ライフサイエンスコーパス: B cell

1 astogenic support provided by Th1, Th17, and B cells.

2 Bcl-6 directly repressed Hhex in GC B cells.

3 ne receptors were up-regulated in CSF memory B cells.

4 ctioning of human IL-10 producing regulatory B cells.

5 e, despite rapid turnover of germinal-centre B cells.

6 ation, and robust generation of Ab-producing B cells.

7 uniquely required by normal and malignant GC B cells.

8 the IgE- and IgG subclass-expressing memory B cells.

9 ting apoptosis and inhibiting necroptosis in B cells.

10 ls during the production phase, or in plasma B cells.

11 th preferential recruitment of high-affinity B cells.

12 a cells, memory cells, and immune regulatory B cells.

13 cing Dsg-specific autoantibody production by B cells.

14 ate antigen receptor signaling in both T and B cells.

15 ectively induce ex vivo expansion of GZMB(+) B cells.

16 initiated the transformation of premalignant B cells.

17 ype possessing the ability to suppress naive B cells.

18 orable outcome were age >18 years; activated B-cell (ABC) DLBCL profile, HGBCL, NOS, high genetic com

19 : A subpopulation of B cells (age-associated B cells [ABCs]) is increased in mice and humans with inf

20 antigen acquisition by B cells, duration of B cell access to antigen and the timing of T cell help m

21 view, we summarize the emerging knowledge of B cells across the NSAb-mediated diseases.

22 ~2,200 IgG-secreting activated human memory B cells, activated ex vivo, demonstrating its versatilit

23 nance therapy with belimumab, an antibody to B-cell activating factor.

24 1 monoclonal antibody targeting the cytokine B cell-activating factor (BAFF).

25 pha activation lowered surface BCR, CD19 and B cell-activating factor receptor and increased expressi

26 B-cell-activating factor (BAFF) is associated with donor

27 The "two-signal" model of B cell activation has long been invoked to explain alter

28 uction role in antibody expression following B cell activation.

29 ity to effectively recruit T cell help after B cell activation.

30 initiating oncogenic lesion in patients with B cell acute lymphoblastic leukemia (B-ALL), making B-AL

31 and adults with Philadelphia chromosome-like B cell acute lymphoblastic leukemia (Ph-like B-ALL) expe

32 %] of 7 patients) and PDGFRB fusion-positive B-cell acute lymphocytic leukaemia (43 [88%] of 49 patie

33 Children with ABL-class fusion B-cell acute lymphocytic leukaemia have poor outcomes wh

34 of paediatric patients with ABL-class fusion B-cell acute lymphocytic leukaemia in the pre-tyrosine-k

35 DFD regimen favors persistence of functional B cells after the third dose.

36 Rationale: A subpopulation of B cells (age-associated B cells [ABCs]) is increased in

37 Surprisingly, AID(S38A/S38A)UNG(-/-) mouse B cells also cannot complete CSR or affinity maturation

38 onal programs in circulating T(FH) cells and B cells among patients with ABMR, which markedly differe

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

40 In addition, both transitional B cell and plasmablast levels were significantly elevate

41 its substrate Notch, a critical regulator of B cell and T cell development.

42 detected activated B cells, germinal centre B cells and ASCs within the tumour microenvironment.

43 Single cell RNA-sequencing of activated B cells and construction of differentiation trajectories

44 that a longer PLP antigen may better engage B cells and designed a peptide encompassing the extracel

45 lls required CXCL12-dependent crosstalk with B cells and dictated GC output by retaining B cells in t

46 ecreased MHCII expression in germinal center B cells and diffuse large B cell lymphoma.

47 ration of long-lived plasma cells and memory B cells and highlight the challenges for successful vacc

48 ein EBNA3A is expressed in latently infected B cells and is important for efficient EBV-induced trans

49 ssed only on plasma cells, a small subset of B cells and MM cells, which makes it a suitable target a

50 Tumours often contain B cells and plasma cells but the antigen specificity of

51 fector memory T cells, as well as monocytes, B cells and stromal fibroblasts.

52 regimen is associated with a breakthrough of B cells and their aggressive graft infiltration.

53 the appropriateness of specific therapy when B cells and/or plasma cells are found.

54 B-cell and antibody responses to Plasmodium spp., the pa

55 igin and alter interactions between lymphoma B-cells and other cells within the microenvironment.

56 ntibodies, frequency of germinal center (GC) B cells, and antigen-specific plasma cells induced durin

57 and in vivo against MM plasma cells, memory B cells, and MM-propagating cells.

58 capabilities relative to alphabeta T cells, B cells, and NK cells, allowing immunosurveillance for s

59 In addition to inducing Tregs, B cell antibody production and antigen-presenting cell a

60 B cell antigen receptor (BCR) signals induce Syk activat

61 individuals, indicating strong selection of B cell antigen receptors even in the absence of microbio

62 ence that primary FCRL4-bearing human memory B cells are constitutively bound to IgA.

63 Memory and Naive B cells are good potential predictors of LC and HCCin di

64 Tumor-infiltrating B cells are heterogeneous, and their roles in tumor immu

65 nodes of SLE patients, and colocalized with B cells at the margins of follicles.

66 sociated with increased plasma levels of the B-cell-attracting chemokine CXCL13.

67 otypic and functional abnormalities of T(FH)-B cell axis.

68 MS, adoptive transfer of IL-10(+) regulatory B cells (B(regs)) has been shown to reverse EAE by promo

69 However, the role of B cells beyond antibody-producing cells is less well def

70 ults are not only valuable for understanding B cell biology, but also have important implications for

71 to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma ce

72 ls provide help to autoreactive TG2-specific B cells by involvement of gluten-TG2 complexes, and they

73 Patients with T- or B-cell CAEBV had increased phosphorylation of Akt and S6

74 and expressed in developing germinal center B cells, can induce Kaposi's sarcoma-associated herpesvi

75 w that high-affinity vaccines targeting rare B cells capable of broadly protective antibody responses

76 r reference samples (breast cancer cells and B cells), captured either separately or in mixtures, we

77 lls (CD3(+)CD8(+)CD161(+)PD1(+)), and memory B cells (CD3(-)CD19(+)CD20(+)CD24(+)CD27(+)) were found

78 ts of bacterial antigens on the emergent B-1 B cell clonal repertoire.

79 (SPF) mice contain highly dominant 'winner' B cell clones at steady state, despite rapid turnover of

80 Thymus-associated B cell clones were detected in the circulation by both m

81 Many circulating thymus-associated B cell clones were inferred to have originated and initi

82 sensitivity and specificity for identifying B cell clones.

83 er, infection failed to stimulate the memory B cell compartment in preimmunized mice, although they w

84 latency and lytic programmes to navigate the B-cell compartment and evade immune responses.

85 s thought to be a disorder of the peripheral B-cell compartment, in 25% of patients, early B-cell dev

86 sights into the nature and function of human B-cell compartments across multiple tissues.

87 Interclonal B cell competition to complex antigens, particularly in

88 al organization of T(FH) cells to form T(FH):B cell conjugates in germinal centers.

89 phase 1b study, percentages of transitional B cells decreased, naive B cells increased, and senescen

90 Here, we show that at 1 month postinfection, B cell deficiency alone enhanced resistance to splenic i

91 ficient B6.BTg.muMT mice, and BAFF-deficient/B cell-deficient B6.Baff(-/-) muMT mice demonstrated tha

92 -deficient B6.muMT mice, BAFF-overexpressing/B cell-deficient B6.BTg.muMT mice, and BAFF-deficient/B

93 h BAFF-deficient B6.Baff(-/-) Bcl2(Tg) mice, B cell-deficient B6.muMT mice, BAFF-overexpressing/B cel

94 esponse were analyzed by using wild-type and B-cell-deficient (muMT) mice and transfer of IL-10-profi

95 uced by half compared with parental WT Ramos B cells, demonstrating that the CTNNBL1 M466V mutation i

96 ctor kappa-light-chain-enhancer of activated B cells)-dependent inflammation, caspase-dependent apopt

97 These results establish a novel, efficient B cell-dependent EAE model.

98 robust clinical responsiveness of IgG4-RD to B cell depletion and by the identification of multiple s

99 The success of clinical trials of selective B-cell depletion in patients with relapsing multiple scl

100 Our approach was to utilize differential B-cell depletion with anti-CD20 to retain B cells whose

101 B-1 B cells derive from a developmental program distinct fro

102 copy number profiles revealed that malignant B cells derived from different patients with VRL had no

103 presence of concurrent donor-specific memory B cell-derived HLA antibodies (DSA-M) in renal allograft

104 ring the important contributions of CXCR4 to B cell development and function, we investigated the glu

105 We studied B cell development in the presence/absence of autoantige

106 enes related with class-switching and memory B cell development, including Aicda, Ski, Bmi1, and Klf2

107 models is that bnAb expression often hinders B cell development.

108 ally under negative selection during primary B cell development.

109 -cell compartment, in 25% of patients, early B-cell development in the bone marrow is impaired.

110 tic interaction of MYC and MNT in neoplastic B-cell development, but the underlying mechanism remaine

111 bone marrow environment is not permissive to B-cell development.

112 Stroke induced significant bilateral B cell diapedesis into remote brain regions regulating m

113 Thus, B cell diapedesis occurred in areas remote to the infarc

114 t contemporaneously developing memory and GC B cells differ in their affinity for antigen throughout

115 nal expansion, isotype switching, and memory B cell differentiation in response to T cell-independent

116 ignancy, namely follicular lymphoma (FL), GC B cell-diffuse large B cell lymphoma (GCB-DLBCL), and Bu

117 the biology and therapeutic rationale behind B-cell-directed therapeutics in MS, and proposes strateg

118 In addition, CTNNBL1 466V/V Ramos B cells displayed a decreased incidence of SHM that was

119 onsider all the complexities associated with B cell diversification such as the V(D)J rearrangement p

120 llular environment of antigen acquisition by B cells, duration of B cell access to antigen and the ti

121 ation of multiple self-antigens that promote B cell expansion.

122 wever, it is unclear which subpopulations of B cells express GZMB under normal conditions and which p

123 parallel, MCL cells as compared with normal B cells expressed elevated levels of WNT16, a NF-kappaB

124 ry activated phenotype, whereas EBV-infected B cells expressed plasma cell differentiation markers.

125 ed upon antigen re-encounter, whereas memory B cells expressed receptors capable of neutralizing viru

126 ated with specific expansion of transitional B cells, extrafollicular IgG2c-producing plasma cells, a

127 We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1

128 cine design and offer important insight into B cell fate decisions.

129 However, how apoptotic caspases regulate GC B cell fate has not been fully characterized.

130 timing of T cell help may affect follicular B cell fate, including death, survival, anergy, and recr

131 cquisition of founder mutations in activated B cells favors the development of aberrant MBs prone to

132 -) T(FH) cells and loses the ability to help B cells for antibody production.

133 te that detection of Borrelia burgdorferi (B.b.) cell-free DNA (cfDNA) in plasma can improve diagnosi

134 th B cells led to greater tissue like memory B cell frequencies.

135 SG3-CAART specifically lysed human anti-DSG3 B cells from PV patients and demonstrated activity consi

136 revealed a high degree of similarity between B cells from the same patient with VRL, with extensive g

137 downregulation of critical genes involved in B cell function (PAX5, CD79A, CD22, and FCRL1) and upreg

138 CL, NOS was predominantly of germinal center B-cell (GCB) subtype and carried gene mutations similar

139 CD11c(+) T-bet(+) B cells generated during ehrlichial infection require CD

140 l RNA sequencing analyses detected activated B cells, germinal centre B cells and ASCs within the tum

141 Memory B cells had reemerged in 2 of 10 (20%) relapses in patie

142 However, over the last decade B cells have been increasingly recognized as modulators

143 Central nervous system B cells have several potential roles in multiple scleros

144 tors and toward a more complex paradigm with B cells having an essential role in both the inflammator

145 Follicular T helper (TFH) cells provide B-cell help and are crucial for generating long-term hum

146 In normal resting B cells, IFITM3 was minimally expressed and mainly local

147 Furthermore, IL-21 significantly induced B cell IgA production in vitro, with the increased expre

148 Our aim was to analyze the role of B cells in a house dust mite (HDM)-based murine asthma m

149 ing confirms the accumulation of T cells and B cells in adipose tissue-including plasma cells that ex

150 in spleen and early depletion of Vi-specific B cells in bone marrow, resulting in hyporesponsiveness

151 er in germ-free than in SPF mice, and winner B cells in germ-free germinal centres are enriched in 'p

152 This study supports an important role for B cells in indirect T cell priming and further emphasize

153 The role of B cells in MS was selected as the topic of the 27th Annu

154 al expansion and unique functional states of B cells in responders.

155 jugate induced late apoptosis of Vi-specific B cells in spleen and early depletion of Vi-specific B c

156 so observed greater frequencies of activated B cells in the COVID-19 patients.

157 In particular, the central role of B cells in the disease has been demonstrated by both the

158 B cells and dictated GC output by retaining B cells in the follicle and steering their interaction w

159 Recent work has uncovered a role for B cells in the induction and activation of Tregs during

160 ECT domain leads to a block in maturation of B cells in the spleen and upregulation of proteins assoc

161 for efficient EBV-induced transformation of B cells in vitro In this study, we used a cord blood-hum

162 nable to support the constant development of B cells in vitro, indicating a possible low frequency or

163 Immature/transitional B cells increase remarkably in diabetic CHCpatients and

164 ges of transitional B cells decreased, naive B cells increased, and senescent CD8 T cells decreased (

165 00 monoclonal antibodies (mAbs) derived from B cells induced by numerous influenza virus vaccines and

166 ctor kappa-light-chain-enhancer of activated B cells inhibitor that blocks IL-1beta maturation.

167 iation of high-affinity germinal center (GC) B cells into memory B cells versus plasma cells is a maj

168 d naive IL-4Ralpha(-/lox) or IL-4Ralpha(-/-) B cells into muMT(-/-) mice a day before sensitization o

169 hat at low doses these SCFAs directly impact B cell intrinsic functions to moderately enhance class-s

170 tent to which antiviral effects of IRF-1 are B cell intrinsic, we generated mice with conditional IRF

171 In contrast, in testing, B cell-intrinsic IRF-1 expression promoted the MHV68-dri

172 er response, indicating that MHV68 may, in a B cell-intrinsic manner, usurp IRF-1 to promote the germ

173 IL-4 activation of B cells is essential for class switching and contributes

174 he antigen specificity of these intratumoral B cells is not well understood(1-8).

175 Culture of MAIT cell supernatants with B cells led to greater tissue like memory B cell frequen

176 Pre-B cell leukemia factor 1 (PBX1) is an essential developm

177 t a significant source of variation in daily B-cell levels or any CD4+ functional subset, it accounte

178 compound led to tumor stasis in an activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL)

179 e delineation of the CD22 interactome in the B cell line DT40.

180 Fundamentally, the autoantigen-specific B cell lineage leads to production of the pathogenic aut

181 In Ifitm3(-/-) B cells, lipid rafts were depleted of PIP3, which result

182 cision medicine approaches for diffuse large B cell lymphoma (DLBCL) is confounded by its pronounced

183 cular lymphoma (FL), GC B cell-diffuse large B cell lymphoma (GCB-DLBCL), and Burkitt lymphoma (BL).

184 is in noninfected bystander cells.IMPORTANCE B cell lymphoma 2 (Bcl-2) family proteins play important

185 in germinal center B cells and diffuse large B cell lymphoma.

186 Members of the B-cell lymphoma (BCL-2) protein family regulate mitochon

187 We analyze human diffuse large B-cell lymphoma (DLBCL) and non-DLBCL pathologic images

188 n follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) within the context of prior know

189 an activated B-cell-like (ABC) diffuse large B-cell lymphoma (DLBCL) xenograft model, but this compou

190 biological overlap with primary mediastinal B-cell lymphoma and conferred excellent prognosis.

191 Re-expression of individual miRNAs in B-cell lymphoma cells down-regulated expression of PRMT5

192 hanism conferring selective advantage during B-cell lymphoma development.

193 2 models without eliminating A20-luciferase B-cell lymphoma graft-versus-leukemia (GVL).

194 cers such as acute leukemia or diffuse large B-cell lymphoma that require rapid interventions.

195 uding mantle cell lymphoma and diffuse large B-cell lymphoma, and supports constitutive expression of

196 with histologically confirmed diffuse large B-cell lymphoma, who relapsed or had refractory disease

197 L) include venetoclax, the oral inhibitor of B-cell lymphoma-2, and inhibitors of kinases in the B-ce

198 s-gender imbalance and splenic marginal zone B-cell lymphoma-emerged in combination with gene dose re

199 issemination of cancer, including aggressive B-cell lymphoma.

200 t NLRC5 signaling in macrophages can promote B-cell lymphomagenesis during chronic Helicobacter infec

201 ainst recurrent and refractory diffuse large B cell lymphomas (DLBCL).

202 Other B cell lymphomas have acquired an oncogenic mutation in

203 Pediatric large B-cell lymphomas (LBCLs) share morphological and phenoty

204 tients experience relapse and die, targeting B-cell lymphomas with a NMT inhibitor potentially provid

205 he immune environments associated with major B-cell lymphomas with an emphasis on the immune escape p

206 f hematological cancer cell lines, including B-cell lymphomas, to the potent pan-NMT inhibitor PCLX-0

207 emerging precursor to neoplastic high-grade B-cell lymphoproliferation among people with HIV, especi

208 We demonstrate that lytic MHV68 infection of B cells, macrophages, and fibroblasts leads to robust ac

209 Complete remissions of a variety of B-cell malignancies lasting >= 3 years occurred after 51

210 (BTK), is a leading therapeutic strategy in B-cell malignancies, including chronic lymphocytic leuke

211 vity in patients with relapsed or refractory B-cell malignancies.

212 d demonstrated that, when compared to normal B cells, malignant plasma cells showed an extensive acti

213 B cell maturation antigen (BCMA) is expressed only on pl

214 ignaling, resulting in aberrations in T- and B-cell maturation and function.

215 gens, cluster of differentiation 3 (CD3) and B-cell maturation antigen (BCMA).

216 role for the HIV-1 protein NEF in preventing B-cell maturation into antibody-producing plasma cells.

217 Memory B cells (MBCs) expressing the transcription factor T-bet

218 use today depend on their ability to induce B cell memory, we have not yet succeeded in developing v

219 nstrate that, following selection in the LZ, B cells migrated to specialized sites within the canonic

220 Activated B cells modulate infection by differentiating into patho

221 for the brain data and granulocytes/T cells/B cells/monocytes for the blood data.

222 ceptible strains of mice show increased lung B cell, natural killer and T cell effector responses in

223 04 patients comprising different subtypes of B cell neoplasms, we demonstrate that IgCaller identifie

224 ctor kappa-light-chain-enhancer of activated B cells (NF-kappaB) as key signaling pathways in NFKBIZ/

225 Mantle cell lymphoma (MCL) is an uncommon B-cell non-Hodgkin lymphoma (NHL) that is incurable with

226 Drug Administration for relapsed aggressive B-cell non-Hodgkin lymphoma in part on the basis of dura

227 than 18 years of age with high-risk, mature B-cell non-Hodgkin's lymphoma (stage III with an elevate

228 ase-5 (PRMT5) is overexpressed in aggressive B-cell non-Hodgkin's lymphomas, including mantle cell ly

229 es, decreased T cell infiltration, increased B cell numbers, and decreased macrophage recruitment.

230 sing mAbs (n = 14) generated from peripheral B cells of two patients.

231 The influence of B cells on lung function, tissue remodeling, and the imm

232 th autoantibodies being produced by ignorant B cells on provision of T cell help.

233 additional to the BAFF-independent effect of B cells on Treg cells.

234 not impact bacterial burden, indicating that B cells only enhance susceptibility to infection when T

235 e was associated with an increased number of B cells (P = .016) and activated CD4 T cells (P = .016).

236 The authors revealed a distinct tolerant B cell phenotype possessing the ability to suppress naiv

237 cterized clinical parameters, mortality, and B cell phenotypes in blood and cerebrospinal fluid (CSF)

238 B cells play a key role in the development of IgE-mediat

239 B cells play an important role in allergies through secr

240 cells goes beyond its ability to expand the B cell population and is additional to the BAFF-independ

241 ecent advances in understanding the roles of B cell precursor frequency, B cell receptor affinity for

242 to coordinate both the proper positioning of B cell progenitors in the bone marrow (BM) microenvironm

243 In pro-B cells PTBP1 ensures precise synchronisation of the act

244 Here, we used direct labeling of B cells reactive with the N-acetyl-D-glucosamine (GlcNAc

245 However, engagement of the B cell receptor (BCR) induced both expression of IFITM3

246 t from that of conventional B cells, through B cell receptor (BCR)-dependent positive selection of fe

247 ing the roles of B cell precursor frequency, B cell receptor affinity for antigen, antigen avidity, a

248 Inhibition of the B-cell receptor pathway, and specifically of Bruton tyro

249 lymphoma-2, and inhibitors of kinases in the B-cell receptor signaling pathway, like Bruton tyrosine

250 e to external signals, such as in binding of B cell receptors (BCR) to antigen, which initiates signa

251 Because poor B-cell reconstitution after hematopoietic stem cell tran

252 n has long been invoked to explain alternate B cell recruitment into immune response to foreign antig

253 much more frequently than predicted in naive B cell repertoires.

254 The B cell response showed converging IGHV3-driven BCR clust

255 udes to wild-type mice, suggesting that this B cell response was independent of cognate T cell help.

256 Within lymph nodes, we observed augmented GC B cell responses and the promotion of T(h)1 gene express

257 We performed detailed characterization of B cell responses through high-dimensional flow cytometry

258 3 play partially redundant roles to restrain B cell responses to antigen in the absence of co-stimula

259 that can substantially alter the outcomes of B cell responses to complex antigens.

260 cts of M.tb infection and BCG vaccination on B cell responses to heterologous pathogen recall antigen

261 ow-valency antigens induced smaller effector B cell responses, with preferential recruitment of high-

262 We inferred that tolerant alloreactive B cells retained their ability to sense alloantigen beca

263 matched circulating T(FH) cell and activated B cell RNA-sequencing profiles identified highly coordin

264 show that TMEM30A loss-of-function increases B-cell signaling following antigen stimulation-a mechani

265 Here we show that OCA-B, a B cell-specific coactivator essential for germinal cente

266 ve DNA binding of MEF2A and into its role in B cell-specific gene regulation.

267 Surprisingly, B cell-specific IRF-1 deficiency attenuated the establis

268 tatus of signaling proteins across different B cell subpopulations present in a single sample.

269 Both human and mouse B cell subpopulations showed different basal and BCR sti

270 In chronic viral infections, the deranged B cell subset signifies uncontrolled disease.

271 Further, paired CSF and blood B cell subsets (RRMS; n = 7) were isolated using fluores

272 The roles distinct B cell subsets play in clonal expansion, isotype switchi

273 is associated with the apoptosis of multiple B cell subsets.

274 ECD) induced EAE not only in WT mice, but in B cell-sufficient mice incapable of secreting antibodies

275 cluding epithelial cells, endothelial cells, B cells, T cells and hepatocytes.

276 ires intracellular signaling in EBV-infected B cells that optimizes cell survival and proliferation,

277 olled a unique transcriptional program in GC B cells that promoted optimal GC polarization and choles

278 ead to germinal centers that are composed of B-cells that come from a single strain-specific clone, a

279 ce demonstrated that, in a host that harbors B cells, the effect of BAFF on Treg cells goes beyond it

280 functional TCRs or MHC class II molecules on B cells, the liposomal particles also elicited IgM, IgG1

281 l program distinct from that of conventional B cells, through B cell receptor (BCR)-dependent positiv

282 sfer of IL-10-proficient and IL-10-deficient B cells to muMT mice.

283 All vaccines rely on the ability of B cells to remember pathogen infections and respond more

284 ed gradients created by this network promote B cell trafficking.

285 ategies to optimize the use of existing anti-B-cell treatments and provide future directions for rese

286 n epithelial cells using Keratin14-Cre or in B cells using CD19-Cre, female mice have a normal life s

287 ity germinal center (GC) B cells into memory B cells versus plasma cells is a major quest of adaptive

288 ed the potential functional contributions of B cells via bulk and single-cell RNA sequencing, which d

289 y maturation and terminal differentiation of B-cells via the germinal center reaction is a complex mu

290 Of note, AMPKalpha1 in B cells was dispensable for stability of the bone marrow

291 potential for MAIT cells to provide help to B cells was evident during both vaccination and infectio

292 In vitro effects of MWF exposure on murine B cells were assessed.Measurements and Main Results: An

293 NA) profiles of individual vitreous-isolated B cells were characterized.

294 memory Th cells as well as regulatory T and B cells were increased.

295 Alternatively, subsets of memory B cells were lower in abundance in cirrhotic relative to

296 Upon infection of primary B cells, which require latency III for growth in vitro,

297 al B-cell depletion with anti-CD20 to retain B cells whose presence were required to achieve EAE reco

298 tors determining whether an individual naive B cell will proliferate following Ag encounter remains u

299 ll enforced, and there was selection against B cells with high affinity for self-antigen.

300 id arthritis (RA)-rmAbs derived from CD19(+) B cells within RA human synovial tissues frequently reac