ライフサイエンスコーパス: plasmablast

1 differentiation into autoantibody-producing plasmablasts.

2 IgG(+) CD138(+) Blimp-1(+) innate B1b B cell plasmablasts.

3 differentiation into autoantibody secreting plasmablasts.

4 induced the appearance of IL-10(+)Blimp-1(+) plasmablasts.

5 21 monoclonal Abs (MAbs) from singly sorted plasmablasts.

6 nterest: CD138(+) plasma cells, and CD138(-) plasmablasts.

7 -like B cells, and CD138(+) plasma cells and plasmablasts.

8 of Ig and are mostly found among short-lived plasmablasts.

9 ntation of activated CD4 and CD8 T cells and plasmablasts.

10 ributed to Igk, Igh, and Prdm1 activation in plasmablasts.

11 imp-1 promoted the migration and adhesion of plasmablasts.

12 esentation and class-switch recombination in plasmablasts.

13 come activated but do not differentiate into plasmablasts.

14 antagonizing IRF4-driven differentiation of plasmablasts.

15 nd increased frequencies of peripheral blood plasmablasts.

16 interleukin-6 (vIL-6) produced by lymph node plasmablasts.

17 he proportion of germinal center B cells and plasmablasts.

18 st frequencies but decreased IL-10-producing plasmablasts.

19 4(+) T cells, homologous memory B cells, and plasmablasts.

20 ites displayed significant CTCF occupancy in plasmablasts.

21 tion between immature B cells and regulatory plasmablasts.

22 ith B cells detected among early circulating plasmablasts.

23 f KSHV vIL-6 in XBP-1s-expressing lymph node plasmablasts.

24 differentiation of human memory B cells into plasmablasts.

25 ation of ER expansion in IRE1alpha-deficient plasmablasts.

26 erentiated, antigen-induced peripheral blood plasmablasts.

27 sient wave of circulating antibody-secreting plasmablasts(1-3).

28 rus-specific antibodies that are produced by plasmablasts a few days after natural secondary infectio

29 tion cytokine secretion and T lymphocyte and plasmablast activation were detected.

30 ifferentiation of B-1 cells to IgM-producing plasmablasts after infections.

31 pec-seq framework, which we applied to human plasmablasts after influenza vaccination in order to cha

32 ntly enhanced H5 hemagglutinin (HA)-specific plasmablast and antibody responses compared to the nonad

33 nce and B cell ELISPOTs were used to measure plasmablast and memory B cell responses (MBC) in APTB ca

34 We analyzed RSV-specific peripheral blood plasmablast and memory B-cell frequencies and antibody l

35 nti-H9, and anti-H18 IgG antibody titres and plasmablast and memory B-cell responses in peripheral bl

36 nd highlight an important role for UBE2L3 in plasmablast and plasma cell development.

37 rs140490 genotype correlated with increasing plasmablast and plasma cell differentiation in patients

38 activation in primary human cells, and with plasmablast and plasma cell expansion in SLE, consistent

39 allele correlated with increased circulating plasmablast and plasma cell numbers in SLE individuals,

40 idosis, had increased numbers of circulating plasmablasts and CD21(low) B cells, as well as TH2 and r

41 trigger that drives expansion of circulating plasmablasts and CD4(+) cytotoxic T cells in patients wi

42 proliferating cells that partially resemble plasmablasts and early plasma cells.

43 ed somatic mutation in activated B cells and plasmablasts and emergence of distinct plasmablast clone

44 vercome the metabolic constraints imposed by plasmablasts and enhanced parasite clearance and the for

45 clonal antibodies (MAbs) from sorted patient plasmablasts and found that DENV-reactive MAbs were larg

46 om single-cell clones of dominantly expanded plasmablasts and generate recombinant human mAbs to iden

47 val and antigen-induced differentiation into plasmablasts and germinal center B cells due to reduced

48 related B-cell subsets of short-lived IgE(+) plasmablasts and IgG(+) memory B cells.

49 eration of extrafollicular T-bet(+) CD11c(+) plasmablasts and IgM memory B cells.

50 The frequency of plasmablasts and IL-10- and/or IL-1RA-producing Breg cel

51 prior to differentiation into GC B cells or plasmablasts and is greatly diminished in GCs.

52 e B cell differentiation into class-switched plasmablasts and led to downregulation of chemokine rece

53 identified antibody-producing B cell-lineage plasmablasts and macrophages as principal target cells f

54 nv-binding cells were measured in the blood (plasmablasts and memory B cells) and in the bone marrow

55 the immunized NHPs were isolated from single plasmablasts and memory B cells, and their immunogenetic

56 IIV increased frequencies of plasmablasts and memory B cells.

57 ystems were used to determine frequencies of plasmablasts and naive, memory, transitional, and activa

58 study, we show that SpA altered the fate of plasmablasts and plasma cells (PCs) by enhancing the sho

59 cle that a discrete population of CD5(-) IgM plasmablasts and plasma cells in the bone marrow (BM) pr

60 pression was 3-4 times higher in circulating plasmablasts and plasma cells than in other B-cell subse

61 sites of infection with that of bone marrow plasmablasts and plasma cells to control viremia during

62 stantially elevated UBE2L3 protein levels in plasmablasts and plasma cells.

63 ting in the generation of antibody-producing plasmablasts and plasma cells.

64 Our characterization of plasmablasts and plasmablast-derived MAbs provides a foc

65 om the depletion of pathogenic immune cells (plasmablasts and plasmacytoid dendritic cells).

66 ly eliminated the omental Ehrlichia-specific plasmablasts and reduced antigen-specific serum IgM, ide

67 ents with NMO, induces AQP4-ab production by plasmablasts and represents a novel therapeutic target.

68 and a 2.5- and 5-fold expansion of CD138(+) plasmablasts and T-bet(+) memory cells, respectively.

69 apidly differentiating into T-cell-dependent plasmablasts and T-cell-independent plasma cells.

70 a positive-feedback loop between circulating plasmablasts and Tfh cells that could sustain autoimmuni

71 ccination, the frequency of vaccine-specific plasmablasts and the binding reactivity of plasmablast-d

72 ted by the relative levels of cross-reactive plasmablasts and the cross-reactive PPAb binding reactiv

73 Increased frequency of plasmablasts and very few activated B cells were observe

74 ntre (GC)-like B cells, (ii) IgE(+) PC-like 'plasmablasts' and (iii) IgE(+) PCs.

75 al and chronically activated CD27(+) memory, plasmablast, and IgE-expressing memory subsets.

76 on induces robust antigen-specific antibody, plasmablasts, and CD4(+) T cells yet limited CD8(+) T ce

77 sion of LLT1 on GC-associated B cells, early plasmablasts, and GC-derived lymphomas.

78 equency of Der p 1-specific IgG4(+) B cells, plasmablasts, and IL-10(+) and dual-positive IL-10(+)IL-

79 IgG(4)-expressing Der p 1-specific B cells, plasmablasts, and IL-10(+) and/or IL-1RA(+) Breg cells.

80 nd IgG(4)-switched Der p 1-specific B cells, plasmablasts, and IL-10- and IL-1 receptor antagonist (I

81 anifested by higher numbers of granulocytes, plasmablasts, and inflammatory Ly6C(hi) CCR2(+) monocyte

82 ture B cells, tissue-like memory B cells and plasmablasts, and low proportions of naive B cells when

83 SFTSV-infected post-germinal center B cells, plasmablasts, and macrophages affect systemic immunopath

84 itch isotype, expand into short-lived IgE(+) plasmablasts, and serve as a potential target for therap

85 iche for antibody secreting plasma cells and plasmablasts, and that inflammation and immunization inc

86 38 during acute infection, characteristic of plasmablasts, and transitioned into memory B cells (CD38

87 e identified clonally expanded CD8+ T cells, plasmablasts, and, to a lesser extent, CD4+ T cells not

88 that produce inflammatory cytokines; CXCR3+ plasmablasts; and IL1B+ macrophages and monocytes.

89 l population that appears closely related to plasmablasts appearing in patients with acute respirator

90 nally expanded CD19(+)CD27(+)CD20(-)CD38(hi) plasmablasts are a hallmark of active IgG4-RD.

91 As key antibody producers, plasma cells and plasmablasts are critical components of vaccine-induced

92 se data suggest IgG and IgA vaccine-positive plasmablasts are largely similar, whereas IgA vaccine-ne

93 Peripheral blood plasmablasts are normally highly clonally diverse but th

94 procal interaction whereby circulating human plasmablasts are potent inducers of the Tfh cell-differe

95 that aberrant memory B cells (MBs), and not plasmablasts, are the true cells-of-origin for these tum

96 diated differentiation of resting B cells to plasmablasts as well as immunoglobulin G (IgG) and IgM s

97 oduced as many PE-specific, isotype-switched plasmablasts as wild-type mice.

98 ients with systemic lupus erythematosus with plasmablast-associated flares.

99 ecific B cells promoted differentiation into plasmablasts at the expense of germinal center B cells.

100 in heavy and light chain genes from expanded plasmablasts at the peak of disease reveals that disease

101 responses expanded before the appearance of plasmablast B cells.

102 oth the CD24(hi)CD27(+) and CD27(hi)CD38(hi) plasmablast B-cell compartments.

103 antly increased PC-specific CD138(+) splenic plasmablasts bearing a B-1a phenotype, and produced PC-r

104 sted in the distribution of plasma cells and plasmablasts between macaques that exhibited high or low

105 d function of blood-stage Plasmodium-induced plasmablasts but they also reveal new targets and strate

106 ation, is dispensable for the development of plasmablasts, but is required for immunoglobulin product

107 ulation of MYD88(L265P) B cells as CD19(low) plasmablasts by 10- to 100-fold.

108 in human antigen-specific antibody-secreting plasmablasts can be enriched in vivo, in a severe combin

109 The antigen-specific plasmablasts can then be sorted by flow cytometry, enabl

110 )IgD(-)CD38(-) or CD27(-)IgD(-)CD38(-)), and plasmablast (CD27(+)IgD(-)CD38(high)) subsets.

111 nd circulating follicular T-helper cells and plasmablast cells were measured in serum and whole blood

112 h a focus on HIV-specific memory B cells and plasmablasts/cells that are responsible for sustaining h

113 flammatory disease yet distinct from PCs and plasmablasts circulating in the blood.

114 mAbs expressed from the 2 dominant plasmablast clones of a patient with multiorgan IgG(4)-R

115 s and plasmablasts and emergence of distinct plasmablast clones on relapse indicate that the disease

116 Expanded plasmablast clones were detected only in MS and SCNI sub

117 ed heavy and light chain cDNAs from dominant plasmablast clones were expressed as mAbs and used to pu

118 ated macaques had increased plasma cells and plasmablasts compared to vaccinated animals.

119 The markedly increased propensity of plasmablasts, compared with naive B cells, to induce Tfh

120 selection of escaped cells in activated and plasmablast compartments, further underscoring the centr

121 Signatures of innate immunity and plasmablasts correlated with and predicted influenza ant

122 the antibody repertoire of plasma cells and plasmablasts could enable the discovery of useful antibo

123 Total B-lymphocyte, activated B-cell, and plasmablast counts were also elevated in NiV survivors.

124 lls are also required for the development of plasmablasts derived from germinal center and extrafolli

125 suggest a role of CD24(hi)CD27(+) B-cell and plasmablast-derived IL-10 in the regulation of human cGV

126 Our characterization of plasmablasts and plasmablast-derived MAbs provides a focused analysis of

127 also characterized a panel of DENV-specific plasmablast-derived monoclonal antibodies (mAbs) for act

128 We isolate and characterize a panel of plasmablast-derived monoclonal antibodies from an infect

129 c plasmablasts and the binding reactivity of plasmablast-derived polyclonal Abs are reduced and do no

130 nation, as well as the binding reactivity of plasmablast-derived polyclonal Abs to the hemagglutinin

131 as analyzed by determining the reactivity of plasmablast-derived polyclonal antibodies (PPAbs) to inf

132 Additionally, we isolated plasmablast-derived polyclonal antibodies and compared r

133 tiation has implications for extrafollicular plasmablast development within inflamed tissue.

134 tients showed increased T-bet expression and plasmablast development.

135 RT-PCR, protein immunoblots, and in vitro plasmablast differentiation assays were performed on pat

136 is cross-talk was compromised; pDCs promoted plasmablast differentiation but failed to induce Breg ce

137 Here we studied its functions in plasmablast differentiation by identifying regulated Bli

138 Inhibition of B cell plasmablast differentiation by reduction of Aiolos and I

139 In vitro plasmablast differentiation increased the frequency of I

140 luded ex vivo class switch recombination and plasmablast differentiation models as well as in vivo im

141 However, when using an in vitro plasmablast differentiation protocol, we obtained only 2

142 immunoglobulin G (IgG) class switching, and plasmablast differentiation through a rapamycin-sensitiv

143 ndent inducer of human B cell proliferation, plasmablast differentiation, and IgG secretion from circ

144 s and BAFF- and CD40L-induced proliferation, plasmablast differentiation, and IgG secretion.

145 terms of immunoglobulin isotype expression, plasmablast differentiation, and regulatory B (Breg) cel

146 the debate concerning the role of miR-182 in plasmablast differentiation, strongly suggesting that 18

147 on, and germinal center reaction, as well as plasmablast differentiation.

148 ivation, entry into the germinal center, and plasmablast differentiation.

149 rt that the rapid development of short-lived plasmablasts during experimental malaria unexpectedly hi

150 Omental plasmablasts elicited during Ehrlichia infection lacked

151 upregulation of chemokine receptor CCR10 on plasmablasts, enabling their exit from germinal centers

152 Here we use an in vivo plasmablast enrichment technique to isolate a human mono

153 tained significantly elevated frequencies of plasmablasts, especially those that expressed the extraf

154 hR represses differentiation of B cells into plasmablasts ex vivo and antibody-secreting plasma cells

155 mAbs derived from these plasmablasts exhibited minimal SHM (naive B cell origin)

156 ed pathway that elicited class switching and plasmablast expansion via a combination of T cell-indepe

157 Infected patients generate VH3 plasmablast expansions and increased VH3 idiotype Ig; ho

158 We show that a number of KSHV-MCD lymph node plasmablasts express vIL-6 but do not have full lytic KS

159 ia, the proportion of S. pneumoniae-specific plasmablasts expressing L-selectin was high, the proport

160 olved KSHV-MCD lymph nodes reveals that most plasmablasts expressing vIL-6 also coexpress XBP-1.

161 dicate that many Th cell subsets can promote plasmablast formation by providing CD40 signals to naive

162 LSD1 is an epigenetic modifier that promotes plasmablast formation, but its role in B cell developmen

163 ells is required for IgE class switching and plasmablast formation.

164 roduction, which was correlated with reduced plasmablast formation.

165 Plasmablast frequencies and IgE expression were highest

166 Patients with cGVHD had increased plasmablast frequencies but decreased IL-10-producing pl

167 Plasmablast frequencies were 10-50% of B cells, compared

168 Likewise, plasmablast frequency in the mesenteric lymph node corre

169 However, in bone marrow, plasmablast frequency negatively correlated with viremia

170 We isolated single peripheral blood plasmablasts from children with KD 1-3 weeks after onset

171 tility of the assay by isolating Ag-reactive plasmablasts from cryopreserved PBMC obtained from volun

172 ntified by transcriptomic analysis of single plasmablasts from DENV-infected individuals.

173 Finally, we show that most vIL-6-producing plasmablasts from lymph nodes of KSHV-MCD patients coexp

174 We show that a number of plasmablasts from lymph nodes of patients with KSHV-MCD

175 additional subclassification based on memBc/plasmablast function.

176 almost normal memBc/immunoglobulin-secreting plasmablast functionality in some patients if sufficient

177 Dengue plasmablasts had high degrees of somatic hypermutation,

178 oclonal antibodies (mAbs) derived from these plasmablasts had high levels of somatic hypermutation (S

179 ASCs (plasmablasts) have been extensively studied in humans, b

180 ally differentiated antigen-secreting cells (plasmablasts) have long been regarded as cells-of-origin

181 Plasmablast heavy and light chain immunoglobulin messeng

182 led to a reduction in GC B cells, CD138(hi) plasmablasts, IFN-gamma-dependent IgG2c production, and

183 ion of Spn polysaccharide-specific and total plasmablasts in blood.

184 F B cells preferentially differentiated into plasmablasts in EF zones.

185 normal levels of germinal center B cells and plasmablasts in periphery, they produced significantly r

186 B cells were not responsible for generating plasmablasts in response to Ehrlichia muris.

187 he number of autoreactive CD4(+) T cells and plasmablasts in the joint-draining lymph nodes.

188 in mesenteric lymph nodes, IgG(+) and IgA(+) plasmablasts in the lamina propria, and Abs in intestina

189 found a high frequency of Ehrlichia-specific plasmablasts in the omentum of both conventional and SLP

190 N memory-like B cells to become Ab-producing plasmablasts in the presence of BAFF and proinflammatory

191 the number of follicular helper T cells and plasmablasts in the spleen, and led to elevated levels o

192 rimarily by a population of CD11c-expressing plasmablasts in the spleen.

193 ontrol human B cells decreased production of plasmablasts in vitro, and IRF2BP2 transcripts and prote

194 +) B1 B cells decreases while that of IgG(+) plasmablasts increases, correlating with potential isoty

195 gh levels of autoantigen specific peripheral plasmablasts indicate recent activation of naive or memo

196 ually lytic; production of vIL-6 by involved plasmablasts is a central feature of KSHV-MCD.

197 The induction of circulating plasmablasts is increased in pregnant women versus contr

198 is, their independency from supply with new plasmablasts, is consistent with long-term stability of

199 In addition, both transitional B cell and plasmablast levels were significantly elevated in COVID-

200 e can be reconciled in human melanomas where plasmablast-like cells also express T cell-recruiting ch

201 Plasmablast-like cells also increase PD-1(+) T cell acti

202 -inflammatory factors and differentiate into plasmablast-like cells when exposed to autologous melano

203 This plasmablast-like phenotype can be reconciled in human me

204 on and drove B cell differentiation toward a plasmablast-like phenotype.

205 ) CD27(hi) ) showed higher expression of the plasmablast marker CD38 compared with B cells (CD19(hi)

206 related with increased B-cell activation and plasmablast maturation in patients after transplant.

207 PIs provide efficient elimination of plasmablast-mediated humoral responses; however, long-li

208 owever, when we analyzed the vaccine-induced plasmablast, memory, and serological responses to the tr

209 re evaluated for induction of cross-reactive plasmablasts, memory B cells, and cytokine-secreting CD4

210 aft infiltration, germinal center B cell and plasmablast numbers, as well as production of donor-spec

211 -term transcriptional specialization between plasmablasts of different isotypes.

212 whereas TIV elicited an increased number of plasmablasts on day 7.

213 immunoglobulin A and immunoglobulin G (IgG) plasmablast or memory B-cell response, although these we

214 ow-derived plasma cells, but not circulating plasmablasts or memory B cells.

215 l-dependent IgM(+) and IgG(+)B220(+)CD138(+) plasmablasts or T cell-independent B220(-)CD138(+) IgM(+

216 ces were seen in Env-specific memory B cell, plasmablast, or plasma cell frequencies in the three com

217 +)CD38(lo/int)CD43(+)) cell and conventional plasmablast (PB) (CD20-CD27(hi)CD38(hi)) cell population

218 Removal of plasmablast (PB) plus PC resulted in exacerbated EAE tha

219 he knowledge of antigen targets, we screened plasmablast (PB)-derived monoclonal antibodies (mAbs) fo

220 al responses are composed of a short wave of plasmablasts (PBs) arising from EF sites, followed by GC

221 Acutely activated B cells, or plasmablasts (PBs), were analyzed to dissect the ongoing

222 response to Ehrlichia muris is dominated by plasmablasts (PBs), with few-if any-germinal centers (GC

223 lls and that CD30 was upregulated in IRF4(+) plasmablasts (PBs).

224 ads to the identification of ISG15-secreting plasmablasts/PCs in patients with active systemic lupus

225 Both groups showed increased frequencies of plasmablasts, PLA-specific memory B cells, and IL-10-sec

226 Infection studies showed that plasmablast, plasma, transitional, and mature naive B ce

227 ed positive for CD19 and CD138 immune cells (plasmablast/plasma cell markers).

228 nflammatory and clonally expanded memory and plasmablast/plasma cell phenotype.

229 While we identified memory B cells and plasmablast/plasma cells with highly similar Ig heavy-ch

230 GC area was smaller and plasmablasts/plasma cell numbers lower in anti-BAFF-trea

231 ulatory protein programmed death-1 (PD-1) on plasmablasts/plasma cells in blood (median, 7%) at prese

232 subsets, elevated frequencies of memory and plasmablasts/plasma cells most clearly distinguished the

233 ted a persistent population of IgA-secreting plasmablasts/plasma cells, despite depletion of CD20(+)

234 athogen-specific antibody-producing effector plasmablasts/plasma cells, memory cells, and immune regu

235 ng rituximab, cannot eliminate IgA-secreting plasmablasts/plasma cells, which are likely central to t

236 egies that target autoreactive IgA-secreting plasmablasts/plasma cells.

237 GF-beta1 signaling was down-regulated in CSF plasmablasts/plasma cells.

238 ed an approximately 70-fold expansion of the plasmablast population.

239 Streptococcus pneumoniae-specific plasmablasts presumably originating in the lower respira

240 es to IIV and may have increased circulating plasmablast production compared to control women.

241 Plasmablast production of IL-6 is critical for initiatio

242 inal center formation along with a defect in plasmablast production.

243 ppropriate class-switching can be coupled to plasmablast proliferation to enforce type 2 immunity.

244 In contrast, plasmablast reactivity to a control antigen, tetanus tox

245 Plasmablast response after the first immunization was ex

246 on and immunopathology, we characterized the plasmablast response in four secondary DENV type 2 (DENV

247 The cross-reactive plasmablast response to heterovariant strains, as indica

248 The extrafollicular (EF) plasmablast response to self-antigens that contain Toll-

249 A plasmablast response, as well as a greater plasmablast response to the conserved influenza nuclear

250 Second immunization induced a plasmablast response to the highly variable HA head regi

251 l A(H1N1)pdm09 infection, did not affect the plasmablast response to vaccination, whereas repeated im

252 a greater vaccine-specific immunoglobulin A plasmablast response, as well as a greater plasmablast r

253 d88, or both and studied the extrafollicular plasmablast response.

254 at this cell subset is essential for the IgE plasmablast response.

255 epitopes that were not targeted by the early plasmablast response.

256 preexisting immunity affected virus-specific plasmablast responses and fold-change of T-cell response

257 reveal a regulatory role for cDCs in B cell plasmablast responses and provide a mechanistic explanat

258 SynGEM induced systemic plasmablast responses and significant, durable increases

259 iable alternative for monitoring Ag-specific plasmablast responses at early time points after infecti

260 ater magnitude and persistence, and enhanced plasmablast responses compared to those achieved with al

261 e for CD14(+)CD16(+) monocytes in generating plasmablast responses during dengue virus infection.

262 ystemic memory B cells, contributed to early plasmablast responses following challenge infection.

263 ermore, we used the ICA to track Ag-specific plasmablast responses in HIV-vaccine recipients over a p

264 characteristic of acute viral infection and plasmablast responses reaching >30% of circulating B cel

265 During acute infection, robust plasmablast responses to the infecting virus were detect

266 ive serum IgG antibody, and peripheral blood plasmablast responses.

267 Matsumoto et al. (2014) report that IL-10(+) plasmablasts restrain autoimmune inflammation and sugges

268 Metabolic hyperactivity of plasmablasts resulted in nutrient deprivation of the ger

269 d a prevalent IFN signature and identified a plasmablast signature as the most robust biomarker of DA

270 e tool for single-cell sorting of peripheral plasmablasts, streamlining subsequent Ab analysis, and c

271 relationships between rectal and bone marrow plasmablasts suggested that efficient trafficking to the

272 ritical for the expansion of a population of plasmablasts that correlated with increased SEA-specific

273 vers of control mice contained proliferative plasmablasts that originated from Peyer's patches and pr

274 ent in infected subjects but correlated with plasmablasts that peaked around Day 10.

275 pse after rituximab therapy, and circulating plasmablasts that re-emerge in these subjects are clonal

276 cells are activated by self-antigen to form plasmablasts that secrete high titers of germline-encode

277 dentify the presence of phenotypic CD19(neg) plasmablasts, the proliferative precursor state to matur

278 underlying transition of the GCB cell to the plasmablast--the transient B-cell stage targeted in ABC-

279 he CD19(neg) state can be established at the plasmablast to PC transition, that CD19(neg) PCs increas

280 occur during the maturation of proliferating plasmablast to quiescent plasma cell under survival cond

281 ted individuals and the ratio of TT-specific plasmablasts to MBCs in the APTB cases was 7:1.

282 -cell recruitment to GALT and of T cells and plasmablasts to the small intestine are well described.

283 Our results suggest that plasmablast trafficking to and retention in the bone mar

284 B-cell (ABC)-like subgroup resembles post-GC plasmablasts undergoing constitutive survival signaling,

285 R and TLR7/9 ligation and differentiate into plasmablasts via an extrafollicular (EF) route.

286 -10-producing CD24(+)CD38(hi) Breg cells and plasmablasts, via the release of IFN-alpha and CD40 enga

287 cyte antigen (CLA) on S. pneumoniae-specific plasmablasts was examined in patients with pneumonia (n

288 Generation of the omental plasmablasts was route dependent, as they were detected

289 o frequency of IgG-, IgM-, and IgA-secreting plasmablasts was significantly diminished by 27.2-, 2.4-

290 h Heligmosomoides polygyrus Specific Igs and plasmablasts were determined by ELISA and ELISpot, Cyp27

291 MN) titers, and the frequency of circulating plasmablasts were evaluated in pregnant versus control w

292 Many of these proliferating plasmablasts were IgG-positive, and this finding coincid

293 We found that plasmablasts were resistant to VACV binding, while other

294 the peripheral blood of normal individuals, plasmablasts were the major B cell subpopulation that ex

295 to mature naive B cells, memory B cells, and plasmablasts, were hypersensitive to a range of H2O2 con

296 Numbers of CD19(+)CD27(+)CD20(-)CD38(hi) plasmablasts, which are largely IgG4(+), are increased i

297 from IgM(+) and then from IgG(+) B1b B cell plasmablasts, which may represent important emergency ce

298 which some cells rapidly differentiate into plasmablasts while others undergo affinity maturation in

299 HCV RNA reduction, expansion of memory B and plasmablasts, while negatively associated with exhausted

300 luated by exploring homing receptors on such plasmablasts, yet no data have thus far described homing