ライフサイエンスコーパス: memory B-cell

1 riptional reprogramming (germinal center and memory B cells).

2 RSV monoclonal antibody derived from a human memory B-cell.

3 E memory resides in allergen-specific IgG(+) memory B cells.

4 f short-lived IgE(+) plasmablasts and IgG(+) memory B cells.

5 eages from ~1,000 single-sorted Env-specific memory B cells.

6 chemokine receptors were up-regulated in CSF memory B cells.

7 etions and with SIV-specific tissue resident memory B cells.

8 walls' - namely, long-lived plasma cells and memory B cells.

9 no associations between C-IRIS and total or memory B cells.

10 AIT on the IgE- and IgG subclass-expressing memory B cells.

11 nse to ensure latent infection of long-lived memory B cells.

12 s to establish life-long latent infection in memory B cells.

13 ic viral infections that periodically engage memory B cells.

14 E2 peptide-binding immunoglobulin G-positive memory B cells.

15 entiation to achieve a lifelong infection of memory B cells.

16 antigen-specific long-lived plasma cells and memory B cells.

17 cular T-bet(+) CD11c(+) plasmablasts and IgM memory B cells.

18 onses than cd/Tdap and increased PT-specific memory B cells.

19 response, to establish long-term latency in memory B cells.

20 scriptional differences between effector and memory B cells.

21 al killer T cells, nonclassical T cells, and memory B cells.

22 matic hypermutation, and differentiated into memory B cells.

23 i.e., activated memory cells and tissue-like memory B cells.

24 re CD5(+), IgM(+) memory, and class-switched memory B cells.

25 differentiation to produce plasma cells and memory B cells.

26 cells, antibody-secreting plasma cells, and memory B cells.

27 reting cells, as well as germinal center and memory B cells.

28 clones, especially among non-class-switched memory B cells.

29 e was observed for CD19(+)CD24(-)CD38(-) new memory B cells.

30 result in the production of Ab-secreting and memory B cells.

31 nters, and they affinity matured, and formed memory B cells.

32 omatic hypermutation, and differentiate into memory B cells.

33 ferentiate into Ab-secreting plasma cells or memory B cells.

34 B-cell dysregulation with decreased switched memory B cells.

35 o the conserved HA stem region and came from memory B cells.

36 rvoir and to establish lifelong infection in memory B cells.

37 apy), decreased percentages of IgM+CD21-/low memory B cells (35.7% +/- 6.1% before therapy vs 14.9% +

38 ogammaglobulinemia (88.9%), reduced switched memory B cells (60.3%), and respiratory (83%) and gastro

39 These results reveal that circulating memory B cells act as a rapidly inducible source of muco

40 es from ~2,200 IgG-secreting activated human memory B cells, activated ex vivo, demonstrating its ver

41 These findings suggest that IgG(+) memory B cell activity in individuals with P. vivax stra

42 isolation and characterization of AHAs from memory B cells, although anti-hinge-reactive B cells wer

43 attribute this to the expansion of atypical memory B cells (AMB), which express multiple inhibitory

44 The formation of effective memory B cell and Ab responses is highly dependent on th

45 mediators that support the durability of the memory B cell and long-lived plasma cell populations are

46 center reaction, limiting the generation of memory B cell and long-lived plasma cell responses.

47 in one case revealed a decrease in naive and memory B cells and a reduction in T follicular helper ce

48 sponses due to the production of Ag-specific memory B cells and Ab-secreting plasma cells.

49 utive years on circulating IgE(+) and IgG(+) memory B cells and allergen-specific Ig levels.

50 type, with a deficiency in marginal zone and memory B cells and an increased frequency of transitiona

51 numbers were normal, but the proportions of memory B cells and EBV-specific effector memory CD8(+) T

52 minal centers (GCs) to produce high-affinity memory B cells and follicular PCs.

53 he generation of long-lived plasma cells and memory B cells and highlight the challenges for successf

54 allergen exposures that recurrently activate memory B cells and identify these as a therapeutic targe

55 ilitated by IgG(+) memory B cells, as IgE(+) memory B cells and IgE(+) plasma cells are extremely sca

56 cantly increased the generation of both TI-2 memory B cells and long-lived antibody secreting cells.

57 cdB involves development of antigen-specific memory B cells and long-lived plasma cells that encode T

58 r affinity maturation and the development of memory B cells and plasma cells, while regulatory CD4(+)

59 ations, including the distinct precursors of memory B cells and plasma cells.

60 erminal centers leading to the generation of memory B cells and plasma cells.

61 While we identified memory B cells and plasmablast/plasma cells with highly

62 human B cells, with a focus on HIV-specific memory B cells and plasmablasts/cells that are responsib

63 ctor that is highly expressed by a subset of memory B cells and restrains the magnitude and duration

64 also significantly increased class switched memory B cells and serum immunoglobulin G (IgG).

65 correlation between numbers of IgM+CD21-/low memory B cells and T-regulatory cells (P = .03), and pos

66 GA binds preferentially to the memory B cells and the activation of sorted B cell subse

67 Single IgG(E)(+) memory B-cell and IgE(+) preplasmablast transcriptomes e

68 hese data define a crucial role for atypical memory B-cells and anti-PS autoantibodies in human malar

69 ctivated B cells and circulating tissue-like memory B cells, and expansion of the B regulatory cells

70 ed frequencies of plasmablasts, PLA-specific memory B cells, and IL-10-secreting CD73(-) CD25(+) CD71

71 alignancies, establishes latent infection in memory B cells, and intermittently produces infectious v

72 n vitro and in vivo against MM plasma cells, memory B cells, and MM-propagating cells.

73 d with levels of Dsg-specific CD19(+)CD27(+) memory B cells, and patients with acute pemphigus showed

74 numbers of naive CD8(+) T cells and switched memory B cells, and TH1/TH2 cytokine imbalance improved

75 s were isolated from single plasmablasts and memory B cells, and their immunogenetic properties were

76 ed rare affinity-matured human NANP-reactive memory B cell antibodies elicited by natural Pf exposure

77 aracterized the immunoglobulin repertoire of memory B-cell antibodies against a linear epitope in the

78 ncreased somatic mutations in virus-specific memory B cell antibody genes, and had persistent higher

79 de evidence that primary FCRL4-bearing human memory B cells are constitutively bound to IgA.

80 Memory B cells are found in lymphoid and non-lymphoid ti

81 and CD8(+) T lymphocytes as well as switched memory B cells are mostly targeted by the injection-only

82 precursors are enriched in antigen binding, memory B cells are not.

83 Circulating memory B cells are recruited to the vaginal mucosa in a

84 es and specificities in the intestine, where memory B cells are repeatedly stimulated by commensal ba

85 he production of long-lived plasma cells and memory B cells are subjects of intensive research and ha

86 this B-cell subset, this establishes IgM(+) memory B cells as a general target of lymphoproliferatio

87 humans by effectively recruiting preexisting memory B cells as well as naive B cells into the respons

88 immunity is primarily facilitated by IgG(+) memory B cells, as IgE(+) memory B cells and IgE(+) plas

89 portantly, vaccination can induce long-lived memory B cells at frequencies comparable to those seen i

90 lls, including follicular memory T cells and memory B cells (B(mems)), that are either pre-positioned

91 nd percentages of peripheral blood total and memory B cells between 27 HIV-infected patients with CM

92 -IL-7 improved the percentages of long-lived memory B cells (Bmem) in the draining LNs and plasma cel

93 However, a role for virus-specific memory B cells (Bmem) within the CNS is poorly explored

94 y influenza infection elicited lung-resident memory B cells (BRM cells) that were phenotypically and

95 BTB32 is highly expressed by mouse and human memory B cells but not by their naive counterparts.

96 lergen-specific germinal centers and IgG1(+) memory B cells by flow cytometry, evaluated humoral resp

97 +) T cells (CD3(+)CD8(+)CD161(+)PD1(+)), and memory B cells (CD3(-)CD19(+)CD20(+)CD24(+)CD27(+)) were

98 numbers of T-regulatory cells, IgM+CD21-/low-memory B cells, CD4+CXCR5+ interleukin 21+ cells, and T-

99 production and find that two subsets of IgG1 memory B cells, CD80(+)CD73(+) and CD80(-)CD73(-), contr

100 spleen and bone marrow IgG plasma cells and memory B cells, compared with controls.

101 1 in B cells supports recall function of the memory B cell compartment by promoting mitochondrial hom

102 election into germinal centers (GCs) and the memory B cell compartment in mice immunized with an HIV-

103 Further, infection failed to stimulate the memory B cell compartment in preimmunized mice, although

104 Thus, the polyclonal memory B cell compartment is composed of B cells that we

105 ith that, failed to significantly expand the memory B cell compartment.

106 Depletion of the memory B-cell compartment contributes to the immunosuppr

107 sensitive method to assess the HLA-specific memory B-cell compartment using luminex SAB technology.

108 analysis does not provide information on the memory B-cell compartment.

109 whereas no effect was observed on the IgE(+) memory B-cell compartment.

110 yet little is known about the effect on the memory B-cell compartment.

111 Lung BRM cells, but not systemic memory B cells, contributed to early plasmablast respons

112 between B-cell/T-cell ratio and nonswitched memory B-cell counts (r = 0.42, P = .03).

113 CVID) present with severely reduced switched memory B-cell counts, and some display an increase of CD

114 in rhesus macaques for years after sustained memory B cell depletion.

115 In this subpopulation, memory B-cell depletion was unable to prevent relapse, w

116 te the presence of concurrent donor-specific memory B cell-derived HLA antibodies (DSA-M) in renal al

117 l culture supernatants can be used to detect memory B cell-derived HLA antibodies, low IgG concentrat

118 .277] 10 cells/L) and selective depletion of memory B cells despite normal B cell survival ligand con

119 Thus, CD11c(+) memory B cells develop normally without T-bet but requir

120 mote aberrant GC responses with autoreactive memory B cell development and plasma cell-derived autoan

121 on of genes related with class-switching and memory B cell development, including Aicda, Ski, Bmi1, a

122 in clonal expansion, isotype switching, and memory B cell differentiation in response to T cell-inde

123 g conserved epitopes and the newly generated memory B cells directed toward H7 strain-specific epitop

124 by increased numbers of exhausted CD21(neg) memory B cells, driven by continuous antigen-specific an

125 ed by loss of naive B cells, loss of resting memory B cells due to their redistribution to the gut, i

126 Ebola-specific memory B cells early in convalescence were low in freque

127 ting HCoVs, suggesting recall of preexisting memory B cells elicited by prior HCoV infections.

128 ependent B-cell responses, while circulating memory B cells, except for those expressing IgG4 and IgE

129 Phospholipase A2-specific IgG4-switched memory B cells expanded after bee venom exposure.

130 expanded upon antigen re-encounter, whereas memory B cells expressed receptors capable of neutralizi

131 d the transcription of genes associated with memory B cell formation and maintenance and maturation o

132 ants with B cells led to greater tissue like memory B cell frequencies.

133 nes that augment B-cell responses and higher memory B-cell frequencies correlate with stronger respon

134 es were increased in STAT3-HIES, while other memory B-cell frequencies except for IgG4(+) cells were

135 Peripheral blood IgE(+) memory B-cell frequencies were increased in STAT3-HIES,

136 Sequencing of the switch regions of memory B cells from European blood donors revealed frequ

137 e isolated monoclonal antibodies (MAbs) from memory B cells from four survivors treated for Ebola vir

138 cell repertoire but are rarely found in IgG memory B cells from healthy individuals.

139 Analysis of single memory B cells from immunized human donors has led us to

140 Strikingly, HBsAg-specific memory B cells from natural controllers mainly produced

141 We previously showed that memory B cells from relapsing-remitting multiple scleros

142 As a consequence, the scarce IgG+ memory B cells from the CTNNBL1 466V/V patient showed a

143 Analysis of memory B cells from the immunized macaque suggests that

144 BPII, we sorted single DBPII-specific IgG(+) memory B cells from three individuals with high blocking

145 While memory B-cells from cirrhotic patients were resistant to

146 ter re-infection, somatically mutated IgM(+) memory B cells function as first responders by rapidly d

147 ect memory B cells, leading to inhibition of memory B-cell function and persistent HCV infection in H

148 Memory B cells had reemerged in 2 of 10 (20%) relapses i

149 Low vaccine responders generated fewer memory B cells, had reduced activation by CD4(+) and CD8

150 velope-specific antibody-secreting cells and memory B cells, higher IgG antibody titers, and better p

151 ces between newly generated and pre-existing memory B cells, highlighting the challenges in achieving

152 to fast reactivation of previously generated memory B cells; however, there is increasing evidence th

153 Frequencies of AF DENV(+) class-switched memory B cells (IgD(-)CD27(+) CD19(+) cells) reached up

154 y of gp41-reactive memory B cells than gp120-memory B cells in adult and neonatal RMs.

155 ies on antigen-dependent activation of human memory B cells in culture.

156 te the role of the CD19(+)CD24(-)CD38(-) new memory B cells in disease progression in CHC patients.

157 e consistent with generation of Env-specific memory B cells in GCs and elicitation of prolonged Env-s

158 investigate the function of subsets of IgG1 memory B cells in IgE production and find that two subse

159 cell tetramer to define Plasmodium-specific memory B cells in parasite-infected mice and demonstrate

160 revealed increased numbers of blood IgG4(+) memory B cells in patients with IgG4-RD.

161 f RTX was considered significant with <0.05% memory B cells in peripheral blood lymphocytes.

162 ession analysis to evaluate antigen-specific memory B cells in peripheral blood of virally-suppressed

163 ium, the percentage of IgA(+)CD38(+)CD138(-) memory B cells in Peyer's patches and LP was decreased o

164 production as well as IgA(+)CD38(+)CD138(-) memory B cells in Peyer's patches and LP.

165 cross-reactive antibodies derived from blood memory B cells in RMs as observed in the HVTN 505 vaccin

166 in priming the human immune system, inducing memory B cells in six V160 recipients at frequencies com

167 s previously identified for T cell-dependent memory B cells, including CD80, PDL2, and CD73, although

168 further reveal that SARS-CoV-2-specific IgG memory B cells increased over time.

169 PT-specific memory B cells increased significantly after r-aP + Td b

170 ll dysfunction (defined by loss of total and memory B cells, increased B regulatory cell [Breg] count

171 ver, only delayed reconstitution of switched memory B cells, independent of immunosuppressive treatme

172 sought to study the population of individual memory B cells induced early in convalescence.

173 heories that reactivation/differentiation of memory B cells into plasma cells is required to sustain

174 d the TLR7-mediated differentiation of human memory B cells into plasmablasts.

175 gE and the clonal selection of high affinity memory B cells into the plasma cell fate, our findings p

176 oth infants and toddlers upon infection, and memory B cells isolated from individuals who previously

177 es the Breg functions mainly by shifting the memory B cells known to contribute to the T cell-depende

178 ptor B7.2 enabled lymphotropic HCV to infect memory B cells, leading to inhibition of memory B-cell f

179 ween cryptococcal meningitis and reduced IgM memory B cell levels, and studies in IgM- and/or B cell-

180 disease relevant genes, as for instance the memory-B cell marker CD27 and PTPRC genes, providing us

181 B cells arose in germinal centers, acquired memory B cell markers, and persisted indefinitely.

182 c mutations but lack expression of classical memory B cell markers.

183 emerging pathogen variants and describe how memory B cells may anticipate infections by such variant

184 HLA-specific memory B cells may contribute to the serum HLA antibody

185 response toward generating abnormal immature memory B cells (MB), while impairing plasma cell differe

186 totoxicity, CD4+ T-cell cytokine production, memory B cell (MBC) activation, and recognition of non-v

187 These involve reengagement of memory B cell (MBC) clones, the diversity and specificit

188 The early memory B cell (MBC) response was mediated by both classi

189 Little is known about enduring memory B cell (MBC) responses to Zika virus (ZIKV) and t

190 followed by GC producing somatically mutated memory B cells (MBC) and long-lived plasma cells.

191 eonates had greater proportions of activated memory B cells (MBC) compared with United States neonate

192 Memory B cells (MBC) respond to secondary antigen challe

193 similar B-blasts can differentiate to become memory B cells (MBC), in which EBV persistence is establ

194 the signals that control differentiation of memory B cells (MBCs) and long-lived plasma cells (LLPCs

195 tures specific for B-cell subsets, including memory B cells (MBCs) and plasma cells (PCs).

196 Memory B cells (MBCs) are critical for the rapid develop

197 Memory B cells (MBCs) are essential for long-lived humor

198 Memory B cells (MBCs) are key determinants of the B cell

199 Memory B cells (MBCs) are key for protection from reinfe

200 Memory B cells (MBCs) are long-lived and produce high-af

201 Memory B cells (MBCs) can respond to heterologous antige

202 Memory B cells (MBCs) expressing the transcription facto

203 a, in which case a subpopulation of atypical memory B cells (MBCs) greatly expands and these MBCs sho

204 nctional properties of T-bet(+) and T-bet(-) memory B cells (MBCs) in the context of the influenza-sp

205 generates protective immunoglobulin M (IgM) memory B cells (MBCs) that express the transcription fac

206 utbreak area were assayed for antibodies and memory B cells (MBCs) to mumps, measles, and rubella.

207 The development of polyclonal memory B cells (MBCs) to the 4 DENV serotypes and ZIKV d

208 inducing long-lived plasma cells (LLPCs) and memory B cells (MBCs), cell types canonically generated

209 We comprehensively review memory B cells (MBCs), covering the definition of MBCs a

210 Decreased counts of blood PCs, memory B cells (MBCs), or both expressing distinct IgA a

211 rom activation of preexisting virus-specific memory B cells (MBCs).

212 ortion of total atypical and total activated memory B cells (MBCs).

213 lity in the frequencies and isotype of CD27+ memory B cells (MBCs).

214 in MCD/C5s and PENLs, suggest that aberrant memory B cells (MBs), and not plasmablasts, are the true

215 The frequencies of IgG memory B cells measured on day 28 after vaccination were

216 to the biological effect of RTX monitored by memory B-cell measurement.

217 y-site comparisons for biochemical and human memory B-cell mutational spectra in an IGHV3-23*01 targe

218 zation had higher total B and CD27(+) IgA(+) memory B-cell numbers (15.2% [95% CI 3.2; 28.7], 22.5% [

219 r Th2, Treg, Treg-memory, and CD27(+) IgA(+) memory B-cell numbers compared to children without atopi

220 clones were seen predominantly among IgM(+) memory B cells of all HCV-infected patients analyzed.

221 tein of SARS-CoV-2, which we identified from memory B cells of an individual who was infected with se

222 The demonstration of gp41 immunodominance in memory B cells of both adult and neonatal RMs indicated

223 the viral surface glycoproteins (HBsAg) from memory B cells of HBV vaccinees and controllers.

224 ceptor expressed on a subpopulation of human memory B cells of mucosa-associated lymphoid tissue.

225 ymphomas, was specifically seen among IgM(+) memory B cells of the patients.

226 selection and eventual differentiation into memory B cells or long-lived plasma cells.

227 01), but higher proportions of IgM+CD21-/low memory B cells (P < .05), CD4+IFNgamma+ cells (P < .01),

228 subsets, including a significant decrease in memory B cells, particularly of marginal zone (MZ) B cel

229 Antibodies produced by memory B cells play an essential role in many of these r

230 rther suggest that establishing an optimized memory B cell pool should be an aim of 'universal' influ

231 ificantly contribute to the TI-2 Ag-specific memory B cell pool.

232 Isolated bNAbs derived from memory B cell pools have been the focus of intense studi

233 We identified the CD19(+)CD27(+) memory B cell population as the major source of IL-10(+)

234 dividuals, particularly in the IgD(-)CD27(-) memory B-cell population in ACPA(+) RA.

235 ue VH and VL sequences from sorted naive and memory B cell populations.

236 ation, and maintenance of antibody-secreting memory B-cell populations to the plasma cell stage.

237 s, lymph node follicular helper T cells, and memory B cell proliferation.

238 ntage for donor-derived T cells and switched memory B cells promoted restoration of cellular and humo

239 highlight the importance of novel subsets of memory B cells rather than plasma cells combined with an

240 olleagues challenge current perceptions that memory B cells readily participate in secondary germinal

241 vation phenotype of established pre-existing memory B cells recognizing conserved epitopes and the ne

242 eutralizing antibody responses, we mined the memory B cell repertoire of a convalescent severe acute

243 ge-scale abnormalities in both the naive and memory B cell repertoires.

244 A and immunoglobulin G (IgG) plasmablast or memory B-cell response, although these were severely imp

245 LISPOTs were used to measure plasmablast and memory B cell responses (MBC) in APTB cases and healthy

246 lls, together with induction of CSP-specific memory B cell responses after the second dose that persi

247 GC Env-specific memory B cell responses elicited early post-systemic boo

248 n mature lymphocytes, leading to compromised memory B cell responses in old individuals.

249 osures in childhood can establish long-lived memory B cell responses that can be recalled later in li

250 Vaccine-induced memory B cell responses to evolving viruses like influen

251 e, induces autophagy in vivo and rejuvenates memory B cell responses.

252 responses, as well as long-lived plasma and memory B cell responses.

253 on the mechanisms of antibody production in memory B cell responses.IgE is an important mediator of

254 -H18 IgG antibody titres and plasmablast and memory B-cell responses in peripheral blood.

255 r 2 virus NAb responses, we performed single memory B cell sorting from the peripheral blood of a rhe

256 ic infections with regard to dynamics of the memory B cell subsets point to their role in the pathoge

257 osylation sites in Ab V regions of naive and memory B cell subsets.

258 27(+) and CD27(-) IgG(+) , IgE(+) and IgA(+) memory B cells, Th1, Th2, Th17, and Treg-memory cells fr

259 elicited a higher frequency of gp41-reactive memory B cells than gp120-memory B cells in adult and ne

260 center-activated B cells and CD4bs-directed memory B cells than those inoculated with parental immun

261 Most are antigen-experienced memory B cells that arise during responses to microbial

262 a unique population of IgM(+) and/or IgD(+) memory B cells that contain a high load of somatic mutat

263 associated with a dearth of isotype-switched memory B cells that displayed significantly lower somati

264 nge with herpes simplex virus 2, circulating memory B cells that enter the female reproductive tract

265 zing antibody titers have expanded clones of memory B cells that express the same immunoglobulin VH3-

266 aled the expansion of clones of RBD-specific memory B cells that expressed closely related antibodies

267 asked a marked, long-term depletion of CD19+ memory B cells that may underpin efficacy in MS.

268 demonstrate that VACV preferentially infects memory B cells that play an important role in a rapid an

269 ng-lived antibody secreting plasma cells and memory B cells that protect against subsequent infection

270 mmune systems of infected hosts to recall of memory B cells that recognized the lateral patch, the pr

271 is conferred by allergen-specific long-lived memory B cells that replenish the IgE(+) PC compartment.

272 viral latency is maintained in tumors or in memory B cells, the reservoir for lifelong EBV infection

273 are able to activate and expand Ag-specific memory B cells; these cultured cells are highly effectiv

274 e of the following parameters: IgG, IgA, and memory B cells to B. pertussis antigens.

275 ic differences in the responses of naive and memory B-cells to antigen.

276 h-affinity germinal center (GC) B cells into memory B cells versus plasma cells is a major quest of a

277 desmoglein (Dsg)-specific autoantibodies by memory B cells was evaluated in coculture experiments.

278 , after: 25.1 +/- 3.5%); 2) the frequency of memory B cells was reduced (before: 36.7 +/- 3.1%, after

279 Memory B cells were counted monthly and when relapse occ

280 Mass cytometry showed that switched memory B cells were enriched in the tumours of responder

281 and regulatory B cells were declined whereas memory B cells were expanded post DAA therapy.

282 ients, while CD19(+)CD24(+)CD38(-) primarily memory B cells were higher in CHC-N and CHC-HCC groups t

283 revealed that frequencies of class-switched memory B cells were increased in the patients, whereas f

284 T-bet-deficient memory B cells were largely indistinguishable from their

285 Alternatively, subsets of memory B cells were lower in abundance in cirrhotic rela

286 ells were resistant to VACV infection, while memory B cells were preferentially infected.

287 ed cytotoxicity and degranulation, levels of memory B cells were reduced, and serum IgG4 levels were

288 (+) B cells as well as CD38(+)CD138(-)IgA(+) memory B cells were significantly increased in intestina

289 st patients, naive-like and CD27(-) switched memory B cells were the most prominent CD21(low) subpopu

290 numbers, as well as IgA + and IgG + switched memory B cells, were reduced while naive B cells and T c

291 the frequencies of IgG(2) (+) and IgG(4) (+) memory B cells, whereas no effect was observed on the Ig

292 B viruses promotes the induction of Abs and memory B cells, which can provide strain-specific protec

293 in humans primarily stimulates pre-existing memory B cells, which differentiate into a transient wav

294 hancing BCR signal strength permitted IgE(+) memory B cells-which essentially do not exist under norm

295 also affected, with decreased IgD(+)CD27(+) memory B cells while transitional B cells were increased

296 reveal that memory B cells, while failing to re-enter the germinal c

297 s induced a relative decrease in circulating memory B cells with concomitant expansion of circulating

298 Compared to their naive counterparts, memory B cells with less DM(free) concentrate a higher p

299 s on H7 HA involved a transient expansion of memory B cells with little observed adaptation.

300 rated via class-switch recombination in IgG1 memory B cells without additional somatic hypermutation.