ライフサイエンスコーパス: B-cell subset

1 e activation and temporary expansion of this B cell subset.

2 strong orientation toward the marginal zone B cell subset.

3 ting in a reduction in the size of the naive B cell subset.

4 ecognized CD5(+)CD27(+) post-germinal center B cell subset.

5 cells, suggesting an important role for this B cell subset.

6 riphery that gives rise to a tissue-specific B cell subset.

7 and activation of the T dependent follicular B cell subset.

8 revealed that they were enriched in a CD9(+) B cell subset.

9 organ cellularity, most prominent among the B-cell subset.

10 ing a chemotactic effect of eotaxin on these B cell subsets.

11 turation status of human CD21/CD24 nonmemory B cell subsets.

12 sequent changes in proportions of individual B cell subsets.

13 hat seen in old follicular and marginal zone B cell subsets.

14 are expressed at different levels by various B cell subsets.

15 elatively constant level throughout numerous B cell subsets.

16 transitional and anergic IgD(+)IgM(-)CD27(-) B cell subsets.

17 4(high)CD21(low)) and T2 (CD24(high)CD21(+)) B cell subsets.

18 ng fungal load that was independent of T and B cell subsets.

19 vely selected into the marginal zone and B-1 B cell subsets.

20 cular features of the two RV-specific memory B cell subsets.

21 of germinal center (GC) versus naive mature B cell subsets.

22 the follicular, marginal zone, and B1 mature B cell subsets.

23 s well as decrease the pool of PS-responding B cell subsets.

24 rmed to study the repertoire of DNA-reactive B cell subsets.

25 mobilization in each of the two transitional B cell subsets.

26 ies have mainly focused on B1 and follicular B cell subsets.

27 B1 cell BCR signaling is distinct from other B cell subsets.

28 etermine how CD19 affects CNS recruitment of B cell subsets.

29 related genes and the relative expansions of B cell subsets.

30 mainly derive from T cell-independent innate B cell subsets.

31 7(-)IgM(+), CD27(+)IgM(+), and CD27(+)IgG(+) B cell subsets.

32 inders from the follicular and marginal zone B cell subsets.

33 rongest proliferative response of all memory B cell subsets.

34 ression of IL-10 and are enriched in various B-cell subsets.

35 ing plasma cells and 2 IgE-expressing memory B-cell subsets.

36 uppressive capacity of both memory and naive B-cell subsets.

37 n and internalization of cross-linked BCR in B-cell subsets.

38 ancreatic and splenic suppressive FasL(high) B-cell subsets.

39 4(+) T-cell reduction, and changes in T- and B-cell subsets.

40 to determine the frequencies of circulating B-cell subsets.

41 regulated signatures compared with the other B-cell subsets.

42 g in vivo BAFF dependence of these 2 CD27(+) B-cell subsets.

43 eceptor expression in newly formed and naive B-cell subsets.

44 lular immunity, involving various T-cell and B-cell subsets.

45 ptor after CD40 engagement compared to other B-cell subsets.

46 the four main human IgM(+) and IgG(+) memory B-cell subsets.

47 ular kinases identified activation status of B-cell subsets.

48 BCR-mediated apoptosis of the T1 B cell subset, a major checkpoint for negative selection

49 nct kinetics of proliferation for individual B cell subsets across all developmental stages.

50 examined the dynamics of BAFF induction and B cell subset activation and composition, to investigate

51 terms of their downstream mediators and the B cell subset affected.

52 both the CD27(+) memory population and naive B cell subset after only a brief stimulation in vitro.

53 A newly discovered B cell subset, age-associated B cells, expresses the tra

54 ndard immunophenotyping of circulating human B cell subsets, an in vitro CFSE dilution assay was used

55 dies to polysaccharide antigens by the human B-cell subset analog to murine B-1 cells was reported in

56 The B cell subset analysis confirmed earlier reports of high

57 in diagnostic laboratory methods, including B-cell subset analysis and genetic testing, coupled with

58 2-O was first detected in the transitional 1 B cell subset and high levels were maintained in margina

59 signaling, demonstrate dependence of the T3 B cell subset and IgM surface expression on BTK activity

60 2B low/neg cells in the CD27(+)IgD(-) memory B cell subset and that these changes are associated with

61 enectomized subjects in comparison to memory B cell subsets and Ab responses in healthy controls.

62 s associated with normalization of activated B cell subsets and allows age-dependent accumulation of

63 ress the highest levels of FcgammaRIIb among B cell subsets and are highly susceptible to FcgammaRIIb

64 ich is suitable for longitudinal studies and B cell subsets and biomarkers discovery.

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

66 surface expression of BTLA on various human B cell subsets and confirm its ability to attenuate B ce

67 (T1) stage and leads to a decrease in mature B cell subsets and deficits in T cell-dependent antibody

68 netic maps of BCR signaling in primary human B cell subsets and enable new studies of signaling in B

69 We determined the proportion of B cell subsets and frequencies of Ag-specific memory B c

70 develop normal B1 and B2 immature and mature B cell subsets and have normal levels of naive serum Abs

71 15.) There was no correlation between memory B cell subsets and IgG or IgM Ab responses for controls

72 and activated NK cells, differentiated T and B cell subsets and proinflammatory monocytes, suggesting

73 ar to a previously described FCRL4(+) memory B-cell subset and to an "exhausted," anergic CD21(low) m

74 identified differential effects of different B-cell subsets and helped to clarify the still poorly un

75 in quantitatively greater reduction in some B-cell subsets and qualitatively different effects on bo

76 authors studied by flow cytometry peripheral B-cell subsets and serum levels of BAFF, the main homeos

77 intain stable relative levels of circulating B cell subsets, and a potential mechanism for viral rese

78 ntly up-regulated on monocytes, neutrophils, B cell subsets, and plasma cells in multiple murine mode

79 ti-DNA/antiglomerular autoantibodies, skewed B cell subsets, and profoundly activated B and T cells.

80 chemistry of tissue, flow cytometry of blood B-cell subsets, and serum immunoglobulin levels.

81 ggressive B-cell lymphomas (n = 138), normal B-cell subsets, and stromal cells.

82 replasma and plasma B cells, newly developed B-cell subsets, and their apoptosis was performed 30-60

83 tors regulating Ab production by this unique B cell subset are not well understood.

84 iral replication and alterations in distinct B cell subsets are largely unknown.

85 peripheral B cell compartment, although all B cell subsets are present in relatively normal ratios.

86 asmablast B-cell development, and that these B-cell subsets are dependent on T-cell-derived signals t

87 g cells resided mainly in the CD19(+) CD5(-) B cell subset, as assessed by enzyme-linked immunosorben

88 We sought to define the frequency of B-cell subsets associated with progressive B-cell matura

89 study characterizes longitudinal changes in B cell subsets at both infected anatomical sites.

90 tic stem cell (HSC) gives rise to all of the B-cell subsets [B-1a, B-1b, B-2, and marginal zone (MZ)

91 IL-10-producing CD1d(high)CD5(+) regulatory B cell subset (B10 cells) have been identified during th

92 epleted, particularly a rare IL-10-producing B cell subset (B10 cells) known to regulate inflammation

93 a rare IL-10-producing CD1dhiCD5+ regulatory B cell subset (B10 cells), since the adoptive transfer o

94 Of the major peripheral B cell subsets, B1a cells were most prominently affected

95 We isolated splenic B cell subsets based on their expression of specific cel

96 aluated phenotypic definition of circulating B-cell subsets before and after standard of care and B-c

97 trols, but there was no difference in memory B cells subsets between controls and splenectomized subj

98 This results in significant loss of B cell subsets beyond the T1 stage and disrupted humoral

99 ll compartment with a normal distribution of B-cell subsets both in bone marrow and the periphery, sh

100 t change other previously defined regulatory B-cell subsets (Breg), including CD5CD1d Breg or express

101 antibody results in significant depletion of B cell subsets but does not affect anti-peanut IgE level

102 shared with other mature perinatal or adult B cell subsets but were either unique or variably shared

103 onfer regulatory functions to various mature B-cell subsets but immature B-cell progenitors endowed w

104 l repertoire and the development of distinct B cell subsets, but little is known about what distingui

105 L-10 production was not confined to a single B-cell subset, but enriched in both the CD24(hi)CD27(+)

106 erely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be l

107 Thy-1 autoreactive (ATA) BCR cells in the B1 B cell subset by transgenic expression yielded spontaneo

108 were used to identify C. neoformans-binding B cell subsets by flow cytometry.

109 on at the protein level was confirmed in UCB B cell subsets by intracellular staining and flow cytome

110 allowing independent regulation of different B cell subsets by varying the combination and levels of

111 cent studies in Hep-2 cells; quantitation of B-cell subsets by means of flow cytometry; assessments o

112 depletion of the IL-10-producing regulatory B cell subset called B10 cells.

113 However, specific B-cell subsets can also negatively regulate T-cell immun

114 Specific B-cell subsets can regulate T-cell immune responses, and

115 B cells in three circulating naive or memory B cell subsets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+

116 , depletion of the prominent IL-10-producing B-cell subset, CD1d(hi) cells, resulted in less IL-10(+)

117 characterized a distinct, late transitional B cell subset, CD21(int) transitional 2 (T2) B cells.

118 longitudinal study of its kind, we measured B cell subset composition, as well as PfEMP1-specific Ab

119 We studied blood B-cell subset composition, replication history, somatic

120 servations suggest that B-CLL derives from a B cell subset comprised of restricted BCR structural div

121 biological functions of different peripheral B cell subsets continues to evolve.

122 ormed high-throughput VH sequencing of human B cell subsets defined by IgD and CD27 expression: IgD(+

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

124 reagents were similar, including B cell and B cell subset depletion and prevention of the progressiv

125 ontrast, neither marginal zone nor B1 mature B cell subsets develop from bone marrow precursors under

126 aining glycoprotein is important for splenic B cell subset development, whereas the DC-associated ST6

127 tuted with T2-MZP B cells but not with other B cell subsets displayed accelerated tumor growth, demon

128 Splenic T and B cell subsets displayed constitutive binding of YY1, NF

129 We evaluated B-cell counts, B-cell subset distribution, B cell-activating factor and

130 cells contributed to the alterations in the B-cell subset distribution.

131 to analyze the potential association between B-cell subsets distribution and anti-HLA antibodies befo

132 H2-M, and I-A(b)-CLIP expression patterns in B cell subsets during B cell development and activation.

133 on signals driving CNS migration of distinct B cell subsets during neuroinflammatory insults is criti

134 egulating differentiation and maintenance of B-cell subsets during an immune response is unclear.

135 We analyzed miRNA profiles in B-cell subsets during peripheral B-cell differentiation

136 nse to this virus is contributed by multiple B cell subsets, each generating qualitatively distinct r

137 for the existence of different transitional B-cell subsets, each displaying unique phenotypic and re

138 ntrast, ATA B-CLL did not develop from other B cell subsets, even when the identical ATA BCR was expr

139 ction in each of the major mature peripheral B-cell subsets, exerting the greatest impact on marginal

140 Furthermore, these B cell subsets exhibited an increased steady state dwell

141 in which the major immunoglobulin M (IgM(+)) B-cell subset expresses green fluorescence protein (GFP)

142 Here we report a novel B-cell subset expressing 4-1BBL, which increases with ag

143 CD19 B-cell subsets expressing cell surface kappa and lambda

144 The predominant B-cell subset found in trout NALT are IgT(+) B cells, si

145 Immature transitional and mature activated B cell subset frequencies were increased in HCV-infected

146 re activated, tissue-like memory, and plasma B cell subset frequencies, cell cycling, and intrinsic a

147 nd malaria exposure and also correlated with B cell subset frequencies.

148 criptome analyses of CLL and the main normal B cell subsets from human blood and spleen revealed that

149 B-cell subsets from healthy individuals and patients wit

150 e markedly impaired in both naive and memory B-cell subsets from HIV-infected persons.

151 For clarity, this regulatory B cell subset has been labeled as B10 cells, because the

152 The normal B-cell subsets have well-defined miRNA signatures.

153 es that altered distribution of transitional B-cell subsets highlights different regulatory defects i

154 studied lncRNA expression patterns in normal B-cell subsets, HL cell lines, and tissues.

155 he role of serum Igs in maintaining specific B-cell subset homeostasis at steady state.

156 ciated with an accumulation of heterogeneous B cell subsets; however, their influence on viral load a

157 of two major, functionally distinct, mature B cell subsets, i.e., follicular mature (FM) and margina

158 ising was the finding of an unmutated memory B cell subset identified by the expression of CD80 and C

159 To test this, we analyzed CD27(+) memory B cell subsets, IgG, and IgM pneumococcal Ab responses i

160 Mature B-cell subsets, immune responses, and memory B-cell and

161 s, the proportions of naive and memory T and B cell subsets in A-T patients did not vary in relation

162 Examination of splenic and BM B cell subsets in CD22 and ST6Gal-I knockout mice reveal

163 the characterization of autoantigen-specific B cell subsets in different models of autoimmunity and,

164 hat different Borrelia can activate the same B cell subsets in distinct ways and they each elicit a c

165 g cytokine-producing regulatory and effector B cell subsets in health and disease and discuss how fut

166 ow that changes in P. falciparum Ag-specific B cell subsets in HIV-infected individuals mirror those

167 d CD24 distinguishes transitional and mature B cell subsets in mice.

168 well as the proportion and numbers of major B cell subsets in peripheral lymphoid organs, was unaffe

169 serologic activity and reduce BLyS-dependent B cell subsets in serologically and clinically active SL

170 a B cells are greatly expanded into effector B cell subsets in some autoimmune mice, thus indicating

171 plex interplay of MZ and multiple peritoneal B cell subsets in the early response to infection.

172 To address the roles of B cell subsets in the longevity of humoral responses, ma

173 e findings demonstrate the plasticity of the B cell subsets in virus-infected hosts and show for the

174 to an "exhausted," anergic CD21(low) memory B-cell subset in HIV(+) patients.

175 However, the significance of this B-cell subset in humans is poorly understood.

176 ound that IgT(+) B cells represent the major B-cell subset in the skin epidermis and that IgT is main

177 linked immunospot assay (ELISPOT) to examine B-cell subsets in 59 subjects, including 28 with PBC, 13

178 We analyzed the reconstitution kinetics of B-cell subsets in adult leukemic patients within 6 month

179 t in our understanding of the role of T- and B-cell subsets in atherosclerosis and addresses the role

180 eriphery, (ii) expansion of CD80+ and CD62L- B-cell subsets in BM and the periphery, and (iii) a sign

181 ory and CD19(+)CD24(hi)CD38(hi) transitional B-cell subsets in healthy human donors.

182 The role of B-cell subsets in human leukocyte antigen (HLA)-specific

183 d heavy-chain genes from immature and mature B-cell subsets in mice, we demonstrate a striking gradie

184 mpaired humoral response, we assessed memory B-cell subsets in paired samples collected before and af

185 We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of

186 ic differentiation is skewed toward specific B-cell subsets in the embryo are unanswered questions, b

187 ant early depletion of both naive and memory B-cell subsets in the peripheral blood, with differentia

188 have defined new roles for the B-1a and B-1b B-cell subsets in the response to bacteria and self-anti

189 itors in the bone marrow and of transitional B-cell subsets in the spleen.

190 ore, the altered numbers of naive and memory B-cell subsets in these animals corresponded with increa

191 , whereas they clearly populate 1% of mature B-cell subsets in VH125Tg/NOD mice.

192 rations were associated with an imbalance in B-cell subsets, including a significant decrease in memo

193 with CD19-Cre and found that all peripheral B-cell subsets, including B1 B cells, require YY1 for th

194 HISmice contain several B-cell subsets, including those with the phenotype CD20(

195 rthermore, B2 cells, in the absence of other B-cell subsets, increase splenic regulatory T-cell popul

196 dicated by a marked disruption of peripheral B cell subsets, increased levels of PD-1 expression, and

197 of ART restored the typical distribution of B cell subsets, increasing the proportion of naive B cel

198 variably designed to deplete specific T and B cell subsets, interrupt receptor-ligand interactions,

199 these genes; however, separation of splenic B cell subsets into T1, T2, marginal zone (MZ), and matu

200 Thus, by bolstering the IgM(+)IgD(+)CD27(+) B-cell subset, IRAK-4 and MyD88 promote optimal T-indepe

201 ever, proinflammatory cytokine expression in B-cell subsets is largely unexplored.

202 partment and the relationship between memory B-cell subsets is still limited, although these are cent

203 , it has been unclear whether these distinct B cell subsets make identical or different Abs.

204 The reported microarray analysis of human B cell subsets may now be used to delineate B cell defec

205 und humoral immunodeficiency and lack mature B cell subsets, mirroring deficiency of the cytokine B c

206 In transcriptionally profiled normal B-cell subsets (naive, germinal center, and memory B cel

207 munity, neither the initiating event nor the B cell subset necessary for WP formation has been identi

208 for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus.

209 itution potential derives from a small T/non-B cell subset of one of these populations, or that most

210 proliferation and differentiation of various B cell subsets on TLR stimulation.

211 ejection and pretransplant proportion of any B-cell subset or BAFF serum levels.

212 specifically in CLL but not in normal mature B-cell subsets or after B-cell activation.

213 n), proportion of Bm2 cells but not of other B-cell subsets or BAFF levels was independently associat

214 e global quantitative recovery of T-cell and B-cell subsets or in global T-cell and B-cell function.

215 e or particulation, selective recruitment of B cell subsets, or activation and recruitment of Pn prot

216 B cells play in establishing, and the roles B cell subsets play in maintaining lifelong anti-peanut

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

218 Gene expression profiling of different B-cell subsets positioned the phenotype of putative B-1

219 n leads to an abnormally expanded CD5(+) B1a B-cell subset (present as early as 4 days after birth),

220 re enriched in the IgM(high)CD5(+)CD1d(high) B cell subset previously reported to contain a higher fr

221 To investigate whether perturbation of B cell subsets prior to immunization with recombinant En

222 are still unknown, we studied five precursor B cell subsets (ProB, PreBI, PreBII large, PreBII small,

223 In allergy, some regulatory B-cell subsets producing IL-10 have been recently descri

224 st an important role of BAFF in facilitating B cell subset proliferation and redistribution as a cons

225 rine B-1b and primate IgM(+)CD27(+) "memory" B cell subsets proposed to produce TI-2 Ab responses may

226 Some B cell subsets provide extensive cross-protection agains

227 ng thresholds for tolerance among peripheral B cell subsets reactive with an identical ligand.

228 However, specific regulatory B cell subsets recently were identified that downregulat

229 One functional B cell subset, regulatory B cells (Bregs), has recently

230 l and mature B cell recovery, whereas memory B cell subsets remained significantly depleted.

231 We studied peripheral B- and T-cell subsets, B-cell subset replication history, somatic hypermutation

232 mory T and B cells may limit MS, rapid CD19+ B-cell subset repopulation in the absence of effective T

233 This B cell subset resides within the normal mucosa of the la

234 low cytometric analysis of tetramer-reactive B cell subsets revealed a significantly higher frequency

235 In NOD, btk deficiency mirrors changes in B cell subsets seen in other strains, but also improves

236 infection, a state of activation results in B cell subset skewing that is likely the result of alter

237 Second, we examined colonization by EBV of B-cell subsets sorted from a unique collection of IM ton

238 on, the peripheral CD19CD24CD38 transitional B cell subset strongly declined, regardless of the subse

239 vels of eotaxin receptor CCR3 than the other B cell subsets, suggesting a chemotactic effect of eotax

240 s impaired TLR-induced proliferation of this B-cell subset, suggesting a means by which loss of this

241 The use of B cell-targeted and B cell subset-targeted therapies in humans is illuminati

242 identified IL-10-competent CD1d(high)CD5(+) B cell subset termed B10 cells that represents 1-3% of a

243 st identification of a distinct mature human B cell subset that is naturally autoreactive and control

244 a cells and also the enigmatic marginal zone B cell subset that is poorly understood in humans.

245 ral autoantibodies originate from a distinct B cell subset that may be positively selected by virtue

246 atively regulated by a unique CD1d(hi)CD5(+) B cell subset that was absent in Cd19(-/-) mice, represe

247 al center fate, and we identified a CD11c(+) B cell subset that was not capable of producing IL-10 ev

248 erstanding of the abundance and phenotype of B cell subsets that are induced or perturbed by exogenou

249 Better understanding of the B cell subsets that are responsible for the development

250 ere is also mounting evidence for regulatory B cell subsets that may play a protective role.

251 d this system to characterize the particular B cell subsets that were responsible for secreting autoa

252 We have discovered a distinct mature B-cell subset that accumulates with age, which we have t

253 dentified a novel IL-12-producing regulatory B-cell subset that develops under Th2-mediated intestina

254 Our previous studies have identified a B-cell subset that is induced under inflammatory conditi

255 Marginal zone B (MZB) cells are a B-cell subset that produces T-cell-independent antibodie

256 cted individuals, focusing on the skewing of B-cell subsets that circulate in the peripheral blood an

257 Phenotype of T- and B-cell subsets that expand during the early stages of nu

258 by the functional balance between different B-cell subsets that may be generated by this therapeutic

259 epleting antibody rituximab, the size of all B cell subsets, the T1/T2-ratio, and the cyroglobulin le

260 pite sharing some features with other mature B-cell subsets, they are refractory to BCR and CD40 stim

261 clones in MC and lymphomas derive from this B-cell subset, this establishes IgM(+) memory B cells as

262 e cells self-renew and persist as a minor B1 B cell subset throughout life.

263 tics of LANA/EBNA-1 expression in individual B-cell subsets throughout a course of infection has not

264 ll lymphomas, indicating sensitivity of this B cell subset to transformation caused by p53 deficiency

265 Indeed, disturbances in the ability of B cell subsets to present antigen, produce cytokines, an

266 The contribution of MZ and Fo B cell subsets to this antiviral TI-2 response, however,

267 Despite the differential responses of B cell subsets to various stimuli, and despite the need

268 s showed that BR3-Fc reduced this CD21(high) B-cell subset to a greater extent than it reduced CD21(m

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

270 Here we demonstrate that memory B cell subsets unexpectedly diverged across antibody cla

271 skewing (lower T1/T2-ratio) of the immature B cell subset was noted in MC patients, suggesting that

272 ution of HIV-specific responses among memory B cell subsets was corroborated by transcriptional analy

273 Characterization of B-cell subsets was performed by flow cytometry.

274 HSFC, including analysis of B cell subsets, was performed.

275 Consistent with an increased number of these B cell subsets, we detected elevated levels of IgG3 natu

276 Using large-scale imaging across B cell subsets, we found that, in contrast with naive an

277 n those SLE patients occurred throughout all B cell subsets, we hypothesized that ARID3a expression i

278 whole-genome bisulfite sequencing of normal B cell subsets, we observed broad epigenetic programming

279 ther B-cell lymphomas, cHL lines, and normal B-cell subsets, we show that they differ extensively fro

280 Effects of prolactin on splenic B cell subsets were studied in female BALB/c mice.

281 B-cell subsets were predominantly associated with sex, b

282 Various B-cell subsets were purified and characterized by flow c

283 B-cell subsets were quantified by flow cytometry; annexi

284 phenotype, specificity, and functionality of B-cell subsets were studied in a cohort of pregnant wome

285 oper development and function of the various B cell subsets while counteracting lymphomagenesis.

286 ctivation of the T independent marginal zone B cell subset, while prolactin promotes the survival and

287 ional B cells, including a late transitional B cell subset with a phenotype intermediate between T2 a

288 The spleen regulatory B cell subset with the functional capacity to express IL

289 EBV infection induced redistribution between B cell subsets with enrichment of IgD(+)CD27(+) cells (c

290 B cell subsets with phenotypes characteristic of naive,

291 The discovery of B cell subsets with regulatory properties, dependent on

292 Distinct human IL-10-producing B-cell subsets with immunoregulatory properties have bee

293 KDM6B expression increases in B-cell subsets with increasing stage of differentiation,

294 uction was restricted to this CD1d(hi)CD5(+) B cell subset, with IL-10 production diminished in Cd19(

295 y similar to each other and to IgG(+) memory B cell subsets, with typical upregulation of activation

296 plasmablasts and plasma cells than in other B-cell subsets, with higher levels in patients with SLE

297 Chemokine-dependent localization of specific B cell subsets within the immune microarchitecture is es

298 tinguished FL tumor B-cell and nontumor host B-cell subsets within FL patient biopsies.

299 t the pathologic cytokine-producing effector B cell subsets without impacting the protective regulato

300 he maturation and functionality of all major B cell subsets, yet the molecular players in these signa