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1 revealed that they were enriched in a CD9(+) B cell subset.
2 e activation and temporary expansion of this B cell subset.
3  strong orientation toward the marginal zone B cell subset.
4 ting in a reduction in the size of the naive B cell subset.
5 ecognized CD5(+)CD27(+) post-germinal center B cell subset.
6 cells, suggesting an important role for this B cell subset.
7 L) are highly suggestive that they are a new B cell subset.
8  organ cellularity, most prominent among the B-cell subset.
9 is associated with the apoptosis of multiple B cell subsets.
10 7(-)IgM(+), CD27(+)IgM(+), and CD27(+)IgG(+) B cell subsets.
11 inders from the follicular and marginal zone B cell subsets.
12 rongest proliferative response of all memory B cell subsets.
13 ing a chemotactic effect of eotaxin on these B cell subsets.
14 turation status of human CD21/CD24 nonmemory B cell subsets.
15 sequent changes in proportions of individual B cell subsets.
16 are expressed at different levels by various B cell subsets.
17 elatively constant level throughout numerous B cell subsets.
18 transitional and anergic IgD(+)IgM(-)CD27(-) B cell subsets.
19 4(high)CD21(low)) and T2 (CD24(high)CD21(+)) B cell subsets.
20 duced the highest c-Rel protein levels among B cell subsets.
21 ng fungal load that was independent of T and B cell subsets.
22 vely selected into the marginal zone and B-1 B cell subsets.
23 on sites in Ab V regions of naive and memory B cell subsets.
24 shape the epigenome of expanded SLE effector B cell subsets.
25 etermine how CD19 affects CNS recruitment of B cell subsets.
26 mainly derive from T cell-independent innate B cell subsets.
27 hat seen in old follicular and marginal zone B cell subsets.
28 ies have mainly focused on B1 and follicular B cell subsets.
29 B1 cell BCR signaling is distinct from other B cell subsets.
30 related genes and the relative expansions of B cell subsets.
31 the four main human IgM(+) and IgG(+) memory B-cell subsets.
32 ression of IL-10 and are enriched in various B-cell subsets.
33 ing plasma cells and 2 IgE-expressing memory B-cell subsets.
34 uppressive capacity of both memory and naive B-cell subsets.
35 n and internalization of cross-linked BCR in B-cell subsets.
36 ancreatic and splenic suppressive FasL(high) B-cell subsets.
37 regulated signatures compared with the other B-cell subsets.
38 g in vivo BAFF dependence of these 2 CD27(+) B-cell subsets.
39 ular kinases identified activation status of B-cell subsets.
40 4(+) T-cell reduction, and changes in T- and B-cell subsets.
41  to determine the frequencies of circulating B-cell subsets.
42 eceptor expression in newly formed and naive B-cell subsets.
43 lular immunity, involving various T-cell and B-cell subsets.
44 WM patients in relation to normal plasma and B-cell subsets.
45 ptor after CD40 engagement compared to other B-cell subsets.
46             BCR-mediated apoptosis of the T1 B cell subset, a major checkpoint for negative selection
47 nct kinetics of proliferation for individual B cell subsets across all developmental stages.
48  examined the dynamics of BAFF induction and B cell subset activation and composition, to investigate
49 both the CD27(+) memory population and naive B cell subset after only a brief stimulation in vitro.
50                           A newly discovered B cell subset, age-associated B cells, expresses the tra
51 ndard immunophenotyping of circulating human B cell subsets, an in vitro CFSE dilution assay was used
52 dies to polysaccharide antigens by the human B-cell subset analog to murine B-1 cells was reported in
53                                          The B cell subset analysis confirmed earlier reports of high
54  signaling, demonstrate dependence of the T3 B cell subset and IgM surface expression on BTK activity
55 2B low/neg cells in the CD27(+)IgD(-) memory B cell subset and that these changes are associated with
56 s associated with normalization of activated B cell subsets and allows age-dependent accumulation of
57 ress the highest levels of FcgammaRIIb among B cell subsets and are highly susceptible to FcgammaRIIb
58 ich is suitable for longitudinal studies and B cell subsets and biomarkers discovery.
59 ptosis and is shared by all preimmune murine B cell subsets and CD27- human B cells.
60  surface expression of BTLA on various human B cell subsets and confirm its ability to attenuate B ce
61 (T1) stage and leads to a decrease in mature B cell subsets and deficits in T cell-dependent antibody
62              We determined the proportion of B cell subsets and frequencies of Ag-specific memory B c
63 develop normal B1 and B2 immature and mature B cell subsets and have normal levels of naive serum Abs
64 , several correlations were observed between B cell subsets and liver function.
65 ht the phenotypic heterogeneity of innate B1 B cell subsets and of their possible fates in a relevant
66 and activated NK cells, differentiated T and B cell subsets and proinflammatory monocytes, suggesting
67  isolation of antibodies from all peripheral B cell subsets and revealed the anti-BK virus antibody r
68 ar to a previously described FCRL4(+) memory B-cell subset and to an "exhausted," anergic CD21(low) m
69 ns and thymi from 3-week-old pups for T- and B-cell subsets and epithelial cells did not show any sig
70 identified differential effects of different B-cell subsets and helped to clarify the still poorly un
71 n of anti-PS antibodies or anemia with other B-cell subsets and no association of other antibody spec
72 authors studied by flow cytometry peripheral B-cell subsets and serum levels of BAFF, the main homeos
73 intain stable relative levels of circulating B cell subsets, and a potential mechanism for viral rese
74 atory biomarkers, the proportions of various B cell subsets, and fetal priming to tetanus vaccination
75 ntly up-regulated on monocytes, neutrophils, B cell subsets, and plasma cells in multiple murine mode
76 y receptor on T cells, natural killer cells, B cell subsets, and some dendritic cells.
77                                  Leukocytes, B-cell subsets, and DSA were measured using flow cytomet
78 chemistry of tissue, flow cytometry of blood B-cell subsets, and serum immunoglobulin levels.
79 ggressive B-cell lymphomas (n = 138), normal B-cell subsets, and stromal cells.
80 replasma and plasma B cells, newly developed B-cell subsets, and their apoptosis was performed 30-60
81 tors regulating Ab production by this unique B cell subset are not well understood.
82 iral replication and alterations in distinct B cell subsets are largely unknown.
83  peripheral B cell compartment, although all B cell subsets are present in relatively normal ratios.
84 asmablast B-cell development, and that these B-cell subsets are dependent on T-cell-derived signals t
85 g cells resided mainly in the CD19(+) CD5(-) B cell subset, as assessed by enzyme-linked immunosorben
86         We sought to define the frequency of B-cell subsets associated with progressive B-cell matura
87  study characterizes longitudinal changes in B cell subsets at both infected anatomical sites.
88 tic stem cell (HSC) gives rise to all of the B-cell subsets [B-1a, B-1b, B-2, and marginal zone (MZ)
89  IL-10-producing CD1d(high)CD5(+) regulatory B cell subset (B10 cells) have been identified during th
90 epleted, particularly a rare IL-10-producing B cell subset (B10 cells) known to regulate inflammation
91 a rare IL-10-producing CD1dhiCD5+ regulatory B cell subset (B10 cells), since the adoptive transfer o
92                      Of the major peripheral B cell subsets, B1a cells were most prominently affected
93   Flow cytometry was used to analyze CD19(+) B cell subsets based on the expression of CD24 and CD38.
94 aluated phenotypic definition of circulating B-cell subsets before and after standard of care and B-c
95 trols, but there was no difference in memory B cells subsets between controls and splenectomized subj
96          This results in significant loss of B cell subsets beyond the T1 stage and disrupted humoral
97 ll compartment with a normal distribution of B-cell subsets both in bone marrow and the periphery, sh
98 t change other previously defined regulatory B-cell subsets (Breg), including CD5CD1d Breg or express
99 antibody results in significant depletion of B cell subsets but does not affect anti-peanut IgE level
100  shared with other mature perinatal or adult B cell subsets but were either unique or variably shared
101 onfer regulatory functions to various mature B-cell subsets but immature B-cell progenitors endowed w
102 L-10 production was not confined to a single B-cell subset, but enriched in both the CD24(hi)CD27(+)
103 erely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be l
104 Thy-1 autoreactive (ATA) BCR cells in the B1 B cell subset by transgenic expression yielded spontaneo
105  were used to identify C. neoformans-binding B cell subsets by flow cytometry.
106 on at the protein level was confirmed in UCB B cell subsets by intracellular staining and flow cytome
107 cent studies in Hep-2 cells; quantitation of B-cell subsets by means of flow cytometry; assessments o
108  depletion of the IL-10-producing regulatory B cell subset called B10 cells.
109                            However, specific B-cell subsets can also negatively regulate T-cell immun
110                                     Specific B-cell subsets can regulate T-cell immune responses, and
111 B cells in three circulating naive or memory B cell subsets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+
112 , depletion of the prominent IL-10-producing B-cell subset, CD1d(hi) cells, resulted in less IL-10(+)
113  characterized a distinct, late transitional B cell subset, CD21(int) transitional 2 (T2) B cells.
114  longitudinal study of its kind, we measured B cell subset composition, as well as PfEMP1-specific Ab
115                             We studied blood B-cell subset composition, replication history, somatic
116 ve immune cells, including myriad T-cell and B-cell subsets, compound these complexities.
117 ormed high-throughput VH sequencing of human B cell subsets defined by IgD and CD27 expression: IgD(+
118 tometry analysis of the splenic transitional B cell subsets demonstrated that MZ B cell development w
119 tuted with T2-MZP B cells but not with other B cell subsets displayed accelerated tumor growth, demon
120                  We evaluated B-cell counts, B-cell subset distribution, B cell-activating factor and
121  cells contributed to the alterations in the B-cell subset distribution.
122 to analyze the potential association between B-cell subsets distribution and anti-HLA antibodies befo
123 e study aimed to verify the relation between B cell subsets' distribution and liver disease progressi
124                     Distinct skin-associated B cell subsets drive or suppress cutaneous inflammatory
125       Localized functions of skin-associated B cell subsets during inflammation comprise Ab productio
126 on signals driving CNS migration of distinct B cell subsets during neuroinflammatory insults is criti
127 egulating differentiation and maintenance of B-cell subsets during an immune response is unclear.
128 nse to this virus is contributed by multiple B cell subsets, each generating qualitatively distinct r
129  for the existence of different transitional B-cell subsets, each displaying unique phenotypic and re
130                                        Among B cell subsets, elevated frequencies of memory and plasm
131                         Importantly, not all B cell subsets enhance immune responses.
132 ntrast, ATA B-CLL did not develop from other B cell subsets, even when the identical ATA BCR was expr
133 ction in each of the major mature peripheral B-cell subsets, exerting the greatest impact on marginal
134                           Furthermore, these B cell subsets exhibited an increased steady state dwell
135 in which the major immunoglobulin M (IgM(+)) B-cell subset expresses green fluorescence protein (GFP)
136                                              B cell subsets expressing the transcription factor T-bet
137                       Here we report a novel B-cell subset expressing 4-1BBL, which increases with ag
138                                         CD19 B-cell subsets expressing cell surface kappa and lambda
139                              The predominant B-cell subset found in trout NALT are IgT(+) B cells, si
140   Immature transitional and mature activated B cell subset frequencies were increased in HCV-infected
141 re activated, tissue-like memory, and plasma B cell subset frequencies, cell cycling, and intrinsic a
142 nd malaria exposure and also correlated with B cell subset frequencies.
143 ne cells, we performed RNA-seq in T cell and B cell subsets from either healthy donors or patients wi
144 criptome analyses of CLL and the main normal B cell subsets from human blood and spleen revealed that
145                                              B-cell subsets from healthy individuals and patients wit
146 e markedly impaired in both naive and memory B-cell subsets from HIV-infected persons.
147  subsets, including a newly defined effector B cell subset, from subjects with SLE and healthy contro
148                 For clarity, this regulatory B cell subset has been labeled as B10 cells, because the
149                           The age-associated B cell subset has been the focus of increasing interest
150                        A number of different B cell subsets have been shown to exhibit regulatory act
151                                   The normal B-cell subsets have well-defined miRNA signatures.
152 es that altered distribution of transitional B-cell subsets highlights different regulatory defects i
153 studied lncRNA expression patterns in normal B-cell subsets, HL cell lines, and tissues.
154 he role of serum Igs in maintaining specific B-cell subset homeostasis at steady state.
155 ciated with an accumulation of heterogeneous B cell subsets; however, their influence on viral load a
156  of two major, functionally distinct, mature B cell subsets, i.e., follicular mature (FM) and margina
157                                       Mature B-cell subsets, immune responses, and memory B-cell and
158 ave been shown to be an important regulatory B cell subset in humans.
159 l features revealed activation of T cell and B cell subsets in a proportion of patients.
160 s, the proportions of naive and memory T and B cell subsets in A-T patients did not vary in relation
161                Examination of splenic and BM B cell subsets in CD22 and ST6Gal-I knockout mice reveal
162 the characterization of autoantigen-specific B cell subsets in different models of autoimmunity and,
163 hat different Borrelia can activate the same B cell subsets in distinct ways and they each elicit a c
164 g cytokine-producing regulatory and effector B cell subsets in health and disease and discuss how fut
165 ow that changes in P. falciparum Ag-specific B cell subsets in HIV-infected individuals mirror those
166 d CD24 distinguishes transitional and mature B cell subsets in mice.
167   Additionally, the monitoring of individual B cell subsets in patients may lead to the discovery of
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 e findings demonstrate the plasticity of the B cell subsets in virus-infected hosts and show for the
173  to an "exhausted," anergic CD21(low) memory B-cell subset in HIV(+) patients.
174            However, the significance of this B-cell subset in humans is poorly understood.
175 ound that IgT(+) B cells represent the major B-cell subset in the skin epidermis and that IgT is main
176 linked immunospot assay (ELISPOT) to examine B-cell subsets in 59 subjects, including 28 with PBC, 13
177   We analyzed the reconstitution kinetics of B-cell subsets in adult leukemic patients within 6 month
178 t in our understanding of the role of T- and B-cell subsets in atherosclerosis and addresses the role
179 eriphery, (ii) expansion of CD80+ and CD62L- B-cell subsets in BM and the periphery, and (iii) a sign
180 ory and CD19(+)CD24(hi)CD38(hi) transitional B-cell subsets in healthy human donors.
181                                  The role of B-cell subsets in human leukocyte antigen (HLA)-specific
182 d heavy-chain genes from immature and mature B-cell subsets in mice, we demonstrate a striking gradie
183 mpaired humoral response, we assessed memory B-cell subsets in paired samples collected before and af
184    We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of
185 ic differentiation is skewed toward specific B-cell subsets in the embryo are unanswered questions, b
186 ant early depletion of both naive and memory B-cell subsets in the peripheral blood, with differentia
187 itors in the bone marrow and of transitional B-cell subsets in the spleen.
188 ore, the altered numbers of naive and memory B-cell subsets in these animals corresponded with increa
189 , whereas they clearly populate 1% of mature B-cell subsets in VH125Tg/NOD mice.
190  profiles and transcriptomes from five human B cell subsets, including a newly defined effector B cel
191                              Remarkably, all B cell subsets, including even transitional 1 B cells, w
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 inct DNA methylation signatures specific for B-cell subsets, including memory B cells (MBCs) and plas
195                      HISmice contain several B-cell subsets, including those with the phenotype CD20(
196 rthermore, B2 cells, in the absence of other B-cell subsets, increase splenic regulatory T-cell popul
197 dicated by a marked disruption of peripheral B cell subsets, increased levels of PD-1 expression, and
198  of ART restored the typical distribution of B cell subsets, increasing the proportion of naive B cel
199  variably designed to deplete specific T and B cell subsets, interrupt receptor-ligand interactions,
200  Thus, by bolstering the IgM(+)IgD(+)CD27(+) B-cell subset, IRAK-4 and MyD88 promote optimal T-indepe
201             In addition, the percentage of a B cell subset is significantly lower in the non-responde
202                                         This B-cell subset is IgM(+), but due to low/negative IgD cel
203 ever, proinflammatory cytokine expression in B-cell subsets is largely unexplored.
204 partment and the relationship between memory B-cell subsets is still limited, although these are cent
205 -17, interferon-gamma and differential T and B cell subset lymphopenia.
206 ocystis challenge, suggesting that different B cell subsets may be responsible for the generation of
207    The reported microarray analysis of human B cell subsets may now be used to delineate B cell defec
208 und humoral immunodeficiency and lack mature B cell subsets, mirroring deficiency of the cytokine B c
209         In transcriptionally profiled normal B-cell subsets (naive, germinal center, and memory B cel
210 munity, neither the initiating event nor the B cell subset necessary for WP formation has been identi
211 for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus.
212 boost of 2 clonally and functionally related B-cell subsets of short-lived IgE(+) plasmablasts and Ig
213 proliferation and differentiation of various B cell subsets on TLR stimulation.
214 ejection and pretransplant proportion of any B-cell subset or BAFF serum levels.
215 specifically in CLL but not in normal mature B-cell subsets or after B-cell activation.
216 n), proportion of Bm2 cells but not of other B-cell subsets or BAFF levels was independently associat
217 e global quantitative recovery of T-cell and B-cell subsets or in global T-cell and B-cell function.
218 e or particulation, selective recruitment of B cell subsets, or activation and recruitment of Pn prot
219                           The roles distinct B cell subsets play in clonal expansion, isotype switchi
220  B cells play in establishing, and the roles B cell subsets play in maintaining lifelong anti-peanut
221 ctions with regard to dynamics of the memory B cell subsets point to their role in the pathogenesis o
222       Gene expression profiling of different B-cell subsets positioned the phenotype of putative B-1
223 n leads to an abnormally expanded CD5(+) B1a B-cell subset (present as early as 4 days after birth),
224 re enriched in the IgM(high)CD5(+)CD1d(high) B cell subset previously reported to contain a higher fr
225       To investigate whether perturbation of B cell subsets prior to immunization with recombinant En
226 are still unknown, we studied five precursor B cell subsets (ProB, PreBI, PreBII large, PreBII small,
227                  In allergy, some regulatory B-cell subsets producing IL-10 have been recently descri
228 st an important role of BAFF in facilitating B cell subset proliferation and redistribution as a cons
229 rine B-1b and primate IgM(+)CD27(+) "memory" B cell subsets proposed to produce TI-2 Ab responses may
230                                         Some B cell subsets provide extensive cross-protection agains
231                 However, specific regulatory B cell subsets recently were identified that downregulat
232                               One functional B cell subset, regulatory B cells (Bregs), has recently
233 l and mature B cell recovery, whereas memory B cell subsets remained significantly depleted.
234 We studied peripheral B- and T-cell subsets, B-cell subset replication history, somatic hypermutation
235 mory T and B cells may limit MS, rapid CD19+ B-cell subset repopulation in the absence of effective T
236 low cytometric analysis of tetramer-reactive B cell subsets revealed a significantly higher frequency
237                Further, paired CSF and blood B cell subsets (RRMS; n = 7) were isolated using fluores
238    In NOD, btk deficiency mirrors changes in B cell subsets seen in other strains, but also improves
239  memory B cells and the activation of sorted B cell subsets shows that GA-dependent increased Breg ce
240    In chronic viral infections, the deranged B cell subset signifies uncontrolled disease.
241  infection, a state of activation results in B cell subset skewing that is likely the result of alter
242   Second, we examined colonization by EBV of B-cell subsets sorted from a unique collection of IM ton
243 on, the peripheral CD19CD24CD38 transitional B cell subset strongly declined, regardless of the subse
244 vels of eotaxin receptor CCR3 than the other B cell subsets, suggesting a chemotactic effect of eotax
245 s impaired TLR-induced proliferation of this B-cell subset, suggesting a means by which loss of this
246  identified IL-10-competent CD1d(high)CD5(+) B cell subset termed B10 cells that represents 1-3% of a
247 a cells and also the enigmatic marginal zone B cell subset that is poorly understood in humans.
248     Marginal zone B cells (MZB) are a mature B cell subset that rapidly respond to blood-borne pathog
249 al center fate, and we identified a CD11c(+) B cell subset that was not capable of producing IL-10 ev
250 erstanding of the abundance and phenotype of B cell subsets that are induced or perturbed by exogenou
251                  Better understanding of the B cell subsets that are responsible for the development
252 ere is also mounting evidence for regulatory B cell subsets that may play a protective role.
253         We have discovered a distinct mature B-cell subset that accumulates with age, which we have t
254               Thus, we have identified a new B-cell subset that is critical for immunological toleran
255 in this issue of Blood, identified a pre-pro-B-cell subset that marks the earliest stages of B-cell l
256  and genetic approaches, we discovered a new B-cell subset that, upon adoptive transfer into B cell-d
257 cted individuals, focusing on the skewing of B-cell subsets that circulate in the peripheral blood an
258                          Phenotype of T- and B-cell subsets that expand during the early stages of nu
259  by the functional balance between different B-cell subsets that may be generated by this therapeutic
260 epleting antibody rituximab, the size of all B cell subsets, the T1/T2-ratio, and the cyroglobulin le
261 pite sharing some features with other mature B-cell subsets, they are refractory to BCR and CD40 stim
262  clones in MC and lymphomas derive from this B-cell subset, this establishes IgM(+) memory B cells as
263 e cells self-renew and persist as a minor B1 B cell subset throughout life.
264 tics of LANA/EBNA-1 expression in individual B-cell subsets throughout a course of infection has not
265 ll lymphomas, indicating sensitivity of this B cell subset to transformation caused by p53 deficiency
266       Indeed, disturbances in the ability of B cell subsets to present antigen, produce cytokines, an
267 how viral gene products function in specific B cell subsets to regulate this process is incomplete.
268                The contribution of MZ and Fo B cell subsets to this antiviral TI-2 response, however,
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  mononuclear cells were quantified for T and B cell subsets using flow cytometry, and serum cytokine
272  skewing (lower T1/T2-ratio) of the immature B cell subset was noted in MC patients, suggesting that
273 ution of HIV-specific responses among memory B cell subsets was corroborated by transcriptional analy
274 study, a role for LSD1 in the development of B cell subsets was examined.
275                          Characterization of B-cell subsets was performed by flow cytometry.
276                  HSFC, including analysis of B cell subsets, was performed.
277 Consistent with an increased number of these B cell subsets, we detected elevated levels of IgG3 natu
278             Using large-scale imaging across B cell subsets, we found that, in contrast with naive an
279 n those SLE patients occurred throughout all B cell subsets, we hypothesized that ARID3a expression i
280  whole-genome bisulfite sequencing of normal B cell subsets, we observed broad epigenetic programming
281 ther B-cell lymphomas, cHL lines, and normal B-cell subsets, we show that they differ extensively fro
282              Effects of prolactin on splenic B cell subsets were studied in female BALB/c mice.
283   Using fluorescence-activated cell sorting, B-cell subsets were analyzed.
284                                              B-cell subsets were predominantly associated with sex, b
285                                      Various B-cell subsets were purified and characterized by flow c
286                                              B-cell subsets were quantified by flow cytometry; annexi
287 phenotype, specificity, and functionality of B-cell subsets were studied in a cohort of pregnant wome
288 oper development and function of the various B cell subsets while counteracting lymphomagenesis.
289 ional B cells, including a late transitional B cell subset with a phenotype intermediate between T2 a
290                        The spleen regulatory B cell subset with the functional capacity to express IL
291 EBV infection induced redistribution between B cell subsets with enrichment of IgD(+)CD27(+) cells (c
292                                              B cell subsets with phenotypes characteristic of naive,
293                             The discovery of B cell subsets with regulatory properties, dependent on
294               Distinct human IL-10-producing B-cell subsets with immunoregulatory properties have bee
295                KDM6B expression increases in B-cell subsets with increasing stage of differentiation,
296 y similar to each other and to IgG(+) memory B cell subsets, with typical upregulation of activation
297  plasmablasts and plasma cells than in other B-cell subsets, with higher levels in patients with SLE
298 Chemokine-dependent localization of specific B cell subsets within the immune microarchitecture is es
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

 
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