ライフサイエンスコーパス: GC-B

1 GC B cell (GCB)-type diffuse large B cell lymphomas (DLB

2 GC B cell lymphomas maintain their GC transcriptional si

3 GC B cells are short lived and are prone to caspase-medi

4 GC B cells elicited during Pc infection suffer widesprea

5 GC B cells in TLR7-deficient mice proliferated to a less

6 GC B cells of Cdkn1a (-/-) Ezh2 (-/-) mice have high lev

7 GC B cells receive help signals during transient interac

8 GC B cells, in contrast to mature naive B cells, memory

9 GC B-cell selection can lead to four different outcomes:

10 he allosterically activated conformation, 2) GC-B phosphorylation is required for CNP-dependent activ

11 ng purified human tonsillar GC B cells and a GC B cell-like cell line.

12 In a GC B cell-like human B cell line, although IL-21 alone c

13 88P and R655C missense mutations result in a GC-B conformation that mimics the allosterically activat

14 from resting follicular B cell to activated GC B cell.

15 GC Tfh cell is to selectively help adjacent GC B cells via cognate interaction; thus, GC Tfh cells m

16 Although self-ligands directly affect GC B cell responses, the loss of Mer in dendritic cells

17 Neither mutation affected GC-B concentrations.

18 for the efficient selection of high affinity GC B cell clones.

19 Thus, high-affinity GC B cells are selected by a mechanism that involves pro

20 ive PC differentiation of only high-affinity GC B cells remains unknown.

21 We now show that murine Aicda(-/-) GC B cells accumulate as centrocytes and inefficiently g

22 e reported previously that murine Aicda(-/-) GC B cells have enhanced viability and accumulate in GCs

23 AID(+) GC B cells then undergo class-switch recombination and s

24 prevalent in the GC, with up to half of all GC B cells dying every 6 hours.

25 In contrast, although GC B cell formation was markedly reduced in SAP-deficien

26 that although BCR signaling is reduced among GC B cells, a small population of cells exhibiting GC li

27 s associated with diminished plasma cell and GC B cell formation.

28 e stage of the ongoing follicular T cell and GC B cell response.

29 mbers of follicular helper T (TFH) cells and GC B cells, and accelerated production of broad-affinity

30 pite relatively poor cell viability, eGC and GC B-cell cultures produced the highest yields of IgE(+)

31 and B cells cooperate for optimal T(FH) and GC B cell differentiation in response to both model Ags

32 Evaluations of GC T(FH) and GC B cell dynamics including correlation analyses suppor

33 The increased numbers of T(fh) and GC B cells in Taci(-/-) mice are largely a result of up-

34 l allele restores normal levels of T(fh) and GC B cells in Taci(-/-) mice.

35 rge but transient contacts between T(FH) and GC B cells presenting the highest levels of cognate pept

36 nces from retrovirus-specific hybridomas and GC B cells from infected mice revealed Ig heavy-chain V

37 that contemporaneously developing memory and GC B cells differ in their affinity for antigen througho

38 Both naive and GC B cell synapses required proximal BCR signaling, but

39 ave modeled acute EBV infection of naive and GC B cells in mice through timed expression of LMP1 and

40 We provide an atlas of lncRNAs in naive and GC B-cells that indicates their partition into ten funct

41 follicular helper (T(FH)) cell responses and GC B cells with improved Env-binding, tracked by longitu

42 GC Tfh and GC B cell development were blocked by loss of SAP in K/B

43 alphabeta receptor blockade restored Tfh and GC B cell phenotypes in mice containing STAT3-deficient

44 th different magnitude and kinetics, TFH and GC B cell responses in draining lymph nodes.

45 the regulation and proliferation of TFH and GC B cells in vivo and that a decreased TFR/TFH ratio in

46 Remarkably, this enhancement of TFH and GC B cells is already fully functional in 3-wk-old infan

47 ions that mediate differentiation of TFH and GC B cells remain an important area of investigation.

48 between frequencies of TFR and both TFH and GC B cells, as well as levels of CD4(+) T cell prolifera

49 moted humoral immunity by recruiting Tfh and GC B cells, facilitating the formation of GCs, and incre

50 auses cell-intrinsic accumulation of Tfh and GC B cells.

51 lead to unchecked expansion of both TFH and GC B cells.

52 at late times for maintenance of the Tfh and GC B cells.

53 r the persistence of high numbers of Tfh and GC B cells.

54 146a-deficient T cells, prevents the Tfh and GC B-cell accumulation.

55 inal center T follicular helper (GC Tfh) and GC B cells and antibody-secreting cells in the spleen an

56 or the aspartate in the DYG-loop of GC-A and GC-B failed to decrease enzyme phosphate content, consis

57 r guanylyl cyclase domains, such as GC-A and GC-B, also known as Npr1 and Npr2, respectively.

58 ecause ATP allosterically activates GC-A and GC-B, we investigated how ATP binding to the PKD influen

59 rtate, are conserved in the PKDs of GC-A and GC-B.

60 we find a significant decrease in apoptotic GC B cells in B6.Sle1b mice compared with B6 controls.

61 iated developmental arrest and presenting as GC B cells with constitutive activation-induced cytidine

62 at EZH2 mutations initiate FL by attenuating GC B cell requirement for T cell help and driving slow e

63 Within lymph nodes, we observed augmented GC B cell responses and the promotion of T(h)1 gene expr

64 cin complex 1-dependent canonical autophagy, GC B cell autophagy occurred predominantly through a non

65 ic peptide activation of guanylyl cyclase B (GC-B), also known as natriuretic peptide receptor B or N

66 triuretic peptide (CNP), guanylyl cyclase B (GC-B, also known as Npr2 or NPR-B), increase cellular cG

67 amount of antigen captured and presented by GC B cells to follicular helper T cells in the light zon

68 When dysregulated, the same processes cause GC B cells to become susceptible to lymphomagenesis.

69 induced expanded Ag-specific CD73(+)CD80(-) GC B cells in proximal- and distal-draining lymph nodes,

70 8-fold expansion of GL7(+) CD38(lo) CD95(+) GC B cells, and a 2.5- and 5-fold expansion of CD138(+)

71 formation; however, the signals that commit GC B cells to the memory pool remain unclear.

72 In contrast to this complexity, GC B cells are canonically divided into two principal po

73 Consequently, GC B cells extracted antigen with better affinity discri

74 ositive feedback loop in which EZH2 controls GC B cell proliferation by suppressing CDKN1A, enabling

75 ng the transcriptional network that controls GC B cell and plasma cell differentiation.

76 In contrast, the R655C mutation converted GC-B-7A from CNP-unresponsive to CNP-responsive.

77 Here we show that CXCR4-deficient GC B cells, which are restricted to the LZ, are graduall

78 Dicer-deficient GC B cells express higher levels of cell cycle inhibitor

79 how that dissemination of Galpha13-deficient GC B cells additionally requires an egress-promoting rec

80 kinase-dead mutant donor bone marrow-derived GC B cells still supported BO cGVHD generation.

81 ion suppressed T follicular differentiation, GC B cell frequency, and class switching of GC B cells t

82 mLANA contributes to gammaherpesvirus-driven GC B cell proliferation.

83 mechanisms that are commonly targeted during GC B cell lymphomagenesis.

84 to visualize, purify, and characterize dying GC B cells.

85 f4 was required for the development of early GC B cells.

86 expression in B cells substantially enhanced GC B cell responses and anti-Plasmodium Ab production.

87 factor networks that operate within exiting GC B cells.

88 os(+/+) mice, leading to substantially fewer GC B cells and a decrease in affinity, but not productio

89 portant process shaping the success of T(fh)-GC B cell interactions by influencing costimulatory and

90 malignancy, namely follicular lymphoma (FL), GC B cell-diffuse large B cell lymphoma (GCB-DLBCL), and

91 ed cytokine, provides instructional cues for GC B cell maturation, with disruption of IL-21 signaling

92 stinct genetic and epigenetic etiologies for GC B-cell transformation.

93 e germinal center (GC) stage is required for GC B-cell function.

94 Our study establishes a central role for GC B cell-specific CD84 and Ly108 expression in maintain

95 is crucial to develop targeted therapies for GC B cell dysfunctions, including lymphomas.

96 es in TFH to TFR ratio, GC T cell frequency, GC B cell frequency, and class switching of GC B cells t

97 y expressed in plasma cells, but absent from GC B cells.

98 s, explaining how indolent tumors arise from GC B cells.

99 gene expression diverges significantly from GC B cells, underlying mechanisms that alter the activit

100 lar lncRNA expression pattern, distinct from GC-B cells.

101 Our data explain how GC B cells with the highest affinity for antigen are sel

102 e-specific redox responses distinguish human GC B cells.

103 e-cell (sc) transcriptomic analysis on human GC B cells and identified multiple functionally linked s

104 On human GC B-cells, this sulfate modification is lost, giving ri

105 We show here that IgE(+) GC B cells are unfit to undergo the conventional GC diff

106 erwise predominantly expressed by Il17ra (+) GC B cells in BXD2 mice.

107 IL-23 acts indirectly on Il17ra (+) GC B cells to facilitate CSR-related base excision repai

108 twork of Tfh cells in a different way, as in GC B cells.

109 However, the role of GC T(FH) cells in GC B cell responses following various simian immunodefic

110 protein levels are positively correlated in GC B cells.

111 Mice lacking Crebbp in GC B cells exhibited hyperproliferation of their GC comp

112 gnaling downstream of the BCR is dampened in GC B cells, raising the possibility that Ag presentation

113 l-zone B cells and a significant decrease in GC B cells.

114 cific knockout of caspase-9 had decreases in GC B cells and Ab production after immunization.

115 deficient in miR-155 exhibited decreases in GC B cells and Tfh cells.

116 RELB/NF-kappaB2 deficiency in GC B cells was associated with impaired cell-cycle entry

117 at FOXP1 is physiologically downregulated in GC B cells and that aberrant expression of FOXP1 impairs

118 led the GNA13-deficient state exclusively in GC B cells by crossing the Gna13 conditional knockout mo

119 este homolog 2 (EZH2) is highly expressed in GC B cells and is often constitutively activated in GC-d

120 ncodes a protein that is highly expressed in GC B cells that promotes plasma cell differentiation and

121 LMP expression in GC B cells impeded the GC reaction but, upon loss of T-c

122 d a substantial impact on gene expression in GC B cells including pathways of cell cycle progression,

123 rs by eliciting protracted AID expression in GC B cells.

124 k and in turn stabilizes Bcl-6 expression in GC B cells.

125 The function of EZH2 in GC B cells remains largely unknown.

126 he expression of PC transcription factors in GC B cells.

127 m for future elucidation of LMO2 function in GC B cells and DLBCL pathogenesis.

128 g this integrin has a regulatory function in GC B cells.

129 activated genes with important functions in GC B cells and plasma cells by inducing and maintaining

130 Bcl-6 directly repressed Hhex in GC B cells.

131 This was concomitant with an increase in GC B cells and augmented insulin autoantibody production

132 f the GC reaction, results in an increase in GC B cells and enhances B cell proliferation in mice.

133 es to haptens, clonal diversity increased in GC B cells as early "winners" were replaced by rarer, hi

134 find that UCH-L1 is specifically induced in GC B cells in mice and humans, and that its expression c

135 The chromodomain protein CBX8 is induced in GC B cells, binds to H3K27me3 at bivalent promoters, and

136 essary for efficient expansion of latency in GC B cells, suggesting that the development of pharmacol

137 stark contrast to the regulatory network in GC B cells, Bach2 in Tfh cells is not coexpressed with B

138 ng conditional deletion of relb and nfkb2 in GC B cells, we here report that ablation of both RELB an

139 ates targets in diverse non-Ig passengers in GC B cells at levels similar to those of V exons, defini

140 vation of the canonical NF-kappaB pathway in GC B cells controls GC maintenance and differentiation t

141 to orchestrate gene expression patterning in GC B cells through both transcriptional and biochemical

142 omatic hypermutation process taking place in GC B cells in both mice and humans, thus leaving open wh

143 ntrolled a unique transcriptional program in GC B cells that promoted optimal GC polarization and cho

144 lls, and to higher levels of BCL6 protein in GC B cells.

145 i-IL-21 treatment also led to a reduction in GC B cells, CD138(hi) plasmablasts, IFN-gamma-dependent

146 their genomic loci and are down-regulated in GC B cells.

147 ion by the post-fusion HA antigen results in GC B cells targeting the occluded epitope, and induces a

148 though whether IRF4 plays a distinct role in GC B cells remains contentious.

149 that miR-217 is specifically upregulated in GC B cells.

150 long bone growth, and missense mutations in GC-B cause dwarfism.

151 uency of Tfh cells correlated with increased GC B cells, cGVHD, and BOS.

152 In addition to increasing GC B cells, MF59-adjuvanted HlaH35L also increased the f

153 rapamycin treatment predominantly inhibited GC B cell responses during viral infection and that this

154 ted B cells that can then differentiate into GC B cells.

155 R is triggered prior to differentiation into GC B cells or plasmablasts and is greatly diminished in

156 Thus, intrinsic GC B cell flexibility allows for somatic, noncognate B c

157 d sequential switching, whereas the isolated GC B-cell fraction, the main source of IgE(+) PCs, gener

158 re, high-throughput epitope mapping of local GC B cells is used to identify conserved HA epitope sele

159 n in rapamycin-treated mice was due to lower GC B cell responses that are essential for Tfh generatio

160 a signaling, there was an accumulation of LZ GC B cells and reduced antibody affinity maturation like

161 microRNAs expressed in normal and malignant GC B cells identified microRNA 28 (miR-28) as significan

162 is uniquely required by normal and malignant GC B cells.

163 and continually scanned the surface of many GC B cells, forming short-lived contacts that induced se

164 omote GC confinement of both human and mouse GC B cells via Galpha13-dependent pathways, and they sho

165 ein, we show that Ezh2 inactivation in mouse GC B cells caused profound impairment of GC responses, m

166 onditional MYC transgene expression in mouse GC B cells, promotes lymphomagenesis.

167 J passenger allele system to assay, in mouse GC B cells, sequence-intrinsic SHM-targeting rates of nu

168 are highly expressed and functional on mouse GC B cells, removal of single integrins or their ligands

169 lack a P2RY8 orthologue, we show that mouse GC B cell clustering is also dependent on FDCs acting to

170 We also find that mouse GC B cells upregulate alphavbeta3 and adhere to vitronec

171 Accordingly, deletion of nfkb2 in murine GC B cells resulted in a dramatic reduction of antigen-s

172 deletion of caspase 8 specifically in murine GC-B cells results in larger GCs and a delay in affinity

173 We find that egress of Gna13 mutant GC B cells from lymph nodes in the mouse depends on sphi

174 FOXO1-negative GC B cells displayed normal somatic hypermutation but de

175 ng network than IgG(+) FL B cells and normal GC B cells.

176 h activates or decommissions REs from normal GC B cells and commandeers enhancers from other lineages

177 ifferential expression between HL and normal GC-B cells was observed for 475 lncRNA loci.

178 tigen uptake and processing by naive but not GC B cells depend on Cbl and Cbl-b (Cbls), which consequ

179 Single-cell transcriptomics analysis of GC B cells revealed that whereas Ifngr1, Il21r, and Il4r

180 e find that loss of ATM induces apoptosis of GC B cells, likely due to unresolved DNA lesions in cell

181 oring of GC activity by direct assessment of GC B cells and germinal center CD4(+) T follicular helpe

182 that determine the unique characteristics of GC B cells.

183 The molecular control of GC B cell maintenance and differentiation remains incomp

184 lls in GCs and between survival and death of GC B cells.

185 This decrease of GC B cells was accompanied by increased apoptosis in the

186 aturation of the response and development of GC B cells.

187 role for IRF8 and PU.1 in the development of GC B cells.

188 -Cre completely prevented differentiation of GC B cells and plasma cells.

189 premature activation and differentiation of GC B cells and provides an environment tolerant of the D

190 ion and prevents terminal differentiation of GC B cells, which allows antibody diversification and af

191 signaling to promote the differentiation of GC B cells.

192 To explore the dynamics of GC B cell development beyond the known dark zone and lig

193 of ACs in GCs, resulting in dysregulation of GC B cell and CD4(+) Th cell responses and Th1 cytokine

194 ediated selection and sustained expansion of GC B cells for humoral immunity.

195 Ep300 but not Crebbp impaired the fitness of GC B cells in vivo.

196 kappaB1 led to the spontaneous generation of GC B cells.

197 clonal avidities varied greatly, and half of GC B cells did not bind the immunogen but nonetheless ex

198 rate that RTX treatment results in a lack of GC B cells in human lymph nodes without affecting the Tf

199 -L1 cooperates with BCL6 in a mouse model of GC B-cell lymphoma, but not with the development of mult

200 models that an affinity-dependent number of GC B cell divisions overcomes the dichotomy of quality a

201 isms whereby Tfh cells program the number of GC B cell divisions.

202 tly decreased in the frequency and number of GC B cells during the GC reaction.

203 germinal center (GC) size and the number of GC B cells remained the same, BXD2-p19(-/-) mice exhibit

204 uction or loss led to an increased number of GC B cells, to an altered ratio of GC dark zone to light

205 D28 was associated with decreased numbers of GC B cells and a reduction in overall GC size.

206 A13-deficient mice have increased numbers of GC B cells that display impaired caspase-mediated cell d

207 y WT T cells resulted in elevated numbers of GC B cells, PCs, and serum IgG.

208 BAFF and rRABV induced equivalent numbers of GC B cells, suggesting that rRABV-mBAFF augmented the ex

209 Despite finding a small percentage of GC B cells expressing germline transcripts, phylogenetic

210 lymph nodes, and promoted the persistence of GC B cells, detected up to 4 mo after immunization.

211 n repair genes during the dark zone phase of GC B cell development.

212 cle phase transitions and DNA replication of GC B cells.

213 Although selection of GC B cells is triggered by antigen-dependent signals del

214 how Tfh cells contribute to the selection of GC B cells, with a particular emphasis on how Tfh cell s

215 functions as a cell-extrinsic suppressor of GC B cell lymphomagenesis.

216 GC B cell frequency, and class switching of GC B cells to IgG1.

217 GC B cell frequency, and class switching of GC B cells to IgG1.

218 usly attenuating malignant transformation of GC B cells.

219 EZH2 suppresses G1 to S phase transition of GC B cells in a Cdkn1a-dependent manner.

220 te-substituted phosphomimetic mutant form of GC-B also reduced enzyme activity, consistent with ATP s

221 te the lack of impact of Klhl6 deficiency on GC B cell expansion, mutants could contribute to the onc

222 iency leads to increased ICOSL expression on GC B cells and antigen-presenting cells.

223 are replaced by Neu5Ac-containing glycans on GC B-cells.

224 ulator and cyclophilin ligand interactor) on GC B cells, thus limiting their capacity for BLyS bindin

225 The conserved modulation of CD22 ligands on GC B-cells is striking because high affinity glycan liga

226 e that loss of high affinity CD22 ligands on GC B-cells occurs in both mice and humans through altern

227 humans that loss of high affinity ligands on GC B-cells unmasks the binding site of CD22 relative to

228 igh affinity CD22 ligands, which are lost on GC B-cells.

229 Gc) as the sialic acid, which is replaced on GC B-cells with Neu5Ac.

230 us-associated CD84 and Ly108 specifically on GC B cells in B6.Sle1b mice is sufficient to break B cel

231 that can alter lymphoid tissue organization, GC B cell development, and extrafollicular T-bet(+) B ce

232 Downregulation of Ighg2b in BXD2-p19(-/-) GC B cells was associated with decreased expression of C

233 Finally, Peyer's patch GC B cells generate a reservoir of V exons that are high

234 Pathogenic GC B cell and macrophage reactions culminate in antibody

235 e translocations associated with GC and post-GC B-cell lymphomas, the role of downstream AID-associat

236 lls are clonal B cells considered as GC/post-GC B cells.

237 cell transcription patterns with IgG(+) post-GC B cells and show a faster and more vigorous restimula

238 When primary GC B cells were cultured under PC differentiation condit

239 PNGase F deglycosylation of fully processed GC-B reduced GC activity.

240 sis when overexpressed, and thereby promotes GC B cell survival.

241 ion inhibitory receptor, S1PR2, in promoting GC B-cell confinement to GCs.

242 EZH2 protected GC B cells against activation-induced cytidine deaminase

243 g that a pharmacologic approach could reduce GC-B dependent human skeletal overgrowth.

244 f positively selected GC B cells and reduced GC B cell expansion and PC formation.

245 However, how apoptotic caspases regulate GC B cell fate has not been fully characterized.

246 at MYC and MIZ1 form a module that regulates GC B cell fate.

247 e FL, whose pathogenic circuitries resembled GC B or activated B cells.

248 TI-derived IFN-gamma induces most responding GC B cells and AFCs to express high levels of CXCR3, and

249 s that can augment the fitness of responding GC B cells.

250 ucial to ensure a competent immune response, GC B cells are also the origin of most human lymphomas,

251 Additional deletion of Ripk3 restored GC B cells and Ab production in mice with B cell-specifi

252 iously unidentified cells, designated "rogue GC B cells," are a major driver of autoantibody producti

253 ted repeated rounds of divisions of selected GC B cells.

254 ired cell cycle entry of positively selected GC B cells and reduced GC B cell expansion and PC format

255 of MYC-MIZ1 complexes in positively selected GC B cells led to a gene expression profile alike that o

256 PC) formation, so-called positively selected GC B cells.

257 vaccine, elicited potent SARS-CoV-2-specific GC B and T follicular helper (Tfh) cell responses as wel

258 t clusters of AID(+)PNA(+)GL7(+) Ag-specific GC B cells form within the B cell follicles of draining

259 IF stabilization, decreases antigen-specific GC B cells and undermines the generation of high-affinit

260 follicular helper T cells, antigen-specific GC B cells, and high-affinity class-switched antibody pr

261 ells reduced frequencies of antigen-specific GC B cells, Tfh cells, and overall antigen-specific Ab a

262 dering the maintenance of influenza-specific GC B cells.

263 bust overall GC response-the insert-specific GC B cell and Ab responses induced by modified vaccinia

264 vectored vaccines induce Ag insert-specific GC B cell and Ab responses of a magnitude comparable to

265 cell-intrinsic IFN-gamma and T-bet suppress GC B cell responses and anti-Plasmodium humoral immunity

266 key regulatory loci to transiently suppress GC B cell differentiation.

267 iption factor AP4 was required for sustained GC B cell proliferation and subsequent establishment of

268 mmunity as demonstrated by augmented CD4 TFH/GC B cell numbers and hastened islet allograft rejection

269 cognized by the T cells, it was evident that GC B cells presented a broader repertoire of insulin epi

270 We found that GC B cell-intrinsic sensing of self-RNA, but not self-DN

271 l conformation capture (Hi-C), we found that GC B cells undergo massive reorganization of the genomic

272 We report that GC B cell-specific deletion of the NF-kappaB subunits c-

273 We further show that GC B cells and T cells use different mechanisms to regul

274 cells and as a consequence, compromises the GC B response.

275 Thus, MYC constitutes the GC B cell division timer that when deregulated leads to

276 of the genomic architecture that encodes the GC B cell transcriptome.

277 g CRISPR and deleted Crebbp and Ep300 in the GC B cell compartment of mice.

278 ower class-switch recombination (CSR) in the GC B cells, leading to lower serum levels of IgG2b.

279 nity through the extrafollicular and not the GC B cell pathway.

280 The reduced fitness of the GC B cells did not appear to be due to decreased Ag acqu

281 positioning of DCIR2(+) DCs and rescued the GC B cell response.

282 rdinate expression of genes that specify the GC B cell phenotype-most prominently BCL6-was achieved t

283 ependent ABC-like subgroup compared with the GC B-cell (GCB)-like DLBCL subgroup.

284 nd 4) an ATP analog selectively inhibits the GC-B mutants, indicating that a pharmacologic approach c

285 r, T cells lacking IL-21R induced Ab titers, GC B cell frequency, and arthritis development similar t

286 the HVEM-BTLA axis restrains T cell help to GC B cells.

287 with B cell Bcl-2 overexpression, leading to GC B cell outgrowth.

288 Generation of IgE(+) PCs from tonsil GC B cells occurs mainly via sequential switching from I

289 fferentiation using purified human tonsillar GC B cells and a GC B cell-like cell line.

290 ce of ATP were similar to those of wild-type GC-B assayed in the presence of ATP.

291 cumulation of a population of unconventional GC B cells that underwent somatic hypermutation, survive

292 Unlike GC B cells, which are clonally restricted, T(FH) cells d

293 ronchiolitis obliterans (BO), dependent upon GC B cells, Tfhs, and counterbalanced by T follicular re

294 e findings are consistent with a model where GC B cells change from DZ to LZ phenotype according to a

295 Nevertheless, the process whereby GC B cells differentiate into PCs is uncharacterized, an

296 Thus, GNA13 loss is associated with GC B-cell persistence, in which impaired apoptosis and o

297 hich T follicular helper cells interact with GC B cells to produce antibodies that are associated wit

298 ) formation throughout lymphoid tissues with GC B cells binding insulin.

299 s by as much as 80% but failed to inhibit WT-GC-B.

300 istics of light zone, relative to dark zone, GC B cells.