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 cells adopt a unique activation and transcriptional

3 GC B cells also exhibited greater DNA methylation hetero

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 undergo both somatic hypermutation and isotyp

9 GC B cells were predominantly hypomethylated compared wi

10 GC B cells with high-affinity B cell receptors (BCRs) ar

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

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

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

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

15 V-based vaccines before B cells displaying a GC B cell phenotype (B220(+)GL7(hi)CD95(hi)) are formed,

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

17 optimal production of IL-21, which induces a GC B cell transcriptional profile.

18 88P and R655C missense mutations result in a GC-B conformation that mimics the allosterically activat

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

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

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

22 Neither mutation affected GC-B concentrations.

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

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

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

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

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

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

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

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

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

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

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

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

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

36 onucleotides markedly increased GC T(FH) and GC B cell neonatal responses, up to adult levels.

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

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

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

40 ion and thereby limits the size of T(fh) and GC B-cell compartments and prevents autoimmunity.

41 ory factor-4 (Irf4(-/-)) mice lacked GCs and GC B cells despite developing normal initial hyperplasia

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

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

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

45 l for maintenance of the T(FH) phenotype and GC B cell development.

46 es that contribute to cyclin D stability and GC B cell proliferation.

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

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

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

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

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

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

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

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

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

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

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

58 146a-deficient T cells, prevents the Tfh and GC B-cell accumulation.

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

60 TP binding to the catalytic site of GC-A and GC-B and that ATP increases the magnitude of the inhibit

61 Go6976 inhibits guanylyl cyclase (GC)-A and GC-B.

62 ut reducing the maximal velocity of GC-A and GC-B.

63 of CD80 resulted in an increase in apoptotic GC B cells during the contraction phase of the GC.

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

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

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

67 ranscriptional targets in germinal centre B (GC B) cells are significantly enriched for those differe

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

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

70 Up-regulation of CXCR3 by GC B cells and AFCs and their migration toward its ligan

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

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

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

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

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

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

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

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

79 Here we show that S1P(2)-deficient GC B cells outgrew their wild-type counterparts in chron

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

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

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

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

84 molecules required for T(FH) cells to direct GC B cell responses.

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

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

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

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

89 factor networks that operate within exiting GC B cells.

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

91 t Dicer and probably miRNAs are critical for GC B-cell formation during B-cell terminal differentiati

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

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

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

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

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

97 mum Go6976 increased the potency of ATP for GC-B 4-fold.

98 d WT T(FH) cells reconstituted GC formation, GC B-cell differentiation, and LN cell survival.

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

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

101 ymphomagenesis, which originates mostly from GC B cells and frequently involves MYC chromosomal trans

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

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

104 ver, this subset lacked the capacity to help GC-B cells because of the induction of apoptosis of GC-B

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

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

107 ay disruptions were also identified in human GC B cell lymphoma patient samples.

108 HGAL expression on differentiation of human GC B cells to plasma cell.

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

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

111 e BCL6 and overcome strong autorepression in GC B cells.

112 protein levels are positively correlated in GC B cells.

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

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

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

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

117 of Bim could partially rescue the defect in GC B-cell formation in Dicer-deficient mice.

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

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

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

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

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

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

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

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

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

127 However, its function in GC B cells and DLBCL is currently unknown.

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

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

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

131 he expression of DNA damage-related genes in GC B cells of BXD2-Aicda-DN-transgenic mice.

132 , EZH2-bound promoters are hypomethylated in GC B cells, but many of them are aberrantly hypermethyla

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

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

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

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

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

138 oncogene, latent membrane protein (LMP1) in GC B cells, the presumptive progenitors of HL.

139 th particular emphasis on the role of LRF in GC B cells.

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

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

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

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

144 arked shift in DNA methylation patterning in GC B cells versus resting/naive B cells.

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

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

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

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

149 only DNMT1 was significantly up-regulated in GC B cells.

150 sed expression of caspase 9 messenger RNA in GC B cells, and lower numbers of GCs in the spleens of B

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

152 found that KDM6B transcriptional targets in GC B cells are enriched for genes differentially express

153 eaches expression levels resembling those in GC B cells, and protects pre-B cells from DNA damage-ind

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

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

156 ibition of this pathway results in increased GC B cell proliferation, reduced antibody secretion, and

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

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

159 These observations suggest that EBV-infected GC B cells are a useful model for studying virus-associa

160 it could perform a similar role in infected GC B cells, permitting the survival of potentially patho

161 Moreover, S1P(2) inhibited GC B cell responses to follicular chemoattractants and h

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

163 o undergo expansion and differentiation into GC B cells in the spleen, Ab titers were reduced, and sp

164 Intriguingly, GC B cells in the cell-cycle G(2) period regained respon

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

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

167 erentiation may restore adultlike early life GC B cell responses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 urification of 'untouched' mature GC and non-GC B cells from the spleens of immunized mice and report

183 This protocol can yield GC and non-GC B cells with purities exceeding 90%.

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

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

186 In contrast to its expression in normal GC B cells, IGSF4 was down-regulated and methylated in H

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

188 but not B7-1 was required for acquisition of GC B cell phenotype, plasma cell generation, and virus-s

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

190 that determine the unique characteristics of GC B cells.

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

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

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

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

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

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

197 signaling to promote the differentiation of GC B cells.

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

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

200 me between vaccination and the generation of GC B cells.

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

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

203 We show that EBV infection of GC B cells is followed by upregulation of the DNA methyl

204 ntially expressed following EBV infection of GC B cells were significantly enriched for those reporte

205 pression observed following EBV infection of GC B cells.

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

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

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

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

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

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

212 r, in direct correlation with the numbers of GC B cells and plasma cells elicited.

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

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

215 ice had a significantly higher percentage of GC B cells on days 9, 14, and 21 postimmunization compar

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

217 proximately 1 h and provides a population of GC B cells of sufficient purity and quantity to allow ex

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

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

220 unction to limit selection-based survival of GC B cells could become a novel therapy for the treatmen

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

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

223 ontribute to the malignant transformation of GC B cells into DLBCLs.

224 usly attenuating malignant transformation of GC B cells.

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

226 lls because of the induction of apoptosis of GC-B cells through the FAS/FAS-ligand interaction.

227 Inhibition of GC-B was minimal in the absence of ATP, and 1 mm ATP inc

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

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

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

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

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

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

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

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

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

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

238 ated class switching to IgG1, but few AFC or GC B cells express CXCR3.

239 r staurosporine nor Go6976 activated GC-A or GC-B.

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

241 Pathogenic GC B cell and macrophage reactions culminate in antibody

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

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

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

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

246 show that, surprisingly, most proliferating GC B cells did not demonstrate active BCR signaling.

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

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

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

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

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

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

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

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

255 ivation and migration, S1P(2) helps restrict GC B cell survival and localization to an S1P-low niche

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

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

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 dering the maintenance of influenza-specific GC B cells.

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

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

264 nized GCs and phenotypically defined splenic GC B cells were found in lymph nodes, but not spleens.

265 Bcl2 transgene, FDC ablation led to splenic GC B cell dispersal.

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

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

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

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

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

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

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

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

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

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

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

279 Notably, the GC B cells of Dnmt1 hypomorphic animals showed evidence

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

281 elopmental processes: the termination of the GC B-cell transcriptional program, immunoglobulin (Ig) c

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 g of S1PR2 and S1P biology as it pertains to GC B cells and place this information in the context of

287 ) for survival and proliferation, similar to GC-B cells.

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 igration and interaction dynamics underlying GC B-cell selection events are currently under intense s

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

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 what is known about what determines whether GC B cells become MBCs or PCs.

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

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.