ライフサイエンスコーパス: B cell

1 ty in the activation of the lineage germline B cell.

2 are significantly lower than in SPPL2a(-/-) B cells.

3 immune murine B cell subsets and CD27- human B cells.

4 ukaemia (CLL) is a clonal disorder of mature B cells.

5 rd antigen in activated germinal center (GC) B cells.

6 Ab, yet harbor marginal zone and follicular B cells.

7 ge pre-B cells to small B cells and immature B cells.

8 irus that establishes a latency reservoir in B cells.

9 ery of innate signals to antigen-experienced B cells.

10 ypermutation, and differentiated into memory B cells.

11 elated to their intracellular trafficking in B cells.

12 as impaired in all mature naive CVID-derived B cells.

13 CD4(+) and CD8(+) T cells but no binding by B cells.

14 c leukemia tumor cells while sparing healthy B cells.

15 ctivated memory cells and tissue-like memory B cells.

16 .IMPORTANCE EBV establishes viral latency in B cells.

17 e response and contained hypermutated IgD(+) B cells.

18 at concentrations that did not affect normal B cells.

19 urvival, and tissue infiltration of leukemic B cells.

20 late times for maintenance of the Tfh and GC B cells.

21 quencing method can use as few as 1000 naive B cells.

22 biting proliferation of germinal center (GC) B cells.

23 with less contribution from neutrophils and B cells.

24 o showed superior activation of Env-specific B cells.

25 s to sense alum and, in turn, activate T and B cells.

26 h cells than other lineages of more specific B cells.

27 (VL) sequences of individual and Ag-specific B cells.

28 ctor kappa-light-chain-enhancer of activated B cells.

29 c cells such as in mammalian hepatocytes and B-cells.

30 ed with avoidance of humoral immunity, i.e., B cell activation and antibody neutralization.

31 creased B regulatory cell [Breg] counts, and B cell activation and apoptosis) is specifically associa

32 s BAFF, IL-2, and IL-21 induce memory and DN B cell activation and differentiation has implications f

33 However, B cell activation was only partially normalized post-ART

34 into the RBC cell surface strongly inhibited B cell activation, cytokine secretion, and proliferation

35 d with an hCD22 ligand were shown to prevent B cell activation, increase cell death, and induce toler

36 arabinose residues, decreased the extent of B cell activation.

37 B-cell activation seemed to play a role in B-cell lympho

38 osit MYD88/p100 signaling as a regulator for B-cell activation.

39 phia chromosome (Ph)-positive or Ph-negative B-cell acute lymphoblastic leukaemia who were due to rec

40 d blood cancers and primary, patient-derived B-cell acute lymphoblastic leukemia blasts compared with

41 nsposon screens of 123 mammary tumors and 20 B-cell acute lymphoblastic leukemias, respectively.

42 myeloid cells could contribute to the strong B-cell ALL association of MLL-AF4 leukemia observed in t

43 n, phosphoinositide-interacting protein 2 in B cells alone enhanced this noncanonical autophagy, resu

44 mmune responses by differentially regulating B cell and CD4 T cell responses during acute viral infec

45 fferences in function between MBCs and naive B cells and among MBC subsets and how this leads to memo

46 reported that NP contain elevated levels of B cells and antibodies, making NP an ideal system for st

47 that the IL-12p35 subunit induces regulatory B cells and can be used therapeutically to limit autoimm

48 ution to the gut, increases of the activated B cells and circulating tissue-like memory B cells, and

49 chromosomal rearrangements in primary murine B cells and discovered that RAG1/2 causes aberrant inser

50 eterogeneous expression of Ifnb in wild-type B cells and distinct gene expression patterns associated

51 d CL59, that block membrane fusion with both B cells and epithelial cells.

52 ferentiation from large pre-B cells to small B cells and immature B cells.

53 on, we compared the fate of IgE-ICs in human B cells and in CD23-expressing monocyte-derived dendriti

54 ctor kappa-light-chain-enhancer of activated B cells and negative regulators tumor necrosis factor-al

55 e generated normal levels of germinal center B cells and plasmablasts in periphery, they produced sig

56 Pirfenidone dampened splenic germinal center B-cell and T-follicular helper cell frequencies that col

57 used a significant increase in percentage of B-cells and significantly decreased percentage of myeloi

58 d B cells and circulating tissue-like memory B cells, and expansion of the B regulatory cells (Bregs)

59 is comparable to expression on human primary B cells, and it colocalizes with mCD22 on the cell surfa

60 pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49 recombinant chemokines us

61 ly composed of CD3+ T cells, scattered CD20+ B cells, and relatively few PD-1+ (programmed cell death

62 essment of neutralizing antibodies, T cells, B cells, and safety.

63 liciting local mucosal immunity and systemic B cell- and T cell-mediated memory responses.

64 affinity-matured human NANP-reactive memory B cell antibodies elicited by natural Pf exposure that p

65 tion compromises the activity of the pivotal B-cell antigen receptor (BCR)-proximal effector spleen t

66 B cells are a significant producer of PIBF1 in human cho

67 While circulating B cells are virtually restored to preinfection levels du

68 As recirculating naive Ag-specific B cells arrive in Ag-draining secondary lymphoid organs,

69 tter long-term outcome had higher numbers of B cells at birth than those who developed LTI; no differ

70 s of these receptors in myeloid cells during B cell autoimmune activation remain less clear.

71 complex 1-dependent canonical autophagy, GC B cell autophagy occurred predominantly through a noncan

72 In both mouse and human B cells, BCR ligands that deliver a TLR9 agonist induce

73 The density of CD23 molecules on B cells but not the number of CD23(+) cells correlated w

74 Infection of B cells by HCV inhibited the recall reaction to antigen

75 c antigen receptor (CAR) that target CD19 in B-cell cancers, although data regarding B-cell lymphomas

76 responses depend on competitive selection of B cells carrying somatically mutated B-cell receptors by

77 proportional decrease in splenic follicular B cells (CD21/35(int)CD23(+)) at 1, 2, and 12 months of

78 ed post-ART, with the frequency of activated B cells (CD86(+)CD40(+)) reduced compared with pre-ART l

79 the treatment of B cell neoplasms, including B cell chronic lymphocytic leukemia (B-CLL).

80 nmutated common ancestor knock-in mice Env(+)B cell clones develop anergy and partial deletion at the

81 ne of the main factors limiting entry of new B cell clones into ongoing immunization-triggered GC res

82 ion, somatic hypermutation, and selection of B cell clones.

83 Depletion of the memory B-cell compartment contributes to the immunosuppression

84 B cells contribute critically to an effective immune res

85 B cells contribute to multiple aspects of autoimmune dis

86 f multiple sclerosis suggests that depleting B cells could be useful for treatment.

87 In addition, IL-7-stimulated pro-B cell cultures revealed a reduced differentiation from

88 Therefore, we studied B cell cytokine secretion and/or Ab production across ob

89 In contrast, TIM-4(+) B cells decreased B16-F10 metastasis and s.c. tumor grow

90 Wild-type (WT) and B cell-deficient mice received ovalbumin (OVA) intranasa

91 ed to lethality in infected animals, whereas B cell-deficient mice showed CD4(+) T cell loss but reco

92 old reduced I-A expression on the surface of B cells, dendritic cells, cortical thymic epithelial cel

93 Unlike B cell depletion, pan-T cell aplasia is prohibitively to

94 viral infections due to combined T cell and B cell depletion.

95 lly removed the pericardial AT and performed B-cell depletion and granulocyte-macrophage colony-stimu

96 circulating Ab in mediating CTL responses to B cell-derived exosomes was ruled out using DHLMP2A mice

97 data indicate that the environment in which B cells develop can affect the expressed Ig repertoire b

98 Before birth, B cells develop in the fetal liver (FL).

99 sitional B cell subsets demonstrated that MZ B cell development was blocked at the transitional-1 to

100 s the BCR and coreceptor programs throughout B cell development, promoting enrichment of self-reactiv

101 nduced mTOR activation impairs IL-7-mediated B cell development.

102 artly compensate for loss of Btk activity in B cell differentiation, although the underlying mechanis

103 ntial signaling and provide insight into how B cells discriminate between antigens of different quant

104 n both disease models, IL-4Ralpha-responsive B cells displayed increased IL-4 production as early as

105 oss of naive B cells, loss of resting memory B cells due to their redistribution to the gut, increase

106 E We report here that the HIV/SIV-associated B cell dysfunction (defined by loss of total and memory

107 SIV-associated B cell dysfunction associated with the pathogenic SIV in

108 onstitute a rate-limiting checkpoint against B cell dysregulation by MYD88(L265P) and provide an expl

109 GCs) in lymphoid tissues where self-reactive B cells expand and differentiate.

110 B cells expressed B surface markers compatible with a ma

111 p in this process is the activation of naive B cells expressing germline (gl) antibody precursors tha

112 Conversely, B cells expressing MYD88(L265P) decreased surface IgM co

113 B cells expressing the T-bet transcription factor, a mar

114 lograft tolerance, and this was dependent on B cell expression of TIM-4.

115 decrease in the messenger RNA level of early B cell factor 1 (EBF1) and paired box 5, two critical tr

116 fic mIg/BCR dosage may play a larger role in B cell fate than previously anticipated.

117 innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mecha

118 e homing of Tfh cells and the development of B cell follicles.

119 r helper (pTfh) cells, which provide help to B cells for developing into Ab-secreting cells, were sim

120 significantly associated with gp120-specific B cell frequencies.

121 epertoire but are rarely found in IgG memory B cells from healthy individuals.

122 B cells from hypersensitive patients, but not controls,

123 vate EBV lytic induction in freshly isolated B cells from peripheral blood mononuclear cells (PBMCs)

124 n that six codons in VH4-containing genes in B cells from the cerebrospinal fluid of patients with re

125 Analysis of memory B cells from the immunized macaque suggests that elicita

126 ranscriptomes and proteomes of primary mouse B cells from wild-type and STAT6-deficient mice cultured

127 ts on nonmotile E. coli exposed to polymyxin B, cell-generated frequency noise dropped close to zero

128 onal epitope(s), masked in refp17, to elicit B-cell growth-promoting signals after its interaction wi

129 Human CD40L(+) ILC3s provide innate B-cell help and are involved in an innate immunoregulato

130 Multiple myeloma (MM) is a plasma B-cell hematologic cancer that causes significant skelet

131 PRIL system is best known for its control of B cell homeostasis, and it is a target of therapeutic in

132 expansion of the "exhausted," virus-specific B cells, i.e., activated memory cells and tissue-like me

133 In B cells, Ig class switch recombination (CSR) is initiate

134 ibitory activity for allergen-IgE binding to B cells (IgE-facilitated allergen binding).

135 estions about the establishment of effective B cell immunity elicited by vaccination, not just agains

136 s an innate link between viral infection and B cell immunity.

137 Conditional deletion of T-bet from B cells impaired the formation of germinal centers and m

138 omotes chronic gammaherpesvirus infection of B cells.IMPORTANCE Gammaherpesviruses infect a majority

139 We assessed differentiation of B cells in bone marrow and spleen and analyzed their end

140 Anti-Notch2 antibodies decreased MZ B cells in control and Notch2HCS mice.

141 The potential protective role of B cells in controlling cCMV-related disease and the clin

142 Dendritic cells, monocytes, and B cells in HCC tumors expressed ligands for these recept

143 later found to be present on some subsets of B cells in humans; however, whether CD6 plays any role i

144 dies, making NP an ideal system for studying B cells in the airways.

145 een reported to respond against EBV-infected B cells in the lytic cycle and to control the viral infe

146 ur data suggest that the altered response of B cells in tolerant recipients may contribute to long-te

147 unction (defined by loss of total and memory B cells, increased B regulatory cell [Breg] counts, and

148 B cells influence the pathogenesis of multiple sclerosis

149 the clonal selection of high affinity memory B cells into the plasma cell fate, our findings provide

150 Expression of hCD22 on transgenic murine B cells is comparable to expression on human primary B c

151 t the block of CD74 degradation in CatS(-/-) B cells is incomplete, so that NTF levels are significan

152 Although selection of GC B cells is triggered by antigen-dependent signals delive

153 transduced T cells efficiently lysed primary B-cell leukemia, mantle cell lymphoma, and multiple myel

154 300 are recurrently mutated in the activated B cell-like and germinal center (GC) B cell-like subtype

155 tivated B cell-like and germinal center (GC) B cell-like subtypes of diffuse large B cell lymphoma (D

156 e therefore expected to evolve only when the B cell lineage evolving breadth is consistently capturin

157 two critical transcription factors directing B cell lineage specification and commitment.

158 omic and epigenomic study in patient-derived B-cell lines to investigate the genome-scale effects of

159 infection is characterized by loss of naive B cells, loss of resting memory B cells due to their red

160 ignificantly higher prevalence of monoclonal B cell lymphocytosis, premalignant condition poorly desc

161 r (GC) B cell-like subtypes of diffuse large B cell lymphoma (DLBCL).

162 ly, BCL-W was overexpressed in diffuse large B cell lymphoma and correlated with decreased patient su

163 B cell lymphoma-6 (Bcl-6) is a transcriptional repressor

164 mphomas (DELs) are subtypes of diffuse large B-cell lymphoma (DLBCL) associated with poor outcomes af

165 inical trials of patients with diffuse large B-cell lymphoma (DLBCL).

166 licular lymphoma (FL; n = 29), diffuse large B-cell lymphoma (DLBCL; n = 34), DLBCL arising from chro

167 pression of downstream genes, such as Bcl-2 (B-cell lymphoma 2), c-Myc, MMP7 (matrix metalloproteinas

168 B-cell activation seemed to play a role in B-cell lymphoma development at early stages across diffe

169 CTL019) to treat patients with diffuse large B-cell lymphoma or follicular lymphoma that had relapsed

170 Lymphoma cells from diffuse large B-cell lymphoma patients had high basal phosphorylation

171 ous NHL histologies, including diffuse large B-cell lymphoma, Richter's transformation, mantle cell l

172 evels and causes cell death in EBNA1-induced B cell lymphomas.

173 on and are associated with cancer, including B cell lymphomas.

174 ar lymphoma, and MYC/BCL2/BCL6 in high-grade B-cell lymphomas are essential for diagnosis.

175 9 in B-cell cancers, although data regarding B-cell lymphomas are limited.

176 ed by mutations in JAK2, CALR, or MPL In the B-cell lymphomas, detection of characteristic rearrangem

177 lymphoma, Burkitt's lymphoma, diffuse large B-cell lymphomas, nasopharyngeal carcinoma (NPC), and ly

178 be a crucial part of the pathophysiology of B-cell lymphomas; however, several early attempts to tar

179 mechanism underlying the regulation of early B cell lymphopoiesis is unclear.

180 ndamental differences in the pathogenesis of B-cell lymphoproliferative disorders.

181 re frequently and simultaneously detected in B cell malignancies.

182 cal functions of BACH2 and its regulation of B-cell malignancies in chronic hypoxic microenvironment

183 these data and mutations identified in other B-cell malignancies, 1716 genes were sequenced in 113 FL

184 te (ADC) being investigated for treatment of B-cell malignancies, which has improved potency compared

185 a novel treatment for refractory or relapsed B-cell malignancies.

186 fusion lymphoma (PEL) is a highly aggressive B-cell malignancy that is closely associated with one of

187 V/SIV infections and suggest that monitoring B cells may be a reliable approach for assessing disease

188 B-blasts can differentiate to become memory B cells (MBC), in which EBV persistence is established.

189 Myasthenia gravis (MG) is a prototypical B cell-mediated autoimmune disease affecting 20-50 peopl

190 These antibodies may provide the basis for a B cell-mediated HIV-1 vaccine.

191 nts did not show upregulation of T cell- and B cell-mediated rejection pathways.

192 not a consequence of diminished formation of B cell memory; instead, SpA reduced the proliferative ca

193 on that CD19-independent factors drive early B cell mobilization and recruitment to the infected CNS,

194 0-positive cells did not display the typical B cell morphology, having in general a more dendritic ce

195 hallmark anti-CD20 mAb for the treatment of B cell neoplasms, including B cell chronic lymphocytic l

196 nscriptional regulator Ikaros into mouse pre-B cell nuclei triggered immediate binding to target gene

197 ved that NKG2D deficiency affects peripheral B cell numbers.

198 Flow cytometric analysis of peripheral blood B cells of 30 MC-negative HCV-infected patients and 15 h

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

200 increase in CD21/35(high)CD23(-) splenic MZ B cells of approximately fivefold and a proportional dec

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

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

203 on Network Analysis (WGCNA) was enriched for B cell pathways, and shared seventeen genes with a mouse

204 received renewed interest as an innate-like B cell population of fetal-derived hematopoiesis, respon

205 ance/survival of the mature naive peripheral B cell population.

206 use in patients with relapsed or refractory B-cell precursor ALL on the basis of single-group trials

207 erimental stroke prevents loss of splenic MZ B cells, preserves IgM levels, and reduces bacterial bur

208 icial substrates or live cells, we show that B cells primarily use force-dependent extraction and res

209 s, mTORC1 activation is required for fueling B cells prior to DZ proliferation rather than for allowi

210 ther antigen-specific contexts, such as with B-cell probes.

211 In vitro, IL4I1-deficient B cells proliferate more efficiently than their wild-typ

212 patient suffering from recurrent EBV-induced B cell proliferations including Hodgkin's lymphoma becau

213 ic cells are stiff cells that promote strong B cell pulling forces and stringent affinity discriminat

214 ted with 2 or more mutations, and linked the B cell receptor (BCR) pathway to trisomy 12, an importan

215 We discuss targeting of B cell receptor (BCR) signaling, with emphasis on identi

216 evels of B-lineage transcription factors and B cell receptor (BCR)/pre-BCR-signaling genes.

217 of infiltrating immune cell types, the T or B cell receptor repertoire, and direct the design of a p

218 mediating energy metabolism, cell cycle, and B cell receptor signaling.

219 ese B-ALLs encode proteins implicated in pre-B-cell receptor (BCR) signaling and migration/adhesion,

220 ated to regulate signaling downstream of the B-cell receptor (BCR), Fc receptors (FcRs), and toll-lik

221 ltage-gated proton channel-encoding gene and B-cell receptor signaling modulator, were associated wit

222 Combinatorial disruption of B-cell receptor signalling and PI3K-AKT-mTOR axis leads

223 tion of B cells carrying somatically mutated B-cell receptors by follicular helper T (TFH) cells in g

224 ever, intravital imaging suggests that early B-cell recognition of large foreign antigens may be tran

225 ric form of the toxin, suggesting that human B cells recognize epitopes on the dimerized form of LukA

226 resembling the trafficking block in anergic B cells repeatedly stimulated by self-antigen.

227 collective findings point toward a deformed B cell repertoire as a fundamental component of MG.

228 34-expressing clones are common in the naive B cell repertoire but are rarely found in IgG memory B c

229 an those who developed LTI; no difference in B cell replication was observed.

230 nctions from CH12F3 cells and primary murine B cells, respectively.

231 e have demonstrated that the kinetics of the B cell response are similar for all four FMDV serotypes

232 RATIONALE: Diverse B cell responses and functions may be involved in athero

233 nt resulted in suppression of virus-specific B cell responses by inhibiting proliferation of germinal

234 suppresses follicular helper T cell-mediated B cell responses in the germinal center reaction.

235 Here, we describe B cell responses to C-PfCSP from European donors who und

236 ncreasing the risk for seeding of autoimmune B cell responses.

237 presenting cells support different stages of B cell responses.

238 ory molecule playing a role in physiological B cell responses.

239 mechanisms of antibody production in memory B cell responses.IgE is an important mediator of protect

240 B-cell responses result in clonal expansion, and can occ

241 ation, in the absence of modulation of T- or B-cell responses.

242 -/-)) mice were used as a model for enhanced B-cell responses.

243 alysis of B6 Ifnb(+/+) versus B6 Ifnb(--) T1 B cells revealed heterogeneous expression of Ifnb in wil

244 immunoregulatory signaling in APCs regulates B cell selection and autoimmunity.

245 protective or deleterious effects on loss of B cell self-tolerance in vivo, we depleted neutrophils a

246 assenger allele system to assay, in mouse GC B cells, sequence-intrinsic SHM-targeting rates of nucle

247 Interestingly, PLA-specific B cells showed increased CCR5 expression after high-dose

248 ned a model of specific antibody deficiency, B cell-specific CD79a-Cre x XBP1 (X-box binding protein-

249 B-cell-specific Moloney murine leukemia virus integratio

250 BACH2, a B-cell-specific transcription factor, plays a critical r

251 rtial deletion at the transitional to mature B cell stage, but become Env(-) upon receptor editing.

252 ptosis and is shared by all preimmune murine B cell subsets and CD27- human B cells.

253 tometry analysis of the splenic transitional B cell subsets demonstrated that MZ B cell development w

254 ctions with regard to dynamics of the memory B cell subsets point to their role in the pathogenesis o

255 nerated IgE(+) cells, the capacity of tonsil B-cell subsets to generate IgE(+) PCs and the class swit

256 Residual B cell subtype distribution was disrupted in the spleen,

257 ng a multivalent immunogen, rare VRC01-class B cells successfully competed in germinal centers (GC),

258 In SPPL2a(-/-) B cells, such an NTF impairs endosomal trafficking and B

259 oxin-elicited suppression of early B and pro-B cells, suggesting a role of AHR in regulating B lympho

260 we have exposed a critical role for BCL-W in B cell survival and lymphomagenesis.

261 This dynamic change in B cell survival mechanisms is unique to virus-infected c

262 Delivery of neurotransmitters across the T-B-cell synapse may be advantageous in the face of infect

263 Thus, the mechanical properties of B cell synapses regulate antigen extraction, suggesting

264 ral or mature versus precursor) and lineage (B cell, T cell, and natural killer cell).

265 ), MRD detection method, phenotype/genotype (B cell, T cell, Philadelphia chromosome), and EFS and OS

266 ld cells (M cells) overlay an arrangement of B cells, T cells, and antigen-presenting cells.

267 entify critical immunoregulatory circuits in B cells that may be targeted to promote long-lived humor

268 We discuss the abnormalities in B cells that occur in HIV infection both in the peripher

269 ystems of infected hosts to recall of memory B cells that recognized the lateral patch, the principal

270 erred by allergen-specific long-lived memory B cells that replenish the IgE(+) PC compartment.

271 rom human immature dendritic cells and naive B cells to assess the expression of CD40-downstream gene

272 Mechanistically, DHA did not directly target B cells to elevate Ab levels.

273 H2 histone methyltransferase is required for B cells to form germinal centers (GC).

274 ontributes to the efficacy of SIT by helping B cells to produce neutralizing IgG antibodies.

275 led a reduced differentiation from large pre-B cells to small B cells and immature B cells.

276 strategy to reliably identify blood IgG4(+) B cells to study their cellular and molecular characteri

277 cking of FDC secretion of IFN-alpha restored B cell tolerance and reduced the amount of GCs and patho

278 Thus, upregulation of EBI2 drives the B cells toward the extrafollicular area, whereas downreg

279 Mice with CD1d(hi) CD5(+) B cell transfer demonstrated reduced periodontal bone lo

280 fer group and the group with CD1d(lo) CD5(-) B cell transfer.

281 eveal an important role for RUNX3/CBF during B cell transformation and EBV latency that was hitherto

282 s with RUNX3-a protein induced by EBV during B cell transformation.

283 arrested B-lymphopoiesis at the pro-B to pre-B-cell transition and, contrary to their proposed domina

284 icantly increases CD20 levels in established B-cell tumor cell lines and primary malignant cells.

285 crete proportion of infiltrating T cells and B cells underwent proliferation within the pituitary par

286 differentiation of sorted LPS-stimulated MZ B cells was impaired, and aged bumble mice were unable t

287 hereas frequencies of transitional and naive B cells were decreased.

288 antly, very high numbers of antigen-specific B cells were detected in local genital draining lymph no

289 ed that frequencies of class-switched memory B cells were increased in the patients, whereas frequenc

290 mic or splenic DC, whereas thymic or splenic B cells were poor donors.

291 vitro immunoglobulin production by cultured B cells were quantified by using ELISA.

292 genes in immature dendritic cells and naive B cells were significantly enriched in synovial tissues

293 diating xenobiotic toxicity, is expressed in B cells, which are known targets for environmental pollu

294 Mechanistically, we show that B cells, which express BCRs specific to hen egg lysozyme

295 The chemokine CXCL13 recruits both Tfh and B cells, which is essential for the homing of Tfh cells

296 lly, CpG increased the number of circulating B cells, which produced elevated amounts of tumor necros

297 lymphoid tissues, clusters of proliferating B cells with a GC-like phenotype can be generated in the

298 zing near T lymphocytes early in disease and B cells with advanced disease.

299 Nod1, including follicular and marginal zone B cells with natural autoreactivity.

300 lin light chain editing occurred, generating B cells with up-regulated Nod1, including follicular and

301 protein 3 (EBI3) mRNAs were detected only in B cells, with a trend toward a lower level among patient