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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
32                                     In mice, TFH cells accordingly promote B cell infiltration into t
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
35                                     Added to TFH cell and B-cell cocultures, they inhibited B-cell di
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
39        We first assessed miRNA expression in TFH cells and defined a TFH-specific miRNA signature.
40 nizations, and the putative central roles of Tfh cells and GC in the generation of HIV bnAbs.
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
49  cells, which is essential for the homing of Tfh cells and the development of B cell follicles.
50 ifficulty of quantifying antigen-specific GC Tfh cells and the difficulty of tracking GC in human and
51         This vaccine enhanced the numbers of Tfh cells and the GC responses, resulting in upregulated
52 receptor restricts the expansion of aberrant Tfh cells and the generation of self-reactive antibodies
53 d carry important implications for targeting Tfh cells and/or B cells therapeutically.
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
56 criptional regulator of T follicular helper (Tfh) cells and germinal center B cells.
57  to the hypothesis that T follicular helper (Tfh) cells and germinal centers (GC) play a critical rol
58                         T follicular helper (TFH) cells and infiltrating stromal cells have been show
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-
61 and a positive correlation between tonsillar TFH-cell and systemic IgG induction after LAIV.
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
67                                           As Tfh cells are also required for the development of plasm
68 ly, our results indicate that IL-4-producing Tfh cells are central orchestrators of the type 2 immune
69              Differentiation and function of TFH cells are controlled by the master gene BCL6, but it
70                                              Tfh cells are essential for the formation and maintenanc
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
74 without affecting the protective function of Tfh cells are unknown.
75                         T follicular helper (Tfh) cells are a specialized T cell subset that regulate
76                         T follicular helper (Tfh) cells are essential for germinal center B cell resp
77                  CD4(+) T follicular helper (Tfh) cells are essential for inducing efficient humoral
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
81                       This paradox intimates Tfh cells as key pathologic effectors, consistent with a
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,
86      Altered control of T follicular helper (Tfh) cells can lead to generation of autoantibodies and
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
89 e cytokines showed a significant decrease in Tfh cells compared with in wild-type mice.
90 ession of Aiolos was elevated in Ag-specific TFH cells compared with that observed in non-TFH effecto
91                   We further show that human Tfh cells comprise two effector states producing either
92      Here we show that a proportion of human TFH cells contain dense-core granules marked by chromogr
93 Here, we review current understanding of how Tfh cells contribute to the selection of GC B cells, wit
94                               route had high Tfh cell counts in lymph nodes but low pTfh cell counts
95 r helper (pTfh) cell counts in blood but low Tfh cell counts in lymph nodes.
96 f tonsillar follicles and influenza-specific TFH-cell (CXCR5+CD57+CD4+ T cell) responses in children,
97             Besides lymphoid tissue-resident Tfh cells, CXCR5(+) circulating Tfh (cTfh) cells have be
98                         Genetic depletion of Tfh cells decreased IgE antibody levels and protected mi
99 i) PD-1(hi) circulating T follicular helper (Tfh) cells decreased after rituximab treatment.
100                      In these outer regions, Tfh cells demonstrate multiple interactions between each
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.
103                                     IL-21, a Tfh cell-derived cytokine, provides instructional cues f
104 duction, and autoantibodies, indicating that Tfh cell-derived IL-21 is critical for pathological B ce
105                                Additionally, Tfh cell-derived IL-4 was required to maintain the Th2 r
106  T-cell homeostasis and negatively regulates TFH cell development and autoimmunity.
107 e sought to assess the role of Breg cells on TFH cell development and function.
108  upon allergen exposure play a major role in Tfh cell development, IgE Ab production, and initiation
109 r 9 and CD40 activation of B cells prevented TFH cell development.
110 I(hi) dendritic cells that are implicated in Tfh cell development.
111 te interactions, drives T follicular helper (Tfh) cell development in germinal centers (GCs).
112 responses, but inhibits T follicular helper (TFH) cell development.
113  demonstrate that Bach2 critically regulates Tfh cell differentiation and CD4(+) T cell memory.
114             Advances in the understanding of Tfh cell differentiation and function are discussed, as
115 LRBA deficiency reflects impaired control of TFH cell differentiation because of profoundly decreased
116                               SFB induced PP Tfh cell differentiation by limiting the access of inter
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
119 hat older people and aged mice have impaired Tfh cell differentiation upon vaccination.
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
124 ription factor Bach2 results in preferential Tfh cell differentiation.
125  with Bcl6 to mediate the effect of Thpok on Tfh cell differentiation.
126 g that Etv5 is a critical CIC target gene in TFH cell differentiation.
127 y regulating Id3 to restrain germinal center TFH cell differentiation.
128 dentified activin A as a potent regulator of TFH cell differentiation.
129 , which is known to promote Th1 and suppress Tfh cell differentiation.
130 lyses included in vitro follicular helper T (TFH) cell differentiation and cTFH/naive B-cell cocultur
131 e composed of two distinct areas in terms of Tfh cell distribution and migration.
132                    CD4+ T follicular helper (Tfh) cells dominate the acute response to a blood-stage
133 rstand the contribution of these circulating Tfh cells during human immune responses.
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
136 nsable for the expansion of antigen-specific Tfh cells during vaccination.
137       IL-21 and IFN-gamma are coexpressed by Tfh cells during viral infections, but transcriptional r
138 ing PD1, TIM3, LAG3, and TIGIT, resulting in TFH cell dysfunction.
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
141             It has long been debated whether Tfh cells exit from lymph nodes into the blood as circul
142  or raptor deletion ameliorates the aberrant TFH cell expansion in mice lacking Def6.
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
145 onal induction of Irf4 expression redirected Tfh cell fate trajectories toward those of Teff.
146                                           In TFH cells, Fgl2 induces the expression of Prdm1 and a pa
147                 The possibility of targeting Tfh cells for the treatment of GC-derived lymphomas is d
148 a) demonstrated a more diverse repertoire of TFH cells from female CKO mice than of those from wild-t
149                                 In contrast, Tfh cells from IL-6R-cKO-infected mice exhibited reduced
150                                  Circulating Tfh cells from patients with systemic lupus erythematosu
151                                This diverted Tfh cells from systemic (non-gut) inflamed sites such as
152 es, which are known to antagonize peripheral Tfh cell function.
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
156                         T follicular helper (TFH) cells have been shown to be critically required for
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
159 ch2 regulates the transcriptional network of Tfh cells in a different way, as in GC B cells.
160        We sought to investigate the roles of TFH cells in allergic immune responses.
161 restingly, OX40 was coexpressed with ICOS on Tfh cells in and around the GC, and ICOS-ICOSL interacti
162       Here we develop mathematical models of Tfh cells in germinal centers to explicitly define the m
163 (AIM) methodology to identify Ag-specific GC Tfh cells in human lymphoid tissue.
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
166                          However the role of TFH cells in LAIV-induced immune responses is unknown.
167 , demonstrate an important role of tonsillar TFH cells in LAIV-induced immunity in humans.
168 ir numbers correlating with the magnitude of Tfh cells in lymphoid tissues.
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
171                                        Thus, TFH cells in the B cell follicle progressively different
172                  This includes discussion of Tfh cells in the human immune system.
173 mount of antigen they capture and present to Tfh cells in the light zone.
174          A great deal has been learned about Tfh cells in the past 10 years, particularly regarding t
175            These findings suggest a role for Tfh cells in the pathogenesis of human T1D and carry imp
176                  Despite the central role of Tfh cells in vaccine responses, there is currently no va
177 lity, restricted expansion of antigen-pulsed Tfh cells in vitro, and possessed a unique gene expressi
178                         T follicular helper (Tfh) cells in germinal centers of secondary lymphoid org
179 repertoire of different follicular helper T (Tfh) cells in germinal centers.
180 ted B-cell receptors by follicular helper T (TFH) cells in germinal centres.
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
183 (+) T cells, especially T follicular helper (Tfh) cells, in HIV-infected lymph nodes.
184 o be selective for Treg, Th1, Th2, Th17, and Tfh cells, including CD194 (CCR4)(+)FOXP3(+) Treg and CD
185       Gene expression analysis revealed that Tfh cells induce Myc expression in light-zone B cells in
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
188                                    Increased Tfh-cell induction by COPD cDC2s correlated with increas
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
204 genes characteristic of follicular helper T (TFH) cell lineage, including Bcl6, Tcf7 and Cxcr5.
205 eukin 2 to CD4(+) T cells, thereby enhancing Tfh cell master regulator Bcl-6 in a dendritic cell-depe
206                     Human Breg cells control TFH cell maturation, expand follicular regulatory T cell
207  on stimulated human T cells, characterizing TFH cell maturation.
208                    Cytokine production by GC Tfh cells may be intrinsically limited in comparison wit
209 llicular regulatory T cells, and inhibit the TFH cell-mediated antibody secretion.
210 ely impaired CD4(+) T cell memory, including Tfh cell memory.
211                 In the outer GC light zones, Tfh cells migrate actively and with a high ability to fo
212  our knowledge, the dynamic behavior whereby Tfh cells migrate in human GC and highlight the heteroge
213  proliferative response of human preexisting Tfh cells more efficiently than belatacept.
214 lls, leading to PDL1-mediated suppression of TFH cell motility, alteration of TFH cell differentiatio
215 GC and highlight the heterogeneity of GC for Tfh cell motility.
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
218 ons between B cells and follicular helper T (Tfh) cells occurring in lymphoid germinal centers.
219 tion expansion of follicular helper T cells (TFH cells) occurs in patients with lupus.
220  found to be polyclonal and related to GFP(-)Tfh cells of Peyer's Patches in TCR repertoire compositi
221 une responses toward antibody production via Tfh cells or inflammation by Teff cells.
222 7-producing Th17 cells, follicular T helper (Tfh) cells, or regulatory T (Treg) cells.
223                               Follicular Th (Tfh) cells orchestrate physiological germinal center (GC
224 ), and positive correlations with numbers of Tfh cells (P = .03) and serum levels of cryoglobulin (P
225 4+CXCR5+interleukin 21+ follicular T-helper (Tfh) cells (P < .01).
226 , the transcriptional network sustaining the Tfh cell phenotype and function is still incompletely un
227                                              Tfh cells play a key role in peanut allergy, and the IL-
228      Each can promote antibody responses but Tfh cells play critical roles during germinal center (GC
229                                              TFH cells play critical roles in the regulation of IgE a
230                         T follicular helper (Tfh) cells play a very important role in mounting a humo
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
233  the differentiation of T follicular helper (TFH) cell populations.
234  cluster-independent increase of follicular (TFH) cells potentially driving the known expansion of B
235                                           As Tfh cells predominantly reside within B cell follicles i
236 ral pathways and genes related to DC-induced Tfh-cell priming.
237 have impeded our understanding of the GC and Tfh-cell processes involved in bnAb generation, includin
238                                              TFH cells produce high amounts of dopamine and release i
239                       T-bet is important for Tfh cell production of IFN-gamma, but not IL-21, and for
240                           OX40 deficiency in Tfh cells profoundly impaired the acquisition of germina
241 re efficiently induced key regulators of the Tfh cell program and influenced the functional propertie
242     Here, we examined the mechanisms whereby Tfh cells program the number of GC B cell divisions.
243                         Follicular helper T (Tfh) cells promote germinal center (GC) B cell survival
244 ne, high-affinity T cells and XCR1(+) DCs or Tfh cell-prone, low-affinity T cells and SIRPa(+) DCs po
245                         Follicular T helper (TFH) cells provide B-cell help and are crucial for gener
246                CXCR5(+) T follicular helper (Tfh) cells provide help to B cells, are essential for th
247                                 These CD8(+) Tfh cells regulate the germinal center B cell response a
248 riguingly, this suggests that broadening the Tfh cell repertoire by vaccination may speed up the evol
249 ey can be rescued by a large fraction of the Tfh cell repertoire in the germinal center.
250  the Tfh cell response or the breadth of the Tfh cell repertoire markedly facilitates the evolution o
251 ereby modulated antigen presentation and the TFH cell repertoire to contribute to autoimmunity.
252 6 (BCL6; the master transcription factor for Tfh cells) represses HIV infection of tonsillar CD4(+) T
253             We studied antigen-specific CD4+ Tfh cells responding to Plasmodium infection in order to
254  that age-associated defects in the cDC2 and Tfh cell response are not irreversible and can be enhanc
255                With advancing age the GC and Tfh cell response declines, resulting in impaired humora
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.
258       Increasing either the magnitude of the Tfh cell response or the breadth of the Tfh cell reperto
259 tibody production and antigen-specific B and Tfh cell responses.
260 CoV-2-specific GC B and T follicular helper (Tfh) cell responses as well as LLPCs and MBCs.
261 tem-specific B cell and T follicular helper (Tfh) cell responses in the context of influenza infectio
262               We measured influenza-specific TFH-cell responses after LAIV by flow cytometry and immu
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
266 l center (GC)-promoting T follicular helper (Tfh) cells, resulting in cGVHD.
267                                       CD8(+) Tfh cells share similar gene signatures with CD4(+) Tfh,
268 C B cells, with a particular emphasis on how Tfh cell signals may contribute to lymphomagenesis.
269                       In contrast to PD-1(+) Tfh cells, SIV-enriched CTLA-4(+)PD-1(-) CD4(+) T cells
270         This CTLA-4-dependent inhibition was Tfh cell specific in that CTLA-4 expression by Tfh cells
271 thermore, formation of memory TH1 and memory TFH cells strongly depended on Tcf1 long isoforms.
272                     The T follicular helper (Tfh) cell subset of CD4(+) Th cells promotes affinity ma
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
275                         Follicular helper T (TFH) cells support terminal B-cell differentiation.
276                               LRBA-deficient TFH cells supported in vitro antibody production by naiv
277                                              TFH cells supported the sustained production of IgE anti
278 40L and chromogranin B granules at the human TFH cell synapse and increases the synapse area.
279 uately supported Bcl6 and ICOS expression in TFH cells, Tcf1 long isoforms remained important for sup
280 d phenotype and reduced the diversity of the TFH cell TCR repertoire.
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
284 eA, can induce abnormal T follicular helper (Tfh) cells that are able to kill B cells.
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
287 encing was performed using TCR-stimulated GC Tfh cells to identify candidate markers.
288 find that TFR cells are more permissive than TFH cells to R5-tropic HIV-1 ex vivo TFR cells expressed
289 by signals delivered by follicular helper T (Tfh) cells to B cells.
290             Interleukin-4 high (IL-4(hi)) FL-TFH cells, unlike FL B cells themselves, triggered CXCL1
291                     STAT4, phosphorylated in Tfh cells upon infection, is required for expression of
292 aboration by HIF-deficient in vivo-generated Tfh cells was impaired.
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
295                                        GFP(+)Tfh cells were found to be polyclonal and related to GFP
296       A large number of follicular helper T (Tfh) cells were also detected in draining lymph nodes of
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

 
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