell differentiation in a CTLA4-dependent manner.
118 nd knockdown of Etv5 suppresses the enhanced TFH cell differentiation in Cic-deficient CD4(+) T cells
120 )-specific transcription factor Thpok during Tfh cell differentiation, GC formation, and antibody mat
121 e molecular mechanism underlying the initial Tfh cell differentiation, however, is still incompletely
122 pression of TFH cell motility, alteration of TFH cell differentiation, reduced TFH abundance and supp
123 e, the role of miR-31 is restricted to human TFH cell differentiation, reflecting a species specifici
130 lyses included in vitro follicular helper T (TFH) cell differentiation and cTFH/naive B-cell cocultur
134 this article, we summarize the role of human Tfh cells during humoral immune responses and discuss th
135 ortant insights into the development of CD4+ Tfh cells during Plasmodium infection and highlights the
139 , we show that in vivo, despite enhanced non-Tfh cell effector functions, the deletion of transcripti
140 sialic acid binding activity, with limiting Tfh cell elicitation a potential constraint to the induc
143 helper (TFH) cells, is critical as aberrant TFH cell expansion is associated with autoimmune disease
144 pted as being important for the induction of Tfh cell fate decision, other molecules may play key rol
148 a) demonstrated a more diverse repertoire of TFH cells from female CKO mice than of those from wild-t
153 mulatory signaling in human regulatory T and Tfh cells, further informing on its potential use in dis
154 d to CTLA-4-Ig led to superior inhibition of Tfh cell, germinal center, and DSA responses in vivo and
155 entification of a circulating counterpart of Tfh cells has allowed us to better understand the contri
157 ary lymphoid follicles, follicular helper T (TFH) cells have previously been shown to be highly permi
158 nd is required alongside STAT4 to coordinate Tfh cell IL-21 and IFN-gamma production and for promotio
161 restingly, OX40 was coexpressed with ICOS on Tfh cells in and around the GC, and ICOS-ICOSL interacti
164 juvants is a rational approach for enhancing Tfh cells in humans, thereby supporting the long-lived h
165 n are discussed, as are the understanding of Tfh cells in infectious diseases, vaccines, autoimmune d
169 thors show that Def6 limits proliferation of TFH cells in mice via alteration of mTORC1 signaling and
170 ne responses and discuss the contribution of Tfh cells in promoting immunity to influenza viruses in
177 lity, restricted expansion of antigen-pulsed Tfh cells in vitro, and possessed a unique gene expressi
181 from mucosal sites and T follicular helper (Tfh) cells in lymph nodes are thought to facilitate spec
182 r, naive mice developed T follicular helper (Tfh) cells in their lung draining lymph nodes and produc
184 o be selective for Treg, Th1, Th2, Th17, and Tfh cells, including CD194 (CCR4)(+)FOXP3(+) Treg and CD
186 endritic cells (DCs) in T follicular helper (Tfh)-cell induction, a T-cell subset critically implicat
187 latory OX40L (OX40 ligand)-OX40 axis reduced Tfh-cell induction by control lung cDC2s.Conclusions: In
189 (-) (Tfh1) subset bias was observed among GC Tfh cells infiltrating the pancreas of NOD mice, which w
190 differentiation (CD) 4+ T follicular helper (Tfh) cells interact with B cells in the germinal centers
191 rol naive B and cognate T follicular helper (Tfh) cell interaction and initiation of the GC reaction.
192 the impact of HIV antigenemia on B cells and Tfh cell interactions warrants further exploration.
193 fector cells, as the biological role of a GC Tfh cell is to provide help to individual B cells within
194 on, generating balanced responses of Th1 and Tfh cells is important to induce effective cell-mediated
195 CXCR5(+)PD-1(+)ICOS(+)-activated circulating Tfh cells is increased both in children with newly diagn
196 e regulatory network in GC B cells, Bach2 in Tfh cells is not coexpressed with Bcl-6 at high levels t
197 Kdelta activity in donor T cells that become Tfh cells is required for cGVHD in a nonsclerodermatous
198 stinal helminth infection, IL-4 derived from Tfh cells is required for IgE class switching and plasma
199 lar migratory behavior is performed by human Tfh cells is unclear, as technology to track them in sit
200 However, while preferential infection of Tfh cells is widely thought to create an important viral
201 ranscription factor for T follicular helper (TFH) cells, is critical as aberrant TFH cell expansion i
202 A new T-cell subset, follicular helper T (TFH) cells, is specialized in supporting B-cell maturati
203 ed the interaction between MZB cells and pre-TFH cells, leading to PDL1-mediated suppression of TFH c
205 eukin 2 to CD4(+) T cells, thereby enhancing Tfh cell master regulator Bcl-6 in a dendritic cell-depe
212 our knowledge, the dynamic behavior whereby Tfh cells migrate in human GC and highlight the heteroge
214 lls, leading to PDL1-mediated suppression of TFH cell motility, alteration of TFH cell differentiatio
216 +) T cells resulted in a marked reduction in TFH cell numbers and IgE antibody levels, but type 2 cyt
217 ays, attended by significant upregulation of Tfh cell numbers that altogether might explain the obser
220 found to be polyclonal and related to GFP(-)Tfh cells of Peyer's Patches in TCR repertoire compositi
224 ), and positive correlations with numbers of Tfh cells (P = .03) and serum levels of cryoglobulin (P
226 , the transcriptional network sustaining the Tfh cell phenotype and function is still incompletely un
228 Each can promote antibody responses but Tfh cells play critical roles during germinal center (GC
231 essive expansion of the T follicular helper (TFH) cell pool is associated with autoimmune disease and
232 ubsets, including similarity between Th1-Th2-Tfh cell populations and Th17 cells, as well as similari
234 cluster-independent increase of follicular (TFH) cells potentially driving the known expansion of B
237 have impeded our understanding of the GC and Tfh-cell processes involved in bnAb generation, includin
241 re efficiently induced key regulators of the Tfh cell program and influenced the functional propertie
244 ne, high-affinity T cells and XCR1(+) DCs or Tfh cell-prone, low-affinity T cells and SIRPa(+) DCs po
248 riguingly, this suggests that broadening the Tfh cell repertoire by vaccination may speed up the evol
250 the Tfh cell response or the breadth of the Tfh cell repertoire markedly facilitates the evolution o
252 6 (BCL6; the master transcription factor for Tfh cells) represses HIV infection of tonsillar CD4(+) T
254 that age-associated defects in the cDC2 and Tfh cell response are not irreversible and can be enhanc
256 e sought to discover what underpins the poor Tfh cell response in ageing and whether it is possible t
257 ce did not generate an excessive primary CD4 TFH cell response nor an enhanced alloantibody reaction.
261 tem-specific B cell and T follicular helper (Tfh) cell responses in the context of influenza infectio
263 ic salivary IgA concentrations and tonsillar TFH-cell responses, and a positive correlation between t
264 Ectopic overexpression of Bach2 in murine Tfh cells resulted in a rapid loss of their phenotype an
265 n CD8 T cells leads to an increase of CD8(+) Tfh cells, resulting in the breakdown of B cell toleranc
268 C B cells, with a particular emphasis on how Tfh cell signals may contribute to lymphomagenesis.
273 viously included in the follicular helper T (TFH) cell subset, which consists of cells that are highl
274 n of humoral responses: T follicular helper (Tfh) cells support germinal center formation and provide
279 uately supported Bcl6 and ICOS expression in TFH cells, Tcf1 long isoforms remained important for sup
281 ly capturing and presenting more peptides to Tfh cells than other lineages of more specific B cells.
282 in mice, we show that OX40 was expressed on Tfh cells that accumulated at the T/B borders in the whi
283 les, we identify a population of circulating Tfh cells that are transcriptionally and clonally simila
285 nown to be regulated by follicular helper T (TfH) cells, the mechanism by which B cells initially see
286 e P2X7 receptor as a checkpoint regulator of Tfh cells; thus, restoring P2X7 activity in SLE patients
288 find that TFR cells are more permissive than TFH cells to R5-tropic HIV-1 ex vivo TFR cells expressed
293 h cell specific in that CTLA-4 expression by Tfh cells was necessary and sufficient for the improved
294 l trial of vaccine formulations, circulating Tfh cells were expanded in Tanzanian volunteers when an
297 could be corrected when follicular helper T (Tfh) cells were induced before macrophage ablation or wh
298 naive T cells to become T follicular helper (Tfh) cells, whereas higher-affinity TCRs promoted the fo
299 y impaired formation of follicular helper T (Tfh) cells, which are essential for humoral immunity.
300 of cognate peptides to follicular helper T (Tfh) cells, which provide survival signals to the B cell