ライフサイエンスコーパス: plasma cell

1 cells by inhibiting their differentiation to plasma cells.

2 is expressed in MM and smoldering MM patient plasma cells.

3 c CD8+ T cells, Th1 cells, IgM+ B cells, and plasma cells.

4 ansion of durable bnAb memory and long-lived plasma cells.

5 toid dendritic cells, B cells and especially plasma cells.

6 aling was down-regulated in CSF plasmablasts/plasma cells.

7 al center B (GCB) cells and isotype-switched plasma cells.

8 ith its antithetical prosurvival function in plasma cells.

9 d that these 2 plasma cell subsets are IgG(+)plasma cells.

10 rather than lack of selection against ANA(+) plasma cells.

11 at partially resemble plasmablasts and early plasma cells.

12 yeloma is a malignancy of antibody-secreting plasma cells.

13 direct and indirect interactions with tumor plasma cells.

14 ng B-cell maturation into antibody-producing plasma cells.

15 etect naturally occurring ANA(+) B cells and plasma cells.

16 iximab-TNF complexes and infliximab-specific plasma cells.

17 f donor B cells and elimination of recipient plasma cells.

18 any patients, probably related to long-lived plasma cells.

19 he distinct precursors of memory B cells and plasma cells.

20 ulators were normally expressed in IghPax5/+ plasma cells.

21 is home to the body's largest population of plasma cells.

22 gG production and accumulation of long-lived plasma cells.

23 use and human meninges contain IgA-secreting plasma cells.

24 is universally and strongly expressed on MM plasma cells.

25 rentiation into memory B cells or long-lived plasma cells.

26 s also executed in B cell differentiation to plasma cells.

27 mutated memory B cells (MBC) and long-lived plasma cells.

28 erleukin 6-mediated signaling to B cells and plasma cells.

29 turation antigen (BCMA) is expressed only on plasma cells, a small subset of B cells and MM cells, wh

30 The dominant model holds that nascent plasma cells adapt to increased antibody synthesis by ac

31 and Bcl6, driving both early extrafollicular plasma cell and germinal center responses, in a CD4(+) T

32 pers, as well as B-cell differentiation into plasma cells and autoantibody expression.

33 onic inflammatory infiltrate of lymphocytes, plasma cells and hyalinized fibrous stroma.

34 1 mutant MB cells fail to differentiate into plasma cells and instead preferentially reenter new GC r

35 oclonal antibody that targets CD38, depletes plasma cells and is approved for the treatment of multip

36 CD68) were used to identify T- and B-cells, plasma cells and macrophages.

37 antigen drives the generation of long-lived plasma cells and memory B cells and highlight the challe

38 sses that drive the production of long-lived plasma cells and memory B cells are subjects of intensiv

39 ion, producing long-lived antibody secreting plasma cells and memory B cells that protect against sub

40 n B cell memory 'walls' - namely, long-lived plasma cells and memory B cells.

41 higher levels of antigen-specific long-lived plasma cells and memory B cells.

42 ortantly, these data suggest a novel role of plasma cells and offer potential new mechanistic and reg

43 Mining the antibody repertoire of plasma cells and plasmablasts could enable the discovery

44 althy skin is a niche for antibody secreting plasma cells and plasmablasts, and that inflammation and

45 ckpoint that restricts the generation of IgG plasma cells and protects against IgG ANAs.

46 from malignant immunoglobulin (Ig)-secreting plasma cells and remains an incurable, often lethal dise

47 ile Ufbp1 deficiency impairs ER expansion in plasma cells and retards immunoglobulin production.

48 Dual targeting of both plasma cells and upstream GC responses successfully prol

49 nal B cells, extrafollicular IgG2c-producing plasma cells, and activation of CD4 and CD8 T cells.

50 al capacity to differentiate into memory and plasma cells, and B1 differentiation can be instructed b

51 cells and monocyte/macrophages with B cells, plasma cells, and eosinophils accounting for <5%.

52 luminated the biologic relevance of B cells, plasma cells, and pathogenic antibodies in autoimmunity.

53 tein P3 (FoxP3)+ regulatory T cells and IgG4 plasma cells; and abundant arachidonate 15-lipoxygenase

54 Plasma cells are a logical target of therapy given their

55 Strain-specific plasma cells are capable of producing neutralizing antib

56 Ab-secreting cells (ASC) or plasma cells are essential components of the humoral imm

57 B cells, as IgE(+) memory B cells and IgE(+) plasma cells are extremely scarce and short-lived, respe

58 ness of specific therapy when B cells and/or plasma cells are found.

59 Long-lived plasma cells are implicated in the pathogenesis of syste

60 Plasma cells are of special interest in chronic periodon

61 rkably, we demonstrate that CD138(+) CD38(+) plasma cells are the major immune cell type in CP gingiv

62 e targeting the germinal center response and plasma cells as a desensitization strategy, we sensitize

63 ributions of germinal centres and long-lived plasma cells as sources of autoantibodies, discuss data

64 ipated effects on IgA, IgM, IgE, complement, plasma cells, B cells, or other cells of the innate or a

65 and relapsed/refractory patients, including plasma cells bearing the t(4;14) translocation obtained

66 ecific MBCs were contained mostly within the plasma-cell-biased CD80(+) subset, and few GCs arose fol

67 Multiple myeloma is a plasma cell blood cancer with frequent chromosomal trans

68 ntibody levels are maintained by bone marrow plasma cells (BMPCs), we investigated the production and

69 Tumours often contain B cells and plasma cells but the antigen specificity of these intrat

70 vated and germinal centre B cells as well as plasma cells can be found in the tumour microenvironment

71 Multiple myeloma (MM) is a plasma cell cancer and represents the second most freque

72 Multiple myeloma (MM) is a plasma cell cancer and represents the second most freque

73 Multiple myeloma (MM), a plasma cell cancer, is associated with many health chall

74 37 and is denoted as IL-37/IL-35-coproducing plasma cells (CD138(+)CD38(+)P(IL-35/IL-37)).

75 -37-we denote this subset as IL-37-producing plasma cells (CD138(+)CD38(+)P(IL-37)).

76 Here, we investigated autoantigen-specific plasma cells, CD4(+) T cells, and IgG fraction crystalli

77 xpression of TNFSF13, a cytokine involved in plasma cell class switching to IgA.

78 rs that permit progression from the aberrant plasma cell clone to MGUS and overt MM.

79 dosis, a small B-cell clone, most commonly a plasma cell clone, produces monoclonal light chains that

80 Prospective studies targeting plasma cell clones and/or fibrotic pathways are warrante

81 ed to identify how MGUS and multiple myeloma plasma cell clones responded to anti-multiple myeloma th

82 novel subsets of memory B cells rather than plasma cells combined with antigen re-exposure and T-cel

83 s and a 16-fold increase in bone marrow (BM) plasma cells compared with bolus immunization.

84 Plasma cells constitute the only known cell type capable

85 Long-lived BM resident plasma cells constitutively secrete antibodies, and we d

86 the germinal centers and an abnormally high plasma cell content.

87 Another subset of plasma cells coproduces IL-35 and IL-37 and is denoted a

88 G(4) or esIgD; indicating that IgE-secreting plasma cells could originate from either sequential isot

89 (+) T-lymphocyte and lamina propria CD138(+) plasma cell densities simultaneously proved to be a mean

90 observed increased numbers of ANA(+) IgG(+) plasma cells despite normal tolerance checkpoints in imm

91 Skin plasma cells developed independently of T cells and micr

92 Pax5 repression is not essential for robust plasma cell development and antibody secretion, although

93 different branches of UPR pathway to promote plasma cell development and function.

94 cofactor of the ufmylation pathway, promotes plasma cell development by suppressing the activation of

95 other UPR branch, PERK, is suppressed during plasma cell development.

96 epression of Pax5 by Blimp1 is essential for plasma cell development.

97 ndependent modality that naturally adjuvants plasma cell differentiation and antibody responses to pr

98 highly expressed in GC B cells that promotes plasma cell differentiation and viral reactivation.

99 with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-media

100 type, whereas EBV-infected B cells expressed plasma cell differentiation markers.

101 Finally, plasma cell differentiation of sorted LPS-stimulated MZ

102 onse axis from germinal center activation to plasma cell differentiation remains intact.

103 Notably, MYC abundance decreases with plasma cell differentiation, a key lytic reactivation tr

104 1 expression, CSR, somatic hypermutation and plasma cell differentiation.

105 y hampering gut lymphocyte homing and IgA(+) plasma cell differentiation.

106 fic selection or a global enhancement of IgG plasma cell differentiation.

107 esponses reducing both B-cell activation and plasma cell differentiation.

108 mmature memory B cells (MB), while impairing plasma cell differentiation.

109 f STAT1 and T-bet in TLR7-driven GC, Tfh and plasma cell differentiation.

110 y promoted B-cell class switching to IgE and plasma cell differentiation.

111 ions in autoimmune diseases or use of B cell/plasma cell-directed anticancer therapies have illuminat

112 Plasma cell-directed therapies using lenalidomide and/or

113 olution of symptoms following treatment with plasma cell-directed therapy supports the hypothesis tha

114 hy, organomegaly, endocrinopathy, monoclonal plasma cell disorder, skin changes (POEMS)-associated MC

115 is while receiving proteasome inhibitors for plasma cell disorders at Mount Sinai Hospital in New Yor

116 will help standardise imaging for monoclonal plasma cell disorders worldwide to allow the comparison

117 a of COVID-19 infection in 650 patients with plasma cell disorders, collected by the International My

118 ons were identified in sixteen patients with plasma cell disorders.

119 d costimulation blockade reduces bone marrow plasma cells, disorganizes germinal center responses, re

120 influenced by the activity of the underlying plasma cell dyscrasia (dFLC) and nephrotic-range albumin

121 ltivariable Cox regression analysis revealed plasma cell dyscrasia (difference between serum free lig

122 thy of undetermined significance (MGUS) is a plasma cell dyscrasia and precursor to multiple myeloma.

123 hom BM tests routinely performed to diagnose plasma cell dyscrasia failed to detect lambda+ monoclona

124 rmined significance (MGUS) is a premalignant plasma cell dyscrasia that consistently precedes multipl

125 AL patients are untreated for the underlying plasma cell dyscrasia.

126 Despite high Pax5 expression, plasma cells efficiently developed in young IghPax5/+ mi

127 Although Pax5 significantly deregulated the plasma cell expression program, key plasma cell regulato

128 B cell and plasma cell fates are controlled by different transcript

129 However, the plasma cell free DNA (cfDNA) level can be low and the fr

130 genomic next-generation sequencing (mNGS) of plasma cell-free DNA (cfDNA) is commercially available,

131 Plasma cell-free DNA at baseline showed ERBB2 (HER2) amp

132 by deep Sequencing, [CAPP-Seq]) analyses of plasma cell-free DNA collected from 45 patients before a

133 Furthermore, post-mortem plasma cell-free DNA sequencing (liquid autopsy) can be

134 The post-mortem plasma cell-free DNA was successfully sequenced and 344

135 To characterize plasma cell-free eccDNAs, we performed sequencing analys

136 In CSF supernatant and blood plasma, cell-free HIV RNA was quantified by qPCR with si

137 A population of plasma cells from intestinal biopsies of patients with c

138 In the present study, we examined plasma cells from MM using a multi-epigenomics approach

139 se but was observed in an average 30% of gut plasma cells from patients and controls.

140 IgA(+)CD138(+) plasma cells from Peyer's patches and lamina propria wer

141 invasion requires shifting the production of plasma cells from strain-specific to broadly reactive.

142 reducing cellular stress, thereby distancing plasma cells from the apoptotic threshold, potentially e

143 t atherosclerosis-prone mice with attenuated plasma cell function manifest reduced plaque burden, ind

144 lls utilize mTORC1 to prepare for subsequent plasma cell function, before the onset of antibody synth

145 rent paths to generate short- and long-lived plasma cells, germinal center cells, and memory cells; a

146 ing pathogens and ischemic injury, sustained plasma cell growth, and immunoglobulin production.

147 marrow-resident hematological malignancy of plasma cells, has remained largely incurable despite dra

148 n critical immune regulatory pathways, while plasma cells have uniquely high levels of circular-RNAs

149 report that liver allograft recipients with plasma cell hepatitis had significant decreases of both

150 with adjacent dendritic cells, macrophages, plasma cells, high endothelial venules, supporting folli

151 ty of polymeric immunoglobulin receptors and plasma cells, how and whether antibodies are delivered t

152 in programmed death-1 (PD-1) on plasmablasts/plasma cells in blood (median, 7%) at presentation were

153 r checkpoint for generation of ANA(+) IgG(+) plasma cells in both nonautoimmune mice and healthy huma

154 However, the presence of cytokine-producing plasma cells in CP is unknown.

155 L-37) and P(IL-35/IL-37) exist as subsets of plasma cells in CP lesions and that these 2 new types of

156 pports an emerging role for distinct sets of plasma cells in cytokine production.

157 dy LC protein that is secreted by monoclonal plasma cells in each patient misfolds and/or aggregates,

158 s our understanding of skin associated B and plasma cells in health and disease.

159 tial relevance for manipulation of cutaneous plasma cells in inflammatory skin diseases or cutaneous

160 We sought to study whether autoreactive plasma cells in lupus models and patients with systemic

161 ansion of IgA(+) germinal center B cells and plasma cells in mesenteric lymph nodes and more IgA-coat

162 oncomitant T-cell activation and also killed plasma cells in MM patient samples ex vivo.

163 ting CD38, an antigen uniformly expressed by plasma cells in multiple myeloma and light-chain amyloid

164 (MHCII) was not restricted to these specific plasma cells in patients with celiac disease but was obs

165 re rapidly reactivated to differentiate into plasma cells in subcapsular proliferative foci (SPF).

166 Specifically, we measured antibody-secreting plasma cells in the BM and VZV-specific CD4 T cells in B

167 These results indicate that plasma cells in the gut can function as antigen-presenti

168 ow that primary infection does not establish plasma cells in the lamina propria of the female reprodu

169 There were more IL-5Ralpha(+) plasma cells in the polyp tissue from those with AERD th

170 ncomitantly elicited clonally related IgA(+) plasma cells in the small intestine.

171 t by decreasing both suppressive myeloid and plasma cells in the tumor.

172 IL-5 stimulation of plasma cells in vitro induced changes in a distinct set

173 e quantification of autoreactive B cells and plasma cells in vivo within a native B-cell repertoire i

174 Peri-sinus IgA plasma cells increased with age and following a breach o

175 1B UM is infiltrated with clonally expanded plasma cells, indicative of antibody-mediated immunity.

176 al center (GC) B cells, and antigen-specific plasma cells induced during chronic IL-18-mediated infla

177 ression in activated B cells with or without plasma cell-inductive signals, we find that follicular B

178 Although plasma cell infiltrates tend to be more diffuse, B cells

179 serum IgG4 level, abundance of IgG4 enhanced plasma cell infiltration in the portal region of the liv

180 ealed interface hepatitis with IgG4 positive plasma cell infiltration in the portal region, without e

181 le in inflamed tissues that consisted of IgG plasma cells, inflammatory mononuclear phagocytes, activ

182 nter (GC) B cells into memory B cells versus plasma cells is a major quest of adaptive immunity.

183 Consequently, differentiation of plasma cells is blunted, and Ab responses are transient

184 stinal tract), dimeric IgA secreted by local plasma cells is transported through polymeric immunoglob

185 f an overexpressed antibody LC from a clonal plasma cell leads to organ toxicity and patient death if

186 ;16), t(14;20), del(17p) or amp1q21, primary plasma cell leukaemia and elevated serum lactate dehydro

187 were GEP(hi), seven (7%) of 100 had primary plasma cell leukaemia, five (5%) of 100 had t(14;20), fo

188 ociated with malignant progression of MM and plasma cell leukemia, correlating to worse treatment out

189 nes confer protection by inducing long-lived plasma cells (LLPCs) and memory B cells (MBCs), cell typ

190 node that generate high-affinity, long-lived plasma cells (LLPCs).

191 s in inflammatory skin diseases or cutaneous plasma cell malignancies.

192 Multiple myeloma (MM) is a plasma cell malignancy and most patients eventually succ

193 Multiple myeloma (MM), a plasma cell malignancy, evolves through premalignant pha

194 In multiple myeloma (MM), a plasma cell malignancy, most tumors display hallmarks of

195 in CP lesions and that these 2 new types of plasma cells may regulate periodontitis pathogenesis by

196 of biopsies, B lineage cells (B cells and/or plasma cells) may be found more abundantly.

197 ighly active in vitro and in vivo against MM plasma cells, memory B cells, and MM-propagating cells.

198 fic antibody-producing effector plasmablasts/plasma cells, memory cells, and immune regulatory B cell

199 vated frequencies of memory and plasmablasts/plasma cells most clearly distinguished the CSF from blo

200 onal activation of the MAP kinase pathway in plasma cell myeloma implicates growth factor-like signal

201 tissues that expressed high levels of CD138 plasma cells (N = 4) had a statistically significant imp

202 ry cells, consisting of lymphocytes (n = 9), plasma cells (n = 6), and histiocytes (n = 6).

203 Multiple myeloma (MM) is a plasma cell neoplasm associated with a broad variety of

204 Multiple myeloma is a plasma cell neoplasm characterized by the production of

205 Extramedullary plasmacytoma (EMP) is a plasma cell neoplasm of soft tissue without bone marrow

206 Multiple myeloma (MM) is a plasma cell neoplasm that commonly expresses CD38.

207 Multiple myeloma (MM) is a plasma-cell neoplasm that is treated with high-dose chem

208 nsplantation has not been reported, although plasma cell neoplasms are a rare form of posttransplant

209 % (N = 151) myeloid cancer, and 10% (N = 80) plasma cell neoplasms.

210 Plasma cell numbers in the nasal mucosa increased during

211 GC area was smaller and plasmablasts/plasma cell numbers lower in anti-BAFF-treated rats, whi

212 ivation, reduced autoantibody production and plasma cell numbers, and normalized B and T cell subsets

213 ific monoclonal antibody (SSM5) derived from plasma cells of a patient, along the corresponding contr

214 ein survivin in the autoreactive B cells and plasma cells of MG patients.

215 Specific depletion of meningeal plasma cells or IgA deficiency resulted in reduced funga

216 can further differentiate into Ab-secreting plasma cells or memory B cells.

217 her terminal differentiation (the long-lived plasma cell) or metastable transcriptional reprogramming

218 specific antibodies (P=0.05) and bone marrow plasma cells (P=0.02) compared with controls, with a tre

219 isystem disease resulting from an underlying plasma cell (PC) dyscrasia.

220 ere, we found that Syk degradation restrains plasma cell (PC) formation in GCs and promotes B cell LZ

221 induced in cells fated for GC expansion and plasma cell (PC) formation, so-called positively selecte

222 for the distribution of 41 blood B-cell and plasma cell (PC) subsets, including subsets defined by e

223 Mucosal plasma cells (PC) and Ig production are essential to fen

224 Plasma cells (PC) are found in the CNS of multiple scler

225 ires rapid elimination of antibody-secreting plasma cells (PC) with a proteasome inhibitor, bortezomi

226 hallenging to completely eliminate malignant plasma cells (PCs) and achieve complete cure.

227 re, we analyzed the quantity of VZV-specific plasma cells (PCs) and CD4 T cells in the bone marrow (B

228 s, autoreactive Abs secreted by autoreactive plasma cells (PCs) are considered to play a critical rol

229 Plasma cells (PCs) are essential for protection from inf

230 Plasma cells (PCs) are the major source of pathogenic al

231 Helper T cell induced plasma cells (PCs) that secrete class-switched neutraliz

232 Here, we examined the contribution of plasma cells (PCs) to age-related increases in myelopoie

233 luminated the biologic relevance of B cells, plasma cells (PCs), and pathogenic antibodies and comple

234 rgic inflammation is driven by IgE-producing plasma cells (PCs), which are required for IgE-mediated

235 Antibodies originate from plasma cells (PCs), which are terminally differentiated

236 subsets, including memory B cells (MBCs) and plasma cells (PCs).

237 n intracellular metabolic pathways of clonal plasma cells (PCs).

238 phoid organs as well as increased numbers of plasma cells (PCs).

239 is known about the biology of amyloidogenic plasma cells (PCs).

240 kappa locus, ensuring its production by all plasma cells (PCs).

241 speculate that thymus-associated B cells and plasma cells persist in the circulation after thymectomy

242 a unifying feature underlying the malignant plasma cell phenotype.

243 and clonally expanded memory and plasmablast/plasma cell phenotype.

244 lity of the bone marrow-resident, long-lived plasma cell population, yet absence of this kinase led t

245 rability of the memory B cell and long-lived plasma cell populations are not fully elucidated.

246 between strain-specific and broadly reactive plasma cell production during infections.

247 adth may assist in boosting broadly reactive plasma cells production.

248 nchronized expression pattern with Cxcr5 and plasma cell program genes, Il17ra exhibited a synchroniz

249 y, and a systemic survey to exclude systemic plasma cell proliferative diseases.

250 was due to increased numbers of total IgG(+) plasma cells rather than lack of selection against ANA(+

251 ating recombinant antibodies from single gut plasma cells reactive with discrete antigen domains and

252 Significant depletion of long-lived plasma cells, reduction of interferon type I activity, a

253 m of the B cell identity factor Pax5 and the plasma cell regulator Blimp1.

254 ated the plasma cell expression program, key plasma cell regulators were normally expressed in IghPax

255 to antibody production in lymphoid tissues, plasma cells reside in healthy mouse and human skin.

256 al germinal center architecture and CD138(+) plasma cells residing in the paracortex, which expressed

257 events that lead to improved breadth of the plasma cell response.

258 neutralizing antibody, memory and long-lived plasma cell responses compared to conventional alum-adso

259 e generation of memory B cell and long-lived plasma cell responses.

260 Plasma cell-rich infiltrates tend to occur later, may be

261 Antibody-secreting cells (ASCs) or plasma cells secrete antibodies and form a cornerstone o

262 sociated with increased disease severity and plasma cells secreting potentially pathogenic autoantibo

263 antibodies produced by bone marrow-residing plasma cells, serum analysis does not provide informatio

264 , when compared to normal B cells, malignant plasma cells showed an extensive activation of regulator

265 lications carried the highest interferon and plasma cell signatures as well as activated CD4(+) T cel

266 Although mice continued to develop plasma cells, splenic follicular structure was restored,

267 y-secreting memory B-cell populations to the plasma cell stage.

268 We determined that these 2 plasma cell subsets are IgG(+)plasma cells.

269 ssed lymph node and bone marrow, blood B and plasma cell subsets, somatic hypermutations in Ig genes,

270 Our data support a model in which skin plasma cells supply natural and adaptive IgM to the cuta

271 ucleotides (PS-ASOs) interact with a host of plasma, cell-surface and intracellular proteins which go

272 ation and exhibit enhanced interactions with plasma, cell-surface, and intracellular proteins, which

273 Finally, BAFF and APRIL support plasma cell survival, with differential impacts on IgM-

274 ion in affinity maturation of antibodies and plasma cell survival.

275 tigen-specific memory B cells and long-lived plasma cells that encode TcdB-neutralizing antibodies.

276 ells and B cells in adipose tissue-including plasma cells that express immunoglobulin J-which also ac

277 We identified a subset of plasma cells that expresses B-cell receptors (BCR) speci

278 may promote the establishment of long-lived plasma cells that secrete antigen-specific, high-affinit

279 The MG thymus is a reservoir of plasma cells that secrete disease-causing AChR autoantib

280 We found B cells and plasma cells to be the most abundant cells that present

281 A) are constitutively secreted by intestinal plasma cells to coat and contain the commensal microbiot

282 on of proliferating plasmablast to quiescent plasma cell under survival conditions including the pote

283 n in endoplasmic reticulum (ER) expansion in plasma cells via unknown mechanisms; interestingly, anot

284 While IgM and IgA secretion by IghPax5/+ plasma cells was normal, IgG secretion was modestly decr

285 immune signatures, including interferon and plasma cells, was observed during healthy pregnancy.

286 Using intratumoral B cells and plasma cells, we generated several HPV-specific human mo

287 To target plasma cells, we treated sensitized rhesus macaques with

288 IgE(+) plasma cells were abundantly present in STAT3-HIES bone

289 Infliximab-specific plasma cells were detected in patient tissue samples by

290 CD138 expressing plasma cells were identified and quantitatively assessed

291 Increased numbers of IgA-producing plasma cells were observed in healthy humans with defect

292 ding transitional, mature naive, memory, and plasma cells, were highly susceptible to VACV binding.

293 dsDNA titers, and the number of circulating plasma cells, which alleviated kidney pathology and impr

294 ase inhibition reduced viability of CD138(+) plasma cells while sparing CD138(-) cells derived from b

295 ion of Ufbp1 and ufmylation pathway genes in plasma cells, while Ufbp1 deficiency impairs ER expansio

296 esting marginal zone B cells, which generate plasma cells with exceptionally rapid kinetics, reinforc

297 we identified memory B cells and plasmablast/plasma cells with highly similar Ig heavy-chain sequence

298 lls with anti-CD20 monoclonal antibodies and plasma cells with proteasome inhibitors and anti-CD38 mo

299 microscopy analysis to identify a subset of plasma cells with robust cytoplasmic expression of IL-37

300 minary, the significance of CD138 expressing plasma cells within BM specimens should be investigated