ライフサイエンスコーパス: IgD

1 IgD and IgM are produced by alternative splicing of long

2 IgD CSR is a rare event, and its regulation is poorly un

3 IgD CSR occurred via both alternative nonhomologous end-

4 IgD deposition is difficult to diagnose, because routine

5 IgD has remained a mysterious Ig class and a bane to imm

6 IgD is also expressed at high levels on naive follicular

7 IgD monoclonal gammopathies are uncommon.

8 IgD overproduction was dependent on activation-induced c

9 IgD(hi) B cells induced IL-10 production by T cells and

10 IgD(hi) B cells may have a de novo versus induced regula

11 IgD(hi) regulatory B cells represent a novel regulatory

12 IgD/CD27 and CD24/CD38 core gating systems and an 11-col

13 IgD/CD27 and CD24/CD38 core gating systems were used to

14 PN significantly reduced lamina propria (1) IgD (naive), (2) IgDLPAM (antigen-activated homed to the

15 ternatively spliced Zfp318 exon 10 abolished IgD expression on marginal zone B cells, decreased IgD o

16 structural levels, much less is known about IgD.

17 similar recruitment of naive/early-activated IgD(+) IgM(+) B cells into both the brain and spinal cor

18 M-1) in naive B (IgD) and antigen-activated (IgD or IgM) B (CD45R/B220) cells.

19 4 and B cell-activating factor (BAFF), after IgD crosslinking.

20 In light-chain amyloidosis, IgD monoclonal proteins are found in ap-proximately 1% o

21 d Rac2, B cell development is arrested at an IgD- transitional B cell stage that we term transitional

22 odeling and PI3K/Akt and Erk signaling in an IgD-BCR-dependent manner.

23 When an IgD monoclonal protein is found, amyloidosis is often om

24 ated antibodies specific for CD43, CD11c and IgD (for GC enrichment) or GL7 (for non-GC enrichment);

25 from baseline in the frequency of CD20+ and IgD+/CD27- B cells, followed by reductions, although B c

26 nly cells and lacking expression of CD27 and IgD.

27 ervoirs within the germinal center cells and IgD(+)"naive" B cells in SAP-deficient mice, showing a p

28 ells induced IL-10 production by T cells and IgD(lo) B cells.

29 including IgM ["IgM-only"], IgG and IgA) and IgD(-)CD27(-) cells ("double-negative," including IgM, I

30 trasting lectin-binding patterns of IgA1 and IgD shows that Ig O-glycosylation is differentially cont

31 rises, the O-glycosylation of serum IgA1 and IgD was studied in IgAN and controls.

32 profiles of native and desialylated IgA1 and IgD were measured in an ELISA-type system using the lect

33 hed by low surface BAFF receptor and IgM and IgD B cell receptors.

34 Mature B cells coexpress both IgM and IgD B-cell antigen receptor (BCR) classes, which are org

35 Intriguingly, the analysis of IgM and IgD expression by maturing and mature naive B cells demo

36 scripts, which would normally encode IgM and IgD from heterogeneous nuclear RNA transcripts via alter

37 emonstrate very distinct outcomes of IgM and IgD isotype activation in CLL cells, providing novel ins

38 ibrutinib effectively inhibited both IgM and IgD isotype signaling.

39 Most CLL cells express BCRs of IgM and IgD isotypes, but the contribution of these isotypes to

40 IgM and IgD receptor downmodulation, HS1 and ERK activation, che

41 ore investigated differences between IgM and IgD signaling in freshly isolated peripheral blood CLL c

42 lting in a switch from expression of IgM and IgD to expression of IgG, IgE, or IgA; this switch impro

43 s express very low levels of surface IgM and IgD, suggesting that they avoid central deletion and per

44 s punctatus express two Ig isotypes: IgM and IgD.

45 on and higher levels of cell surface IgM and IgD.

46 lusters containing immunoglobulin (Ig) M and IgD that recruit the kinase Syk and transiently associat

47 Secretory delta mRNA and IgD(+) plasma cells were detected in all immune tissues

48 ferentiated B cells into CD138(+) plasma and IgD(-)CD27(+) memory cells and triggered immunoglobulin

49 egulation of IgD class-switched B cells and 'IgD-armed' basophils in autoinflammatory syndromes with

50 ic expansion of the transitional and anergic IgD(+)IgM(-)CD27(-) B cell subsets.

51 Addition of IL-4, IL-5, and anti-IgD dextran to the cultures enhances IgA switching in FO

52 ntified through the use of anti-IgM and anti-IgD mAbs.

53 Moreover, anti-IgD-IC-loaded FDCs induced strong polyclonal IgM respons

54 lcium in response to either anti-IgM or anti-IgD cross-linking and contain a significantly increased

55 However, B cells were activated when anti-IgD-ICs, formed with Fc-specific rabbit anti-rat IgG, we

56 henotype (L-selectin and LPAM-1) in naive B (IgD) and antigen-activated (IgD or IgM) B (CD45R/B220) c

57 CR (IgM-BCR) but not of the IgD-isotype BCR (IgD-BCR).

58 ted to ubiquitously express a membrane-bound IgD-superantigen.

59 equencing of human B cell subsets defined by IgD and CD27 expression: IgD(+)CD27(+) ("marginal zone [

60 This undergalactosylation was not shared by IgD; in contrast, IgD carried more galactosylated O-glyc

61 se to certain pathogens and that the catfish IgD Fc-region, as has been suggested for human IgD, may

62 ation was progressively replaced by CD138(-) IgD(-) IgM(+) B cells, isotype-switched CD138(-) IgD(-)

63 -) IgM(+) B cells, isotype-switched CD138(-) IgD(-) IgM(-) memory B cells (B(mem)), and CD138(+) anti

64 127(-)FOXP3(+) regulatory T cells and CD19(+)IgD/M(+)CD27(-) B cells were increased through 5 years p

65 These modulations were mediated by CD19(+)IgD(low)CD38(+)CD24(low)CD27(-) B cells and needed direc

66 memory B cell subsets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+IgD-CD27+) at the single-cell level.

67 a low frequency of somatic mutations in CD19+IgD-CD27+ class-switched memory B cells in RV-specific m

68 We found an increased frequency of CD19+IgD+CD27+ unclass-switched memory B cells and a low freq

69 ets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+IgD-CD27+) at the single-cell level.

70 ulating naive or memory B cell subsets (CD19+IgD+CD27-, CD19+IgD+CD27+, or CD19+IgD-CD27+) at the sin

71 mbers of circulating immature B cells, CD19+,IgD+,CD38(high),CD10(low),CD24(high) cells, were identif

72 CD19(+), CD5(-), CD1d(-), IgD(hi) regulatory B cells from healthy controls produce

73 CD27(+)IgD(+)IgM(+) "natural effector" B cells showed reduced p

74 cells enriched in the CD24(int)CD38(+)CD27(+)IgD(-)IgM(+/low) subpopulation, which are able to transf

75 levels, whereas these were normal in CD27(+)IgD(-) memory B cells.

76 (-)IgD(+)CD38(+)), unswitched memory (CD27(+)IgD(+)CD38(-)), switched memory (CD27(+)IgD(-)CD38(-) or

77 27(+)IgD(+)CD38(-)), switched memory (CD27(+)IgD(-)CD38(-) or CD27(-)IgD(-)CD38(-)), and plasmablast

78 27(-)IgD(-)CD38(-)), and plasmablast (CD27(+)IgD(-)CD38(high)) subsets.

79 rtment, due to its exclusion from the CD27(+)IgD(+)IgM(+) subset, but this skewing does not affect th

80 equency of CD32B low/neg cells in the CD27(+)IgD(-) memory B cell subset and that these changes are a

81 equency of CD32B low/neg cells in the CD27(+)IgD(-) memory B subset in patients with RA.

82 n parallel to increased naive (CD19(+)CD27(-)IgD(+)) B-cell frequencies.

83 sing the proportion of naive B cells (CD27(-)IgD(+)CD38(-)) and concomitantly decreasing the immature

84 lating CD27(+) memory and memory-like CD27(-)IgD(-) double-negative (DN) B cells, but not CD27(-)IgD(

85 double-negative (DN) B cells, but not CD27(-)IgD(+) naive B cells.

86 tched memory (CD27(+)IgD(-)CD38(-) or CD27(-)IgD(-)CD38(-)), and plasmablast (CD27(+)IgD(-)CD38(high)

87 decreasing the immature transitional (CD27(-)IgD(+)CD38(+)), unswitched memory (CD27(+)IgD(+)CD38(-))

88 increased memory (P=0.02) and CD19+/CD27(-)/IgD(-) double negative (DN) B cells (P=0.02) and decreas

89 popolysaccharide (LPS) on apoptosis of CD27+ IgD- memory B (mB) cells from healthy controls.

90 CD27+IgD+ memory B cells and plasmablasts decreased only afte

91 decreased only after 532 days, whereas CD27+IgD- memory B cells were not affected, and there were no

92 B-cell immunophenotype (CD19/CD20/CD40(+)), IgD and/or IgM expression (67%), and lack of programmed

93 gs also reveal the existence of CD19(+)CD9(+)IgD(+) B-1 cells in the lungs of the muMT animals.

94 germinal center-independent memory B cells (IgD(+) CD27(+)).

95 of AF DENV(+) class-switched memory B cells (IgD(-)CD27(+) CD19(+) cells) reached up to 8% during acu

96 GC B cells (IgD(-)CD38(+)) were subdivided into 3 surface CD45RO fra

97 n-regulated in BCL6+ human GC founder cells (IgD+CD38+), is absent in GC centroblasts, and is re-expr

98 sociated with a specific pattern of cellular IgD distribution resembling that observed in normal B ce

99 investigated interfaces from human IgA CH3, IgD CH3, IgG1 CH3, IgM CH4, T-cell receptor (TCR) alpha/

100 Circulating IgD bound to basophils through a calcium-mobilizing rece

101 se (AID) and generated local and circulating IgD-producing plasmablasts reactive to respiratory bacte

102 intact microbiome, against which circulating IgD, but not IgM, was reactive.

103 ss, CD19 deficiency did not affect early CNS IgD(+) B cell accumulation.

104 ilent mutation ratio of systemic compartment IgD- B cells was >2, consistent with a memory phenotype

105 sylation was not shared by IgD; in contrast, IgD carried more galactosylated O-glycans in IgAN than c

106 anscriptional repressor of CCL3 In contrast, IgD signaling induced activation of the cytoskeletal pro

107 Immunoglobulin D (IgD) is an enigmatic antibody isotype that mature B cell

108 infection was observed in immunoglobulin D (IgD)-negative B cells, which was stably maintained over

109 pression on marginal zone B cells, decreased IgD on follicular B cells, and increased IgM, but only s

110 Microbiota-dependent IgD CSR also was detected in nasal-associated lymphoid t

111 e routine immunofluorescence does not detect IgD.

112 , the activation (CD86) and differentiation (IgD, CD27, and CD38) profiles of B cells were measured l

113 ota signal via Toll-like receptors to elicit IgD CSR.

114 early freezings of the WEHI-231 line express IgD but not CD93, which classifies the cells as more sim

115 ss membrane CD8, IgM, nor IgT, but expressed IgD on the cell surface.

116 subsets defined by IgD and CD27 expression: IgD(+)CD27(+) ("marginal zone [MZ]"), IgD(-)CD27(+) ("me

117 A targeted Zfp318 null allele extinguished IgD expression on mature B cells and increased IgM.

118 the immune system, as a critical factor for IgD expression.

119 d peptides showed a large spectra number for IgD, and immunohistochemistry showed intense glomerular

120 is showed 5% plasma cells, which stained for IgD.

121 intense glomerular and tubular staining for IgD.

122 Our data suggest that frog IgD is expressed on mature B cells, like in mouse/human.

123 Furthermore, B cells from IgD-deficient mice show defects in CXCL12-mediated CXCR4

124 Furthermore, IgD expressed by IgM(-)/IgD(+) B cells preferentially as

125 e human upper respiratory mucosa to generate IgD-secreting B cells that bind respiratory bacteria and

126 defect in proliferative expansion of GL7(+) IgD(-) PNA(+) B cells in Ccnd3(-/-) mice defines an unde

127 rom failed proliferative expansion of GL7(+) IgD(-) PNA(+) B cells.

128 rm twice as many GC progeny as naive IgM(hi) IgD+ counterparts.

129 the marginal zone phenotype (B220(hi)IgM(hi)IgD(lo)CD21(hi)) and to some (CD19(-)CD5(hi)) T cells.

130 oire displayed as low levels of IgM and high IgD on anergic B cells, masking a varying proportion of

131 on activity (CD19(+)CD5(+)Thy-1(int)IgM(high)IgD(high)) that we name "initiator B cells." Analysis of

132 d approximately 70% of total spleen IgM(high)IgD(low) cells during peak infection in both wild-type a

133 lls with its repertoire signature but higher IgD or lower CD27 expression levels) thus appear as the

134 D Fc-region, as has been suggested for human IgD, may function as a pattern recognition molecule.

135 he RV-specific VH and VL repertoire in human IgD- B cells expressing the intestinal homing marker alp

136 in autoinflammatory disorders such as hyper-IgD syndrome, indicating that IgD orchestrates an ancest

137 vaccine response and contained hypermutated IgD(+) B cells.

138 We have identified IgD heavy (H) chain (delta) from the amphibian Xenopus t

139 R clones of any immunoglobulin isotype (IgA, IgD, IgM, and IgG) in blood.

140 Other broader classes of antibodies (IgA1, IgD, IgE and IgM), however, differed in these motif regi

141 ion predominantly composed of surface IgM(+) IgD(+) cells residing in villi of the small intestine an

142 lyses revealed a tendency of activated IgM(+)IgD(+)CD27(+) B cells to migrate to B-cell follicles and

143 i) B cells expressed and maintained an IgM(+)IgD(lo)CD27(+)CD80(+) phenotype following immunization.

144 Burkitt lymphoma-like lymphoma (CD19(+)IgM(+)IgD(+) cells) leads to the development of clonal blastoi

145 set of diagnostic genes discriminating IgM(+)IgD(+)CD27(+) blood and splenic MZB cells from switched

146 nectomized subjects, who also have few IgM(+)IgD(+)CD27(+) B cells, had reduced antibacterial IgM.

147 uction of mu-alpha switch circles from IgM(+)IgD(+) naive human B cells, indicating its role as an Ig

148 ion during the transition from pre-GC (IgM(+)IgD(+)CD38(+)CD27(-)) to GCB cells was followed by a dra

149 memory B-cell characteristics of human IgM(+)IgD(+)CD27(+) B cells in that they share typical memory

150 d to be expressed at greater levels in IgM(+)IgD(+)CD27(+) compared with switched B cells in healthy

151 ority of Ig mutated B cells--including IgM(+)IgD(+)CD27(+) B cells--are post-germinal center (GC) mem

152 Moreover, IgM(+)IgD(+)CD27(+) B lymphocytes preferentially responded to

153 n B cells is the origin of the mutated IgM(+)IgD(+)CD27(+) B cells present in HIGM1 patients, and we

154 within the numerically dominant naive (IgM(+)IgD(+)CD27(-)) or transitional (CD10(+)CD27(-)) subsets.

155 The origin of IgM(+)IgD(+)CD27(+) (IgM memory) cells is controversial.

156 centrated within a small population of IgM(+)IgD(+)CD27(+) (nonswitched) memory cells rather than wit

157 ficiency display a marked reduction of IgM(+)IgD(+)CD27(+) B cells in blood, whereas their switched m

158 the development and/or maintenance of IgM(+)IgD(+)CD27(+) B cells in humans.

159 nd IFN-gamma caused differentiation of IgM(+)IgD(+)CD27(+) B cells into PCs, induced class switching

160 yndrome (HIGM1) support populations of IgM(+)IgD(+)CD27(+) B cells that express mutated Ig genes.

161 In contrast, the numbers of IgM(+)IgD(+)CD27(+) B cells were normal in the absence of TLR3

162 heavy-chain CDR3 size distribution of IgM(+)IgD(+)CD27(+) B cells were not affected in these patient

163 lvap results in a dramatic decrease of IgM(+)IgD(lo) B cells in both the spleen and the peritoneal ca

164 oietic Plvap deletion has no effect on IgM(+)IgD(lo) B cell numbers.

165 nctions of human peripheral blood (PB) IgM(+)IgD(+)CD27(+) B lymphocytes with somatically mutated IgV

166 Resting IgM(+)IgD(+)CD27(-) B cells from human tonsils were labeled wi

167 them with sequences cloned from sorted IgM(+)IgD(+) B cells from neonatal liver and both wild-type an

168 Further linking splenic IgM(+)IgD(+)CD27(+) B cells with production of T-independent I

169 We found that IgM(+)IgD(+)CD27(+) but not switched B cells were strongly red

170 Thus, by bolstering the IgM(+)IgD(+)CD27(+) B-cell subset, IRAK-4 and MyD88 promote op

171 these mutated B cells is unknown; the IgM(+)IgD(+)CD27(+) cells do not express AID and appear to acq

172 ap under the Chd5 promoter rescues the IgM(+)IgD(lo) B cell phenotype.

173 -)CD45R(-)CD19(-), which gives rise to IgM(+)IgD(low)CD45R(low)CD5(+)Mac-1(+)CD19(high)CD43(+)CD23(lo

174 antity of specific IgM correlated with IgM(+)IgD(+)CD27(+) B-cell frequencies.

175 lones consisted of class switched and IgM(+)(IgD(+)) members, a feature that correlated significantly

176 ile and highly diverse compartment of IgM(+)(IgD(+)) and class-switched memory B cells.

177 nalysis revealed a high similarity of IgM(+)(IgD(+))CD27(+) and IgG(+) memory B cells but also pointe

178 Catfish IgM(+)/IgD(+) B cells are small and agranular.

179 Comparatively, IgM(+)/IgD(+) B cells can express any of the four catfish IgL i

180 ly, all secreted IgD transcripts from IgM(+)/IgD(+) and IgM(-)/IgD(+) B cells were V-less and began w

181 In this study, IgM(+)/IgD(+) and IgM(-)/IgD(+) catfish B cell populations were

182 resembled pro-B cells, and were CD19(+)IgM(-)IgD(-)CD93(+)CD43(+)CD21(-)CD23(-)VpreB(+)CXCR4(+) Consi

183 For example, some catfish have <5% IgM(-)/IgD(+) B cells in their PBLs, whereas in others the IgM(

184 gD transcripts from IgM(+)/IgD(+) and IgM(-)/IgD(+) B cells were V-less and began with a leader splic

185 In this study, IgM(+)/IgD(+) and IgM(-)/IgD(+) catfish B cell populations were identified throug

186 Furthermore, IgD expressed by IgM(-)/IgD(+) B cells preferentially associates with IgL sigma.

187 er, these findings imply that catfish IgM(-)/IgD(+) B cells likely expand in response to certain path

188 In contrast, IgM(-)/IgD(+) B cells are larger and exhibit a plasmablast morp

189 membrane IgD transcripts from sorted IgM(-)/IgD(+) B cells contain viable VDJ rearrangements, with n

190 in their PBLs, whereas in others the IgM(-)/IgD(+) B cell population can represent as much as 72%.

191 ciencies have fewer immunoglobulin M (IgM)(+)IgD(+)CD27(+) B cells, a population that resembles murin

192 ular hyperplasia due to an expansion of IgM+ IgD+ B cells and showed increased germinal center format

193 tors (TLRs) in homeostasis of human CD27+IgM+IgD+B cells.

194 BALB/c mice contained normal numbers of IgM+IgD+ B cells in bone marrow and spleen and normal number

195 Although the absolute number of IgM+IgD- B cells in the bone marrow was decreased, homozygou

196 oscopy, we demonstrated that endogenous IgM, IgD, and CD19 exhibited distinct nanoscale organization

197 In striking contrast to IgM, IgD/W is evolutionarily labile, showing many duplication

198 In addition to enhancing mucosal immunity, IgD class-switched B cells enter the circulation to 'arm

199 N is incomplete in IgA1 but more complete in IgD.

200 The defects in CXCR4 signaling in IgD-deficient B cells can be overcome by anti-CD19 antib

201 The presence of virus in IgD-negative B cells indicates that gammaHV68 may either

202 ubdivided human tonsillar B cells, including IgD(-)CD38(+) GC B cells, into different fractions based

203 ion of secreted IgD resulting from increased IgD CSR exclusively within B cells of mucosa-associated

204 uggest that newly formed B cells mature into IgD(hi) B cells simultaneously in the spleen and the bon

205 which newly formed B lymphocytes mature into IgD(hi) naive recirculating B cells, but the existence o

206 ey marker used to distinguish these cells is IgD, which, through alternative RNA splicing of H chain

207 pansions of immunoglobulin M (IgM)(+)kappa(+)IgD(low/-)CD21(low)CD27(+) B cells.

208 opulations, and of B cells naturally lacking IgD.

209 increased plasma BAFF and IFN-gamma levels, IgD(-)CD38(low)CD21(-)CD27(-) atypical B cells showed th

210 ell transfers revealed that anergic IgM(low) IgD+ B cells form twice as many GC progeny as naive IgM(

211 vidence for reactivation of anergic IgM(low) IgD+ IGHV4-34+ B cells and removal of cold agglutinin se

212 cells demonstrated that this leader mediated IgD secretion.

213 CD79a and CD79b molecules, and all membrane IgD transcripts from sorted IgM(-)/IgD(+) B cells contai

214 smablast (IgD(-)CD38(++)CD27(+)) and memory (IgD(-)CD38(-)CD27(+)) transition.

215 In fact, most IgD(+) cells in the gills expressed CCR7.

216 Engagement of BCRs with rat-anti-mouse IgD (clone 11-26) does not activate B cells even when cr

217 ssion: IgD(+)CD27(+) ("marginal zone [MZ]"), IgD(-)CD27(+) ("memory," including IgM ["IgM-only"], IgG

218 cells occur exclusively in the anergic naive IgD(+), IgM(-) B-cell (BND) compartment.

219 unctionally attenuated (referred to as naive IgD(+)IgM(-) B cells [B(ND)]).

220 cGVHD patients was largely composed of naive IgD(+) B cells.

221 ty of CD23 molecules were expressed on naive IgD(+) B cells.

222 an tonsillar B cells demonstrated that naive IgD(+) and CD27(-) B cells are selectively induced to pr

223 s achieved through virus infection of naive (IgD(+)CD27(-)) B cells and their differentiation into me

224 modulating expression of surface IgM but not IgD BCRs, and by modifying basal calcium levels.

225 in infected cord blood cell cultures, and of IgD(-)CD27(+) cells (switched memory) in cell cultures f

226 Here, we describe a unique case of IgD deposition disease.

227 The diagnosis of IgD deposition disease underscores the value of laser mi

228 Recent discoveries of IgD in ancient vertebrates suggest that IgD has been pre

229 By showing dysregulation of IgD class-switched B cells and 'IgD-armed' basophils in

230 on between B cell subsets with enrichment of IgD(+)CD27(+) cells (commonly referred to as non-switche

231 V(-) children, the EBV-induced enrichment of IgD(-)CD27(+) B cells was significantly reduced in infec

232 rmore, we observed the specific expansion of IgD(+)CD27(+) B cells in response to gonococcal infectio

233 species of fish in which a secretory form of IgD has been characterized, and it occurs through the us

234 Also, the frequency of IgD-/CD27+ B cells increased in all tabalumab groups com

235 nt study, we reviewed the natural history of IgD-associated amyloidosis among 53 patients seen over 4

236 s upon Ag receptor cross-linking and lack of IgD expression, cells of the mouse cell line WEHI-231 ha

237 D receptor remains elusive, cross-linking of IgD on basophils stimulates release of immunoactivating,

238 l of IgM gene products and a virtual loss of IgD products.

239 The population of IgD(hi) B cells increased 3-fold as VL progressed.

240 s differed in all participants, with that of IgD suggesting that it is more heavily galactosylated th

241 Among Ig isotypes, only IgD, produced early in B cell development, and IgA1, pro

242 negative for surface IgM and retaining only IgD are autoreactive and functionally attenuated (referr

243 ng other switched isotypes and rarely IgM or IgD, suggesting that IgE is derived from previously anti

244 Their phenotype (IgD(+)CD38(-)CD23(-)FSC(hi)CD71(+)) is unique and sugges

245 matic increase during the GC-to-plasmablast (IgD(-)CD38(++)CD27(+)) and memory (IgD(-)CD38(-)CD27(+))

246 g increase in the number of genome-positive, IgD(-) B cells during chronic infection of both mouse st

247 In silico analysis of several published IgD genes suggested that this unique splicing mechanism

248 Regulation of rare IgD CSR events has been enigmatic.

249 Recently, IgD(-)CD27(-) (double negative, DN) and CD21(-)CD11c(+)

250 vy chain domain 1 as revealed by recombinant IgD/IgG chimeras.

251 ation, while accumulation of early-recruited IgD(+) B cells is CD19 independent.

252 Secreted IgD was found in two heavily glycosylated isoforms, whic

253 Interestingly, all secreted IgD transcripts from IgM(+)/IgD(+) and IgM(-)/IgD(+) B c

254 sed age-dependent overproduction of secreted IgD resulting from increased IgD CSR exclusively within

255 ovel strategy for the generation of secreted IgD.

256 and other innate immune cells with secreted IgD.

257 Our data demonstrate that secretory IgD is more prevalent and widespread across taxa than pr

258 We show that TG2-specific IgD molecules are preferred in the reaction and that bin

259 Following anti-CD40 stimulation, IgD(-)IgM(+/low) B cells were blocked in their plasma ce

260 eded by accumulation of non-isotype-switched IgD(+) and IgM(+) B cells.

261 ith a significant expansion of all switched (IgD(-)) MBC and a decrease of naive B cells.

262 e examined circulating non-isotype-switched (IgD(+)CD27(+)) memory cells, a population that much evid

263 ferentially colonizing the isotype-switched (IgD(-)CD27(+)) memory B-cell pool.

264 flow cytometry, and RT-PCR demonstrated that IgD(+) B cell expression varies among individuals.

265 We have recently demonstrated that IgD(hi) B cells can occupy an extravascular perisinusoid

266 ginous fish and lungfish, demonstrating that IgD/W, like IgM, was present in the ancestor of all livi

267 Based on these findings we hypothesize that IgD-expressing B cells using IGHV5-51 are preferentially

268 with periodic fever, our data indicate that IgD orchestrates an ancestral surveillance system at the

269 This indicates that IgD(+) B cells commonly found early in the CNS do not gi

270 such as hyper-IgD syndrome, indicating that IgD orchestrates an ancestral surveillance system at the

271 ught, and thus illustrate the potential that IgD may have a conserved role in immunity.

272 Also, transfection studies show that IgD functions as a typical BCR, because Igdelta-chains a

273 s of IgD in ancient vertebrates suggest that IgD has been preserved in evolution from fish to human f

274 Our study suggests that IgD/W has played varied roles in different vertebrate ta

275 ing, lack intron and exon sequences from the IgD (Ighd)-encoding region.

276 ith healthy individuals, particularly in the IgD(-)CD27(-) memory B-cell population in ACPA(+) RA.

277 Intriguingly, the IgD(+)CCR7(+) population did not coexpress memIgM.

278 e insight into the enigmatic function of the IgD antibody.

279 ngated hinge found in immunoglobulins of the IgD isotype.

280 Although the nature of the IgD receptor remains elusive, cross-linking of IgD on ba

281 The specific role of the IgD-BCR is still enigmatic, but it is colocalized with s

282 the IgM-isotype BCR (IgM-BCR) but not of the IgD-isotype BCR (IgD-BCR).

283 These results show that the IgD-BCR, CD19, and CXCR4 are not only colocalized at nan

284 ptor CXCR4 is also found in proximity to the IgD-BCR.

285 i also interacted with B lymphocytes via the IgD B-cell receptor, resulting in internalization of bac

286 tivation after challenge with foreign Abs to IgD.

287 of infection or stimulation, in contrast to IgD(lo/neg) B cells.

288 anonical form of class switching from IgM to IgD occurs in the human upper respiratory mucosa to gene

289 discovery of an isotype with similarities to IgD in bony fish are perplexing.

290 ve B cells can be induced to class switch to IgD or that autoreactive B cells that use IgD as the B c

291 ies from B cells that have class switched to IgD via genetic recombination (and thus become class swi

292 cell-dependent and T cell-independent IgM-to-IgD class switching in B cells of the human upper respir

293 Taken together, IgD-binding NTHi leads to an unspecific immune response

294 (+)) and IgG(+) MBC subsets and an unmutated IgD(+) MBC population.

295 to IgD or that autoreactive B cells that use IgD as the B cell receptor are not effectively deleted.

296 ade selectively in immature B cells, whereas IgD is coexpressed with IgM when the cells mature into f

297 Together, these findings are consistent with IgD deposition disease.

298 s developmentally regulated in parallel with IgD, with little in pro-B cells, moderate amounts in imm

299 Similarities with IgD(+)IgM(-) subsets in mammals are discussed.

300 Unexpectedly, Xenopus IgD is orthologous to IgW, an Ig isotype found only in c