ライフサイエンスコーパス: plasmablast

1 antagonizing IRF4-driven differentiation of plasmablasts.

2 nd increased frequencies of peripheral blood plasmablasts.

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

4 he proportion of germinal center B cells and plasmablasts.

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

6 4(+) T cells, homologous memory B cells, and plasmablasts.

7 ites displayed significant CTCF occupancy in plasmablasts.

8 tion between immature B cells and regulatory plasmablasts.

9 ction induces a dramatic expansion of B cell plasmablasts.

10 stic of both long-lived PC and proliferating plasmablasts.

11 the possibility that these might instead be plasmablasts.

12 ly IgG, and correlated with levels of IgG(+) plasmablasts.

13 differentiation of human naive B cells into plasmablasts.

14 autoreactive memory B cells and plasma cells/plasmablasts.

15 nds to cells that differentiate into CD20(-) plasmablasts.

16 n the putative B-1 cells and genuine CD20(-) plasmablasts.

17 the production of numerous antigen-specific plasmablasts.

18 numerous antibody-secreting plasma cells or plasmablasts.

19 with disease activity and frequency of blood plasmablasts.

20 differentiation into autoantibody secreting plasmablasts.

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

22 21 monoclonal Abs (MAbs) from singly sorted plasmablasts.

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

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

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

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

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

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

29 esentation and class-switch recombination in plasmablasts.

30 come activated but do not differentiate into plasmablasts.

31 LAIV in young adults, focusing on peripheral plasmablasts 6-8 days after vaccination.

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

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

34 tive B cells significantly contribute to the plasmablast and memory B cell populations of autoimmune-

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

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 ed, as evidenced by increased proportions of plasmablasts and CD86-expressing cells.

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

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

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

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

46 , dual-kappa B cells represent up to half of plasmablasts and memory B cells in autoimmune mice, wher

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

48 IIV increased frequencies of plasmablasts and memory B cells.

49 ective depletion of short-lived DEX-specific plasmablasts and memory B1b B cells using cyclophosphami

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

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

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

53 1 cells could be differentiated into CD20(-) plasmablasts and plasma cells in vitro, supporting a pre

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

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

56 obulin and higher percentages of circulating plasmablasts and plasma cells were observed in patients

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

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

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

60 The quantities of vaccine-specific plasmablasts and plasmablast-derived polyclonal antibodi

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

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

63 3-activating cytokines, differentiating into plasmablasts and secreting high levels of IgM, IgG, and

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

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

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

67 as well as in circulating antibody-secreting plasmablasts and the more differentiated plasma cells re

68 he capacity of B cells to differentiate into plasmablasts and to produce IgG appeared to be contained

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

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

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

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

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

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

75 38 during acute infection, characteristic of plasmablasts, and transitioned into memory B cells (CD38

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

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

78 These expanded plasmablasts are oligoclonal and exhibit extensive somat

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

80 Plasmablasts are terminally differentiating B cells that

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

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

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

84 omoting spontaneous germinal center (GC) and plasmablast B-cell development, and that these B-cell su

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

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

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

88 s defined for murine B cells and LPS-derived plasmablasts by chromatin immunoprecipitation sequencing

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

90 rentiation assay we find that GAL1-deficient plasmablasts can develop normally but die rapidly, throu

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

92 We also observed an expansion of the total plasmablast (CD19(+) CD27(+) CD38(high)) population in t

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

94 eutralization in vivo, and except for CD138, plasmablast cell surface marker expression was unaffecte

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

96 of this receptor, whereas memory B cells and plasmablasts/cells express variable levels of CD300a.

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

98 However, plasmablasts circulating in enormous numbers during acut

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

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

101 y a small fraction (<5%) of peripheral blood plasmablast clonotypes (CD3(-)CD14(-)CD19(+)CD27(++)CD38

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

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

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

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

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

107 In contrast to memory B cells, most plasmablast-derived Abs bound to the structural E protei

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

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

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

111 Plasmablast-derived polyclonal antibodies (PPAb) from yo

112 ntities of vaccine-specific plasmablasts and plasmablast-derived polyclonal antibodies (PPAbs) in IIV

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

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

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

116 these, 366 genes were associated with human plasmablasts differentiating in vitro.

117 le for CD14(+)CD16(+) monocytes in promoting plasmablast differentiation and anti-DENV antibody respo

118 ferentiation, via its regulation of terminal plasmablast differentiation and/or IgM secretion.

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

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

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

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

123 d colleagues show that KSHV infection drives plasmablast differentiation in a subset of IgM(+) lambda

124 the cytosol, which correlates with impaired plasmablast differentiation in vitro.

125 In vitro plasmablast differentiation increased the frequency of I

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

127 th CD40L/IL-21 induced B-cell proliferation, plasmablast differentiation, and antibody secretion in p

128 l-independent proliferation, Blimp1-mediated plasmablast differentiation, and autoantibody secretion.

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

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

131 S3-specific B-cell expansion, IgG switching, plasmablast differentiation, and spleen and bone marrow

132 ere they contributed to B cell selection and plasmablast differentiation.

133 Omental plasmablasts elicited during Ehrlichia infection lacked

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

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

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

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

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

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

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

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

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

143 mpared them directly with memory B cells and plasmablasts for several functional characteristics.

144 pment, defective in vitro B cell activation, plasmablast formation, and immunoglobulin secretion, and

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

146 roduction, which was correlated with reduced plasmablast formation.

147 Plasmablast frequencies and IgE expression were highest

148 ction was associated with extraordinary peak plasmablast frequencies between 4 and 7 d of illness, av

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

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

151 Plasmablast frequency did not correlate with acute serum

152 Likewise, plasmablast frequency in the mesenteric lymph node corre

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

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

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

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

157 In this study, we analyzed single plasmablasts from two patients by sorting the cells for

158 additional subclassification based on memBc/plasmablast function.

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

160 IL-2 increased plasmablast generation and immunoglobulin secretion from

161 Dengue plasmablasts had high degrees of somatic hypermutation,

162 re rare in vivo and, among them, short-lived plasmablasts have the highest frequency, suggesting an a

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

164 Plasmablast heavy and light chain immunoglobulin messeng

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

166 Assessment of plasmablast immunoglobulin isotype distribution revealed

167 A-1 immunostaining identified HHV-8-infected plasmablasts in 16 of 16 tested cases.

168 creased numbers of switched memory cells and plasmablasts in combination with clonal expansion and si

169 with genetic analyses, we show evidence that plasmablasts in dengue patients are a polyclonal pool of

170 otype distribution revealed increased IgG(+) plasmablasts in early and most prominently during chroni

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

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

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

174 Thus, our data suggest that while plasmablasts in the blood may contribute to the HIV-spec

175 Here we show that only a small fraction of plasmablasts in the blood of viremic individuals is HIV

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

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

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

179 ontinuous Ag-driven formation of short-lived plasmablasts in the spleen and a quiescent population of

180 ved, cyclophosphamide-sensitive DEX-specific plasmablasts in the spleen, and a quiescent, cyclophosph

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

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

183 B-cell differentiation to plasmablasts in vitro in response to CD40 ligand and IL-

184 Addition of BAFF to plasmablasts in vitro rescued IgM secretion, suggesting

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

186 f WASp-deficient B cells into class-switched plasmablasts in vitro, suggesting that WASp-dependent B

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

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

189 Differentiation of dual-kappa B cells into plasmablasts is driven by MRL genes, whereas the mainten

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

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

192 -peripheral blood IgG(+) B cells, peripheral plasmablasts isolated after tetanus toxoid immunization

193 are mainly mature B2 (conventional) CD20(-) plasmablasts lacking markers of terminal differentiation

194 ymph nodes; 3) enrichment in IRF4(+)CD138(-) plasmablast-like cells; and 4) overexpression of IgM in

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

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

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

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

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

200 tibodies generated from the vaccine-specific plasmablasts neutralized more than one influenza strain

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

202 of DENV-specific and serotype cross-reactive plasmablasts occurs in acute secondary DENV infection of

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

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

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

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

207 Memory B cell (P=0.02) and plasmablast (P<0.001) repopulation after 26 weeks was ma

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

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

210 y B cells to differentiate into IgG- and IgA-plasmablasts (PBs) resembling those found in the blood o

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

212 emory B-cell subpopulations and plasma cells/plasmablasts (PC/PB) in blood, bone marrow, and lymph no

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

214 After a proliferative plasmablast phase, PCs persist in the absence of cell di

215 These cells display a plasmablast phenotype, and they spontaneously secrete Ig

216 and plasma cells in vitro, supporting a pre-plasmablast phenotype.

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

218 Plasmablast/plasma cell differentiation was assessed by

219 ctivation, expansion, isotype switching, and plasmablast/plasma cell differentiation.

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

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

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

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

224 subpopulations, 10% of the total IgG and IgA plasmablast population and 23% of the IgM plasmablast po

225 gA plasmablast population and 23% of the IgM plasmablast population were uniquely reactive with PDC-E

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

227 with PDC-E2, detected in the CXCR7+ CCR10low plasmablast population.

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

229 and specificity of the antibodies that these plasmablasts produce.

230 Plasmablasts produced Ab that cross-reacted with heterot

231 athology; however, little is known about the plasmablasts producing these antibodies during an ongoin

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

233 Plasmablast production of IL-6 is critical for initiatio

234 mia, contrasting with a predominantly IgA(+) plasmablast profile in HIV-negative individuals or in av

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

236 ts were more Ag differentiated, with greater plasmablast proportions (3.1 +/- 0.8%) than in normal co

237 entirely made up of IgG-secreting cells, and plasmablasts reached very high numbers at a time after f

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

239 were produced for up to 2 mo by plasma cells/plasmablasts recruited to the ectopic lymphoid tissue by

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

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

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

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

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

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

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

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

248 predominantly IgG-producing vaccine-specific plasmablast response.

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

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

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

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

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

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

255 Herein we present an analysis of plasmablast responses in patients with acute dengue viru

256 Day 7 plasmablast responses induced by both vaccines was more

257 ce of these large, rapid, and virus-specific plasmablast responses raises the question as to whether

258 We found very potent plasmablast responses that often increased more than 1,0

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

260 engendered rapid, isotype-switched secondary plasmablast responses upon restimulation.

261 nct quantitative and qualitative patterns of plasmablast responses were induced by LAIV and IIV in yo

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

263 , dual-kappa B cells that differentiate into plasmablasts retain the capacity to secrete autoantibodi

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

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

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

267 TIV induced higher antibody titers and more plasmablasts than LAIV did.

268 type of putative B-1 cells closer to CD20(-) plasmablasts than to memory B cells.

269 is the predominant immunoglobulin isotype of plasmablasts that arise transiently in the blood followi

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

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

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

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

274 fferentiate into short-lived extrafollicular plasmablasts that secreted modest quantities of Ig.

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

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

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

278 The failure of TI plasmablasts to secrete IgM was not a consequence of alt

279 he migration of circulating antigen specific plasmablasts to the mucosal epithelial ligands CXCL12 an

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

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

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

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

284 -10-producing CD24(+)CD38(hi) Breg cells and plasmablasts, via the release of IFN-alpha and CD40 enga

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

286 de novo generation of anti-U1A plasma cells/plasmablasts was reduced following T cell depletion.

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

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

289 , CD4(+)/CD8(+) T cells, memory B cells, and plasmablasts were assessed.

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 ytes (TIL-B), both switched memory cells and plasmablasts were expanded, as compared with nonmalignan

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

294 Splenic DEX-specific plasmablasts were located in the red pulp with persistin

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 us (DENV) infection induces the expansion of plasmablasts, which produce antibodies that can neutrali

298 e IgM derived from T cell-independent spleen plasmablasts, which was germline-encoded, also bound cyt

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

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