ライフサイエンスコーパス: mature B cell

1 ant genes and are generated through CSR in a mature B cell.

2 is essential for the homeostatic survival of mature B cells.

3 tribution to the survival and maintenance of mature B cells.

4 jor antibody isotypes on the surface of most mature B cells.

5 ment, enabling the expression of VRC26UCA in mature B cells.

6 is a transmembrane glycoprotein expressed by mature B cells.

7 role for Fbw7 in the survival and fitness of mature B cells.

8 o oncogenic translocations/amplifications in mature B cells.

9 were largely demethylated in pro-, pre-, and mature B cells.

10 n later stage B cells, including circulating mature B cells.

11 their ability to differentiate in vitro into mature B cells.

12 quences constructed by NextGen sequencing of mature B cells.

13 ts, and in IgH class switch recombination in mature B cells.

14 ulosclerosis in Jh mice, a strain that lacks mature B cells.

15 sential regulator of cellular homeostasis in mature B cells.

16 blocks by expressing bnAbs conditionally in mature B cells.

17 block at the pro-B cell stage and a lack of mature B cells.

18 ovel function for IRF4 in the homeostasis of mature B cells.

19 clonal deletion fails to rescue survival of mature B cells.

20 vel: HSPCs, common lymphoid progenitors, and mature B cells.

21 g role for CAML in the long-term survival of mature B cells.

22 a CD19-Cre driver strain, we deleted PTIP in mature B cells.

23 a resulted in increased amounts of Foxp1 and mature B cells.

24 B-cell transition, leading to a reduction in mature B cells.

25 differentiation and functional reactivity of mature B cells.

26 1, adaptive immunity, alphabeta T cells, and mature B cells.

27 repertoire, and antigen-driven selection of mature B cells.

28 through editing toward lambda light chain in mature B cells.

29 ytic leukaemia (CLL) is a clonal disorder of mature B cells.

30 previously described, a 2-fold reduction in mature B cells.

31 hrough Nod1 promotes competitive survival of mature B cells.

32 y of Hdac3 is required for the generation of mature B cells.

33 critical for the survival and maturation of mature B cells.

34 on in B-cell development or specifically in mature B cells.

35 characterized by an increased compartment of mature B cells.

36 pacity of EML-TA cells to differentiate into mature B-cells.

37 tic changes that are conserved from HSPCs to mature B-cells.

38 e in which Irf4 was conditionally deleted in mature B cells, after immunization with protein Ags or i

39 Thus, Pdap1 protects mature B cells against chronic ISR activation and ensure

40 yk-deficient mice, the DKO mice can generate mature B cells, albeit at >20-fold reduced B cell number

41 d the expression of 109 lncRNAs in pro-B and mature B cells and 184 lncRNAs in acute lymphoblastic le

42 an inverse correlation between normal human mature B cells and bone marrow plasma cells from patient

43 ng IgG mu heavy chain-null mice deficient in mature B cells and by IgG transfer.

44 urvival and homeostasis of normal peripheral mature B cells and chronic lymphocytic leukemia cells, r

45 ted in a severe loss and reduced lifespan of mature B cells and completely abrogated development of B

46 uch tRNA-derived fragment, cloned from human mature B cells and designated CU1276, in fact possesses

47 s in mice leads to the prolonged survival of mature B cells and expanded B cell compartments in secon

48 rt of the B-cell coreceptor and expressed by mature B cells and follicular dendritic cells.

49 onal BCR is essential for the development of mature B cells and has been invoked in the control of th

50 D20 mAbs that efficiently deplete endogenous mature B cells and homologous CD20+ primary lymphoma cel

51 LC3 subsets with levels intermediate between mature B cells and ILC2.

52 so induced IgG Abs in BAFF-R KO mice lacking mature B cells and in mice deficient in interferon signa

53 8 null allele extinguished IgD expression on mature B cells and increased IgM.

54 cius is unaffected, whereas development into mature B cells and migration from the bursa are blocked

55 the TNF receptor family, is expressed on all mature B cells and on most B-cell lymphomas.

56 tablishes that receptor editing can occur in mature B cells and raises the possibility that this may

57 3 is sufficient to trigger transformation of mature B cells and support the notion that p53 deficienc

58 eath and proliferation in antigen-stimulated mature B cells and that mutations in this switch represe

59 tion and mutation process takes place in the maturing B cell and is responsible for the diversity of

60 -)Mb1-Cre(+/-) mice were virtually devoid of mature B cells, and B220(+)CD43(+) B-cell progenitors ac

61 itch recombination (CSR) occurs in activated mature B cells, and causes an exchange of the IgM isotyp

62 Both CD20 and CD19 mAbs effectively depleted mature B cells, and CD19 mAb treatment depleted plasmabl

63 eficient CD19(-/-) mice, in mice depleted of mature B cells, and in mice treated with CD22 mAb to pre

64 crucial survival factor for transitional and mature B cells, and is a promising therapeutic target fo

65 self renew, continuously differentiate into mature B cells, and thereby maintain peripheral B cell h

66 Cancers arising from mature B cells are characterized by clonal production of

67 In normal adult mice, most mature B cells are enriched for Nod1 up-regulated cells,

68 In response to T cell-dependent antigens, mature B cells are stimulated to form germinal centers (

69 udy, we used conditional deletion of Irf4 in mature B cells as well as wild-type and Irf4-deficient m

70 B-cell receptor (BCR)-mediated activation of mature B cells, as well as higher concentrations of plas

71 The exchange of mature B cells between blood and bone marrow is sensitiv

72 CD19(+)CD5(+)CD23(+)sIgdim expressing clonal mature B cells but also its highly variable clinical cou

73 en implicated in inhibiting BCR signaling in mature B cells but promoting pre-BCR signaling during ea

74 feration of B cell progenitors and activated mature B cells, but is dispensable for B cell survival.

75 plays an essential role in the activation of mature B cells, but less is known about the role of IL-4

76 These cells comprise up to 30% of mature B cells by 22 months.

77 owed in wild-type mice that were depleted of mature B cells by anti-CD20 before or different times af

78 ssociated with endemic Burkitt's lymphoma, a mature B cell cancer characterized by chromosome translo

79 Thus, malaria infection favors mature B cell cancers by eliciting protracted AID expres

80 In mature B cells, class switch recombination (CSR) generat

81 Mature B cells coexpress both IgM and IgD B-cell antigen

82 ch gammaherpesviruses may gain access to the mature B cell compartment by recurrent seeding of develo

83 aB signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence o

84 F3B1 mutation) involvement could be found in mature B cells, consistent involvement at the pro-B-cell

85 muMT (mature B-cell deficient) mice were prone to AAA formatio

86 ls, providing insights toward vaccination of mature B cell-deficient individuals and implications in

87 Mice with specific deletion of Ikaros in mature B cells developed systemic autoimmunity.

88 y what we believe to be a new key factor for mature B cell development and provide a rationale for ta

89 consistent with the signal-strength model of mature B cell development being extended to include stim

90 s in regulating lymphoid lineage commitment, mature B-cell development, and the GC response via disti

91 Mature B cell differentiation involves a well-establishe

92 ms regulated by SOX11 including the block of mature B-cell differentiation, modulation of cell cycle,

93 y modifying the immunoglobulin (Ig) genes of mature B cells directly using genome editing technologie

94 Upon antigen exposure, miR-155(-/-) mature B cells displayed significantly higher double-str

95 cell depletion in mice, that a population of mature B cells distinguishable by IgD(low/-) expression

96 Mature B cells diversify their antibody genes by class s

97 show that mice lacking both PU.1 and SpiB in mature B cells do not generate germinal centers and high

98 ymphocytic leukemia (CLL) is a malignancy of mature B cells driven by B-cell receptor (BCR) signaling

99 6 is a transcriptional repressor required in mature B cells during the germinal center (GC) reaction.

100 bination treatment, although this related to mature B-cell engraftment in NOD.Cg-Prkdc(scid) IL2rg(tm

101 ull activation and complete demethylation of mature B cell enhancers.

102 urface TACI expression is usually limited to mature B cells, excess BAFF promotes the expansion of TA

103 Mature B-cell exit from germinal centers is controlled b

104 These results suggest that residual, mature B cells expressing autoreactive BnAbs, like 2F5 a

105 ts identify IL-2 as a crucial early input in mature B cell fate commitment.

106 EML1 cells differentiate to mature B-cells following treatment with IL7; whereas EML

107 ons, the loss of the BCR can be tolerated by mature B cells for some time, whereas HC-deficient B cel

108 Mice with inducible deletion of Cdc42 in mature B cells formed smaller germinal centers and had a

109 om pediatric thymus, and compared these with mature B cells from fetal and pediatric bone marrow.

110 The development of mature B cells from hematopoietic stem cells is a strict

111 of peripheral B cell tolerance that restrain mature B cells from mounting inappropriate responses to

112 Activated mature B cells from wild-type, Unc93b1(3d/3d)-mutant, or

113 te the biologic effects of Btk inhibition on mature B-cell function and the progression of B cell-ass

114 To evaluate its role in mature B cell functions, a conditional gene deficiency i

115 a similar characterization of primary human mature B cells has been lacking.

116 ic region that controls BAFF-R expression in mature B cells (i.e., the TNFRSF13C promoter).

117 IgD(dim)IgM(dim)CD21(neg)) at the expense of mature B cells (IgD(+)IgM(+)CD21(+)).

118 dies in melanoma, support the involvement of mature B cells in cutaneous immunity.

119 ought to be restricted to antigen-activated, mature B cells in germinal centers.

120 older mice we observe a major population of mature B cells in LNs and in the spleens of mice with hi

121 se the Cre/Lox approach to inactivate p53 in mature B cells in mice (referred to as "CP" B cells) and

122 ng is absolutely required for development of mature B cells in mice.

123 Our data therefore reveal that precursors of mature B cells in NOD mice exhibit an altered migration

124 pleen and preferentially differentiates into mature B cells in response to Plasmodium yoelii infectio

125 where we defined pro-B, pre-B, and immature/mature B cells in the adult kidney.

126 down-regulated proapoptotic Bmf, unlike most mature B cells in the adult.

127 Alcohol consumption also decreased mature B cells in the blood.

128 ed significant, albeit incomplete, rescue of mature B cells in the bone marrow, peripheral blood, spl

129 nses to BCR cross-linking and the absence of mature B cells in the bone marrow.

130 ns in myeloma are thought to occur solely in mature B cells in the germinal center through class swit

131 uggest that IRF4 controls the positioning of mature B cells in the lymphoid microenvironments by regu

132 Mature B cells in the mutant mice displayed nuclear accu

133 lusion, Notch2HCS mutant mice have increased mature B cells in the MZ of the spleen.

134 Mature B cells in the periphery are also reduced and cha

135 etion of Spi1 and Spib resulted in a lack of mature B cells in the spleen and a block in B cell devel

136 in the thymus, and a selective reduction in mature B cells in the spleen and bone marrow.

137 the role of intrinsic expression of Cdc42 by mature B cells in their activation and function.

138 canonical NF-kappaB activation potentials in mature B cells in vivo.

139 erarchy, from stem cells, B-cell precursors, maturing B cells in the germinal center, and circulating

140 MEDI551, an anti-CD19 Ab that depletes mature B cells including plasma cells may offer a compel

141 ndin E2 triggers antibody class switching in mature B cells, increasing the levels of anti-alpha-Gal

142 In response to antigenic stimulation, mature B cells interact with follicular helper T cells i

143 P1 expression, and promotes the shift from a mature B cell into the initial plasmacytic differentiati

144 sed recruitment of dendritic cells (DCs) and mature B cells into the draining lymph nodes and the per

145 When a BCR on a mature B cell is engaged by its ligand, the cell becomes

146 ment, its role in the persistence of resting mature B cells is controversial.

147 s known about how this reservoir of infected mature B cells is maintained for the life of the host.

148 ent development of B lineage precursors into mature B cells is stringently controlled by stage-specif

149 development, but whether it plays a role in mature B cells is unknown.

150 s to the sensitivity of B cell precursors as mature B cells largely tolerated their loss.

151 not only for multiple myeloma, but also for mature B cell leukemia and lymphoma.

152 ells, implying a role in the pathogenesis of mature B-cell leukemia.

153 Finally, K13 protected the mature B-cell line Ramos against anti-IgM-induced apopto

154 s an obligate dimer in B cells and regulates mature B cell lineage fate and humoral immune responses

155 ic Kap1-KO mice displayed reduced numbers of mature B cells, lower steady-state levels of Abs, and ac

156 By screening 269 mature B cell lymphoma biopsies, we also identified a so

157 any genes found as translocation partners in mature B cell lymphoma.

158 ed into patient care for various subtypes of mature B-cell lymphoma (e.g., ibrutinib, idelalisib).

159 cents treated on the French-American-British Mature B-Cell Lymphoma 96 (FAB LMB 96) trial.

160 Mantle cell lymphoma (MCL) is a mature B-cell lymphoma characterized by poor clinical ou

161 Seven patients (0.48%) presented mature B-cell lymphoma consisting of 6 DLBCL and 1 FL.

162 tantly, miR-217 overexpression also promotes mature B-cell lymphomagenesis; this is physiologically r

163 l rate, it modifies lymphomagenesis to favor mature B cell lymphomas that are AID dependent and show

164 PURPOSE OF REVIEW: Mature B-cell lymphomas bearing concurrent chromosomal r

165 sed in most MCL but is not detected in other mature B-cell lymphomas or normal lymphoid cells.

166 d to few ALL subtypes (e.g. TCF3-PBX1), most mature B-cell lymphomas rely on BCR signaling provided b

167 within murine HSPCs, and find that it causes mature B-cell lymphomas that lack Bcl6 expression and ta

168 ilarly contribute to c-myc amplification and mature B-cell lymphomas.

169 may be involved in the pathogenesis of human mature B-cell lymphomas.

170 surface BCR expression is conserved in most mature B-cell lymphomas.

171 acquires frequent inactivating mutations in mature B cell malignancies, especially in the MYD88(L265

172 rolase UCH-L1 is frequently overexpressed in mature B-cell malignancies and is a potent oncogene in m

173 ieve promising clinical responses in various mature B-cell malignancies and might also be useful in d

174 Survival and progression of mature B-cell malignancies depend on signals from the B-

175 iagnosis and guides therapeutic decisions in mature B-cell malignancies while enhancing our understan

176 bserved across a broad range of immature and mature B-cell malignancies, thereby providing a rational

177 cally, biologically and genetically distinct mature B-cell malignancies.

178 ling is a successful therapeutic strategy in mature B-cell malignancies.

179 Mantle cell lymphoma (MCL) is a mature B-cell malignancy that continues to have a high m

180 ll prolymphocytic leukemia (B-PLL) is a rare mature B-cell malignancy that may be hard to distinguish

181 s in 8% of cases the translocation occurs in mature B cells mediated by activation-induced cytidine d

182 We also subjected mice deficient in all mature B cells (muMT mice) to renal I/R and found that t

183 Splenic marginal zone lymphoma (SMZL) is a mature B-cell neoplasm characterized by rather indolent

184 Mantle cell lymphoma (MCL) is a mature B-cell neoplasm initially driven by CCND1 rearran

185 Hairy cell leukemia (HCL) is a chronic mature B-cell neoplasm with unique clinicopathologic fea

186 Mature B-cell neoplasms are the fifth most common neopla

187 ive evaluation of large series of aggressive mature B-cell neoplasms reveals recurrent chromosomal ab

188 ne alterations have been identified in other mature B-cell neoplasms that are usually associated with

189 assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms.

190 c miRNA whose expression is lost in numerous mature B-cell neoplasms.

191 of high-grade (52.9%) and low-grade (47.1%) mature B-cell NHL in CSA was also significantly differen

192 th these prognostic factors in children with mature B-cell NHL.

193 re independent risk factors in children with mature B-cell NHL.

194 as improved survival rates for children with mature B-cell non-Hodgkin lymphoma (NHL); however, assoc

195 arge B-cell lymphoma (MLBL) represents 2% of mature B-cell non-Hodgkin lymphoma in patients </= 18 ye

196 1 years) compared with younger children with mature B-cell non-Hodgkin's lymphoma (NHL) have been his

197 younger than 18 years of age with high-risk, mature B-cell non-Hodgkin's lymphoma (stage III with an

198 and adolescents with high-grade, high-risk, mature B-cell non-Hodgkin's lymphoma and was associated

199 cacy and safety in children with high-grade, mature B-cell non-Hodgkin's lymphoma are limited.

200 Although mature B cell numbers were only mildly reduced, bone mar

201 4 end-ligation activity and severely reduced mature B cell numbers, Lig4(R278H/R278H) (Lig4(R/R)) mic

202 ced deaminase initiates isotype switching in mature B cells of secondary lymphoid structures.

203 GS: AID is expressed in many malignancies of mature B-cell origin and contributes to the development

204 immature B cells occurred with conversion to mature B cells over time.

205 t positive histone epigenetic marks, and the mature B cells partially dedifferentiated, induced RAG-1

206 igh-grade disease with a shift toward a more mature B-cell phenotype, increased cycling and gene expr

207 n the context of a normal immune system, the mature B cell pool is naturally maintained by the renewa

208 B cells are selected to enter the peripheral mature B-cell pool only if they do not bind (or bind lim

209 Mature B cell pools retain a substantial proportion of p

210 king PTPRZ, the proportion and number of the mature B cell population are reduced.

211 The presence of the mature B cell population correlates with enhanced IgG an

212 FOB cells are the dominant mature B cell population in the secondary lymphoid organ

213 Memory B cells are a dynamic subset of the mature B cell population that in some cases can reenter

214 gase Fbw7 is required for the maintenance of mature B cell populations in mice.

215 mphoma (DLBCL) genetically resemble specific mature B-cell populations that are blocked at different

216 ath, and that a Bcl2 transgene reconstitutes mature B-cell populations, respectively.

217 s are culled by immunological tolerance from mature B-cell populations.

218 Fetal mature B cells predominantly used proximal V, D, and J g

219 an B cell culture is the capacity to support mature B cell proliferation.

220 ferentiating B cells can directly generate a mature B cell receptor (BCR) and bypass the requirement

221 , most patients exhibited complete total and mature B cell recovery, whereas memory B cell subsets re

222 ly tolerated or positively selected into the mature B cell repertoire as well as at what stage, to wh

223 critical stage in their development when the mature B cell repertoire is shaped.

224 itive selection by endogenous Ags shapes the mature B cell repertoire.

225 (and may even be actively selected into) the mature B cell repertoire.

226 nal unresponsiveness or anergy exists in the mature B-cell repertoire along a continuum, a fact that

227 early hematopoietic progenitors and splenic mature B cells, respectively.

228 cells during B lymphopoiesis and peripheral mature B cells, respectively.

229 ther factors appear to influence the fate of mature B cells responding to antigen in vivo.

230 of newly generated B cells and about 30% of mature B cells show some degree of autoreactivity.

231 resent, but we also found that Tec-deficient mature B cells showed increased activation, proliferatio

232 We show that mature B cell-specific PTEN overexpression enhances CSR.

233 ls specifically at the transitional to naive mature B cell stage in WAS subjects.

234 autoreactivity are mostly deleted before the mature B cell stage, but are positively selected and exp

235 and partial deletion at the transitional to mature B cell stage, but become Env(-) upon receptor edi

236 lation of GL transcription is delayed to the mature B-cell stage is presently unknown.

237 Marginal zone B cells (MZB) are a mature B cell subset that rapidly respond to blood-borne

238 We have discovered a distinct mature B-cell subset that accumulates with age, which we

239 onal 1 (T1) stage and leads to a decrease in mature B cell subsets and deficits in T cell-dependent a

240 ) mice develop normal B1 and B2 immature and mature B cell subsets and have normal levels of naive se

241 CD21 and CD24 distinguishes transitional and mature B cell subsets in mice.

242 t profound humoral immunodeficiency and lack mature B cell subsets, mirroring deficiency of the cytok

243 imuli confer regulatory functions to various mature B-cell subsets but immature B-cell progenitors en

244 combined heavy-chain genes from immature and mature B-cell subsets in mice, we demonstrate a striking

245 ne mice, whereas they clearly populate 1% of mature B-cell subsets in VH125Tg/NOD mice.

246 ion severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers cou

247 Mature B-cell subsets, immune responses, and memory B-ce

248 Despite sharing some features with other mature B-cell subsets, they are refractory to BCR and CD

249 oject (IGP) to identify unique biomarkers of mature B cell subtypes.

250 ne marrow data, CCAST also reveals two major mature B-cell subtypes, namely CD123+ and CD123- cells,

251 MAP kinase signaling pathway in BAFF-induced mature B cell survival and homeostatic maintenance of B2

252 which are also important for BAFF to promote mature B cell survival.

253 aB family of proteins in B-cell development, mature B-cell survival and B-cell function.

254 e found that, although the Igalpha-deficient mature B cells survive for >20 d in vivo, the HC-deficie

255 tion factor that is expressed exclusively in mature B cells, T-cell progenitors, and plasmacytoid den

256 Taken together, these data indicate that in mature B cells, Tec and Btk may compete for activation o

257 lower median percentages of transitional and mature B cells than age-matched healthy controls (P<0.00

258 el negative selection mechanism for deleting mature B cells that acquire reactivity to self-Ag.

259 crucial survival factor for transitional and mature B cells that acts as rheostat for the maturation

260 mia (CLL) is a disease of an accumulation of mature B cells that are highly dependent on the microenv

261 ignancy characterized by clonal expansion of mature B cells that are resistant to apoptosis.

262 ymphocytic leukemia (CLL) is a malignancy of mature B cells that depend on host factors in the tissue

263 low level (BD(L)) are a novel population of mature B cells that emerge in the spleen from the transi

264 BM, but instead appear to be generated from mature B cells that exhaustively expand during the indiv

265 al activity, we conditionally deleted E3' in mature B cells that possessed Ed(-/-) alleles.

266 kappaB signaling was ablated specifically in mature B cells, the differentiation and/or persistence o

267 a critical role for Cdc42 in the motility of mature B cells, their cognate interaction with T cells,

268 ng by acute deletion of Pten specifically in mature B cells, thereby excluding the developmental impa

269 Although HRS cells are derived from mature B cells, they have largely lost their B cell phen

270 microbial products in promoting survival of mature B cells through up-regulated Nod1, providing a po

271 remia had increased proportions of activated mature B cells, tissue-like memory B cells and plasmabla

272 GR deficiency results in impaired homing of mature B cells to bone marrow, whereas migration to othe

273 role in adaptive immune response by enabling mature B cells to switch from IgM expression to the expr

274 The propensity of mature B cells to transform has been linked to their lon

275 oral immunity is dependent on the ability of mature B cells to undergo antibody gene diversification

276 s as a novel marker for this lymphoma across mature B-cell tumors, and support the distinction of NMZ

277 ng cell growth, were enriched in NMZL across mature B-cell tumors, functionally caused the loss of th

278 or the generation and maintenance of several mature B cell types.

279 Because developmentally matured B cells undergo biologically programmed strand-s

280 Furthermore, upon enhancer loss, the mature B cells unexpectedly underwent reversible retrogr

281 Therefore, the effects of depleting all mature B cells using a potent CD20 mAb, or of depleting

282 ed 33% and then shifted to the nearly final (mature) B cell value by the cycling pre-B cell stage.

283 rentiation of immature into transitional and mature B cells via activation of Erk, likely through a p

284 mediate the development of transitional and mature B cells, we examined B cell development using a m

285 nase (PI3K), a major survival determinant in mature B cells, we indeed found that combining constitut

286 Mature B cells were chronically activated, leading to hy

287 Late pre-B and immature and mature B cells were decreased in the bone marrow of Ebf1

288 T cell-mediated anti-tumor immune responses, mature B cells were depleted from wild-type adult mice u

289 wed us to produce chimeric mice in which all mature B cells were derived entirely from IgG1-expressin

290 ll function in promoting T cell homeostasis, mature B cells were either acutely or chronically deplet

291 atients, the CD19(+)CD24(int)CD38(int) naive mature B cells were high in CHC-HCC patients with good p

292 -I and preB-II, and decreased frequencies of mature B cells were observed in bone marrow aspirates of

293 40 and CD86 expression by B cells, iNKT cell-matured B cells were unable to drive proliferation of au

294 trics can be propagated developmentally into mature B cells where they generate new DSBs downstream o

295 Similar to resting mature B cells, where the B-cell antigen receptor (BCR)

296 us human T cells expedites the appearance of mature B cells, whereas in vivo depletion of T cells ret

297 ch allowed us to generate all-iPSC mice from mature B cells, which have until now failed to support t

298 common leukemia in adults and arises from a mature B cell with either mutated or unmutated IGH@ tran

299 cell development but have reduced numbers of mature B cells with poor germinal centers, as well as in

300 D180 rapidly increased both transitional and mature B cells, with especially robust increases in tran