ライフサイエンスコーパス: BCMA

1 BCMA and TACI additionally bind APRIL (a proliferation-i

2 BCMA antibodies were only found in post-DLI responders a

3 BCMA CAR T cells were infused at doses of 50 x 10(6) CAR

4 BCMA expression in murine splenic B cells can be induced

5 BCMA has been implicated as a receptor for both a prolif

6 BCMA is actively cleaved from the tumor cell surface by

7 BCMA responded exclusively to APRIL, while TACI responde

8 BCMA, TACI, and B lymphocyte stimulator receptor 3 (BR3)

9 BCMA-Fc also inhibits production of antibodies against k

10 A BCMA-targeted bispecific antibody presents a promising t

11 n algorithm FoldX to successfully generate a BCMA-specific variant of APRIL, APRIL-R206E, and two TAC

12 We report the initial toxicity profile of a BCMA-directed cellular immunotherapy for patients with r

13 geting BCMA alone resulted in outgrowth of a BCMA-negative tumor.

14 sing both BCMA and TACI in the presence of a BCMA-targeting antibody.

15 Based on these results, a BCMA-Fc fusion with the single I22K mutation was produce

16 We demonstrate that a BCMA deficiency combined with the lpr mutation or the mu

17 the lamprey BAFF-like protein can bind to a BCMA-like receptor Ig fusion protein and to both BCMAL1-

18 B cell maturation Ag (BCMA) is a receptor for BAFF that, under nonautoimmune c

19 pression of BAFF-R and B cell maturation Ag (BCMA) is also highly regulated and we demonstrate that B

20 B cell maturation Ag (BCMA), a member of the TNFR superfamily expressed on B c

21 and interactor (TACI), B cell maturation Ag (BCMA), and BAFF-R.

22 eptors of this system, B cell maturation Ag (BCMA), transmembrane activator and CAML interactor, and

23 interactor (TACI) and B cell maturation Ag (BCMA), which bind both BAFF and APRIL.

24 and interactor (TACI); B cell maturation Ag (BCMA); and BAFF-R.

25 Although BCMA was previously localized to the Golgi apparatus, BC

26 have also been shown to bind BAFF, although BCMA has significantly higher affinity for APRIL than BA

27 icate that BCMA is a receptor for TALL-1 and BCMA activates NF-kappaB through a TRAF5-, TRAF6-, NIK-,

28 (pDCs) show the highest BCMA expression and BCMA-targeted agents eradicate a blastic plasmacytoid de

29 Thus, APRIL-TALL-I and BCMA-TACI form a two ligands-two receptors pathway invol

30 membrane activator and CAML interactor), and BCMA (B cell maturation antigen), while APRIL binds to T

31 d immunohistochemistry identified BAFF-R and BCMA mRNA and proteins in vCTB cells but essentially no

32 mulating CLL cells through TACI, BAFF-R, and BCMA receptors.

33 ne APRIL and two BAFF (ABB) bind to TACI and BCMA and weakly to BAFFR in accordance with the analysis

34 ndogenous BAFF and APRIL by soluble TACI and BCMA decoy receptors attenuates the survival of NHL B ce

35 zation of BAFF and APRIL by soluble TACI and BCMA decoy receptors could be useful to dampen the accum

36 delivering nonredundant signals via TACI and BCMA receptors through both autocrine and paracrine path

37 Also, mice lacking both TACI and BCMA simultaneously exhibit no B cell loss, thus confirm

38 cells lacked BAFF-R, but expressed TACI and BCMA, a phenotype similar to that of plasmacytoid B cell

39 r factor-kappaB (NF-kappaB) through TACI and BCMA, and each ligand stimulated immunoglobulin M (IgM)

40 family member, binds two receptors, TACI and BCMA, and regulates humoral immune responses [1-7].

41 r is unique in that, in contrast to TACI and BCMA, BR3 only binds BLyS.

42 ysically interacting and inhibiting TACI and BCMA, members of the tumor necrosis factor (TNF) recepto

43 ed two TNF receptor family members, TACI and BCMA, that bind zTNF4.

44 BLyS and APRIL share two receptors, TACI and BCMA, whereas a third receptor, BAFF-R, specifically bin

45 es two TNF receptor family members, TACI and BCMA, with another TNF homolog, BLyS/BAFF.

46 known TNF receptor family members, TACI and BCMA.

47 diated tumor clearance of BCMA(+)TACI(-) and BCMA(-)TACI(+) cells, and a single-chain variable fragme

48 The results from TACI(-/-) and BCMA(-/-) mice suggest the existence of additional recep

49 fering RNAs targeting BAFF, APRIL, TACI, and BCMA inhibited HRS cell accumulation in vitro and might

50 ugh cell-surface receptors BAFF-R, TACI, and BCMA.

51 ilin ligand-interactor CD267, TNFRSF13B) and BCMA (B cell maturation antigen, CD269, TNFRSF13C).

52 Anti-BCMA CART may become a powerful tool for improving organ

53 sequent treatment with APRIL or agonist anti-BCMA to similarly induce Ag presentation.

54 LO-715 is a first-in-class, allogeneic, anti-BCMA CAR T cell therapy engineered to abrogate graft-ver

55 humanized and afucosylated antagonistic anti-BCMA antibody-drug conjugate via a noncleavable linker.

56 rated that, in contrast to anti-GPRC5D, anti-BCMA bsAbs also depleted immature and small pre-B cells.

57 t multiple myeloma, but improvements in anti-BCMA CARs are needed.

58 able fragment (scFv) used clinically in anti-BCMA CARs.

59 data from >20 clinical trials involving anti-BCMA CAR T cells have demonstrated that patients with re

60 MM with active development of multiple anti-BCMA T-cell engagers (TCEs) and chimeric antigen recepto

61 f BiFab-BCMA are comparable to those of anti-BCMA chimeric antigen receptor T cell therapy (CAR-T-BCM

62 results indicate that heavy-chain-only anti-BCMA CARs are suitable for evaluation in a clinical tria

63 tes multiple myeloma (MM) resistance to anti-BCMA chimeric antigen receptor T cell (CAR T) or bispeci

64 of ELL2, including B-cell maturation antigen BCMA, a receptor with a defined role in plasma cell surv

65 (TCBs) targeting B-cell maturation antigen (BCMA) and G protein-coupled receptor class C group 5 mem

66 This mAb targets B-cell maturation antigen (BCMA) and has considerable preclinical activity, thus ho

67 nds the receptors B-cell maturation antigen (BCMA) and TACI with high affinity; both of these recepto

68 for BAFF, namely B-cell maturation antigen (BCMA) and the transmembrane activator and calcium modula

69 nt TNF receptors, B cell maturation antigen (BCMA) and transmembrane activator and cylclophilin ligan

70 B cell maturation antigen (BCMA) CAR-T cells have demonstrated promising effects in

71 B-cell maturation antigen (BCMA) chimeric antigen receptor (CAR) T cells are the mo

72 T cells targeting B-cell maturation antigen (BCMA) have activity against multiple myeloma, but improv

73 erapies targeting B-cell maturation antigen (BCMA) in relapsed/refractory multiple myeloma (RRMM) hav

74 B-cell maturation antigen (BCMA) is a key target antigen in MM with active developm

75 B-cell maturation antigen (BCMA) is a prominent tumor-associated target for chimeri

76 B-cell maturation antigen (BCMA) is a promising therapeutic target for multiple mye

77 B-cell maturation antigen (BCMA) is a rational target in multiple myeloma (MM).

78 B cell maturation antigen (BCMA) is a target for various immunotherapies and a biom

79 B cell maturation antigen (BCMA) is a tumor necrosis factor receptor family member

80 B-cell maturation antigen (BCMA) is a validated target for chimeric antigen recepto

81 B-cell maturation antigen (BCMA) is expressed in most cases of MM.

82 B cell maturation antigen (BCMA) is expressed only on plasma cells, a small subset

83 T cells targeting B-Cell Maturation Antigen (BCMA) on MM cells have shown high-response rates, but li

84 B cell maturation antigen (BCMA) target loss is considered to be a rare event that

85 We find that B cell maturation antigen (BCMA), a predicted member of the TNF receptor family exp

86 these studies was B-cell maturation antigen (BCMA), a transmembrane receptor of the tumor necrosis fa

87 The B-cell maturation antigen (BCMA), an essential membrane protein for maintaining the

88 ned expression of B cell maturation antigen (BCMA), and lowered expression of transmembrane activator

89 B cell maturation antigen (BCMA), G protein-coupled receptor family C group 5 membe

90 ractor (TACI) and B-cell maturation antigen (BCMA), has been shown to be important in B-cell biology,

91 rapy that targets B-cell maturation antigen (BCMA), has potential for the treatment of multiple myelo

92 B-cell maturation antigen (BCMA), highly expressed on malignant plasma cells in hum

93 ractor (TACI) and B cell maturation antigen (BCMA), on B cells.

94 to the receptors B cell maturation antigen (BCMA), transmembrane activator and CAML interactor (TACI

95 family receptors (B-cell maturation antigen (BCMA), transmembrane activator and CAML-interactor (TACI

96 decoy receptor of B-cell maturation antigen (BCMA), which can bind both BAFF and APRIL, but not with

97 B-cell maturation antigen (BCMA)-directed chimeric antigen receptor (CAR) T-cell th

98 B-cell maturation antigen (BCMA)-directed chimeric antigen receptor T-cell (CAR T)

99 -multiple myeloma B cell maturation antigen (BCMA)-specific chimeric antigen receptor (CAR) T-cell th

100 B-cell maturation antigen (BCMA)-targeting therapeutics have dramatically improved

101 B-cell maturation antigen (BCMA)-targeting therapies, including bispecific antibodi

102 ation 3 (CD3) and B-cell maturation antigen (BCMA).

103 therapy targeting B-cell maturation antigen (BCMA).

104 previously localized to the Golgi apparatus, BCMA was found to be expressed on the surface of transfe

105 two US Food and Drug Administration-approved BCMA-directed CAR T products.

106 aintenance: BAFF-TACI, APRIL-TACI, and APRIL-BCMA.

107 Modeling of the APRIL-BCMA complex shows the resulting interface is in agreeme

108 rystal structures of APRIL.TACI_d2 and APRIL.BCMA complexes that together reveal the mechanism by whi

109 Our data, therefore, identify a novel APRIL/BCMA signaling pathway in HCC and suggest that APRIL cou

110 and may serve as a model for specific APRIL/BCMA actions.

111 eceptors BCMA and BAFFR, but not TACI; APRIL/BCMA is enhanced in HCC, compared with normal liver tiss

112 -molecule GS inhibitors (GSIs) could augment BCMA-targeted CAR T-cell therapy.

113 se in NZM.Br3-/- mice demonstrates that BAFF-BCMA and/or BAFF-TACI interactions contribute to SLE, an

114 APRIL interact with three receptors, BAFFR, BCMA, and TACI, to play discrete and crucial roles in re

115 BiFab-BCMA lysed target BCMA-positive cell lines up to 20-fold

116 ody against B cell maturation antigen (BiFab-BCMA), which potently and specifically redirects T cells

117 Further, BiFab-BCMA robustly activated T cells in vitro and mediated ra

118 The in vitro and in vivo activities of BiFab-BCMA are comparable to those of anti-BCMA chimeric antig

119 prevented APRIL, but not BAFF, from binding BCMA, their shared receptor.

120 We investigated whether blocking BCMA cleavage by small-molecule GS inhibitors (GSIs) cou

121 d cytolysis of primary tumor expressing both BCMA and TACI in the presence of a BCMA-targeting antibo

122 n and tolerance, binds three receptors: BR3, BCMA, and TACI.

123 t the specific B cell responses regulated by BCMA remain unclear.

124 ings demonstrate antimyeloma activity of CAR-BCMA T cells.

125 Twelve patients received CAR-BCMA T cells in this dose-escalation trial.

126 -eight weeks after this patient received CAR-BCMA T cells, bone marrow plasma cells were undetectable

127 ls expressing the CAR used in this work (CAR-BCMA) specifically recognized BCMA-expressing cells.

128 CART-BCMA cells were manufactured and expanded in all subject

129 CART-BCMA infusions with or without lymphodepleting chemother

130 lophosphamide (Cy) 1.5 g/m2 + 1-5 x 107 CART-BCMA cells; and 3) Cy 1.5 g/m2 + 1-5 x 108 CART-BCMA cel

131 were treated in 3 cohorts: 1) 1-5 x 108 CART-BCMA cells alone; 2) Cyclophosphamide (Cy) 1.5 g/m2 + 1-

132 A cells; and 3) Cy 1.5 g/m2 + 1-5 x 108 CART-BCMA cells.

133 Responses and CART-BCMA expansion were associated with CD4:CD8 T cell ratio

134 ng CD3zeta and 4-1BB signaling domains (CART-BCMA), in subjects with relapsed/refractory MM.

135 nes (e.g., CLEC12B, ILT4, galectin-3, CD160, BCMA, FGL2, LAG3, GPNMB).

136 een initiated, combining GSI with concurrent BCMA CAR T-cell therapy.

137 Circulating human pDCs contained BCMA protein without displaying it on the cell surface.

138 s) in its extracellular region; in contrast, BCMA and BR3, the other known high affinity receptors fo

139 Decreased BCMA expression on residual MM cells was noted in respon

140 CAR), which killed targets expressing either BCMA or TACI (P < .01 and P < .05, respectively, cf. con

141 also encapsulated in LNPs to further elicit BCMA-specific immune response.

142 ell target antigens and methods of enhancing BCMA expression on MM cells.

143 with human pDCs, murine pDCs did not express BCMA, not even after TLR9 activation.

144 both tonsil and bone marrow tissues, express BCMA.

145 All cases tested expressed BCMA, and 39 (78%) of them also expressed TACI.

146 Using transfected cells expressing BCMA, antibodies in patient serum were found to react wi

147 d cells and primary myeloma cells expressing BCMA.

148 nced B cell generation in mice deficient for BCMA or TACI, respectively, suggested that the interacti

149 ggest that APRIL is the preferred ligand for BCMA and show that specificity can be further modified t

150 APRIL) is a natural high-affinity ligand for BCMA and transmembrane activator and calcium-modulator a

151 ctional role for BR3 and a redundant one for BCMA in B cell function.

152 nt for determining binding specificities for BCMA, TACI and BAFF-R.

153 toid dendritic cells (pDCs) show the highest BCMA expression and BCMA-targeted agents eradicate a bla

154 ion between BLyS and another TNFR homologue, BCMA (B cell maturation antigen) [7] [8].

155 lentivirally-transduced with a fully-human, BCMA-specific CAR containing CD3zeta and 4-1BB signaling

156 mouse models deficient in BCMA, we identify BCMA as an important factor in regulating peripheral B c

157 ferent lupus-prone mouse models deficient in BCMA, we identify BCMA as an important factor in regulat

158 sults predicted four amino acid positions in BCMA (Tyr13, Ile22, Gln25, and Arg27) that could impart

159 MA in PC survival was provided by studies in BCMA-/- mice in which the survival of long-lived bone ma

160 TALL-1 has three receptors, including BCMA, TACI, and BAFF-R, which are mostly expressed by B

161 or-bearing NOD/SCID/gammac-/- mice increased BCMA expression on tumor cells, decreased sBCMA in perip

162 mpared to T cells that co-express individual BCMA and CS1 CARs.

163 tion of the Q25D and R27Y substitutions into BCMA produced a dual specificity variant, since it has c

164 In contrast, mice lacking BCMA had normal-appearing B lymphocyte compartments.

165 actor (TACI) and B cell maturation molecule (BCMA)-on B cells play an important role in the humoral i

166 actor (TACI) and B cell maturation molecule (BCMA).

167 racterized the binding affinity of monomeric BCMA for its ligands; BAFF binding affinity (IC50 = 8 +/

168 Binding of the I22K mutant of monomeric BCMA to BAFF was undetectable (IC50 > 100 microm), but a

169 s improved efficacy compared to monospecific BCMA-CAR-T-cell therapy.

170 contrast to monovalent BAFF-R-Fc, monovalent BCMA does not form stable complexes with BAFF.

171 Moreover, BCMA-mediated NF-kappaB activation is inhibited by domin

172 We found that signaling through BR3, but not BCMA or TACI, activated the alternative nuclear factor o

173 emonstrating tumor control in the absence of BCMA, we maintained cytolysis of primary tumor expressin

174 erein provide a dual perspective analysis of BCMA binding to both APRIL and BAFF.

175 terminal sialylation, assists the binding of BCMA with ligands in an in vitro binding assay.

176 as complete ACAR-mediated tumor clearance of BCMA(+)TACI(-) and BCMA(-)TACI(+) cells, and a single-ch

177 The display of BCMA on the surface of human pDCs was accompanied by rel

178 The single cysteine-rich domain of BCMA and BAFF-R both have saddle-like architectures, whi

179 eptor containing the extracellular domain of BCMA blocks the binding of TALL-1 to its receptor on the

180 in consisting of the extracellular domain of BCMA fused to the hinge and CH1 and CH2 domains of human

181 und to react with the cell-surface domain of BCMA.

182 complexed with the extracellular domains of BCMA and BAFF-R at 2.6 and 2.5 A, respectively.

183 Patients who received the highest dose of BCMA-targeting CAR T cells in combination with lymphodep

184 mor cells, and potentially limit efficacy of BCMA-directed adoptive T-cell therapy.

185 al blood, and improved antitumor efficacy of BCMA-targeted CAR T-cell therapy.

186 ELL2 enhances the expression of BCMA (also known as Tnfrsf17), which is important for lo

187 mma-secretase enhanced surface expression of BCMA and reduced the release of sBCMA by pDCs.

188 We quantified surface tumor expression of BCMA and TACI on primary MM cells (n = 50).

189 Increased expression of BCMA, a weak TNFSF receptor for B lymphocyte stimulator

190 A soluble form of BCMA, which inhibited the binding of BAFF to a B cell li

191 effect of N-glycosylation on the function of BCMA and found that the dexamethasone-induced apoptosis

192 The identification of BCMA as a NF-kappaB-activating receptor for TALL-1 sugge

193 Affirmation of the importance of BCMA in PC survival was provided by studies in BCMA-/- m

194 differentiation inhibited both induction of BCMA expression and loss of BAFF-R.

195 es, most patients relapse, and low levels of BCMA on a subset of tumor cells has been suggested as a

196 tage of BCMA+ tumor cells, and the levels of BCMA surface expression in vivo.

197 Overexpression of BCMA activates NF-kappaB, and this activation is potenti

198 atients markedly increases the percentage of BCMA+ tumor cells, and the levels of BCMA surface expres

199 expression is variable, and early reports of BCMA targeting chimeric antigen receptors (CARs) suggest

200 ated with the increased surface retention of BCMA, leading to its elevated level on cell surface.

201 to resting B cells suggests a vital role of BCMA in PC survival.

202 Second, shotgun alanine scanning of BCMA was used to map critical residues for either APRIL

203 A set of BCMA-targeting DVD-ARCs at concentrations as low as 10 n

204 In this study, we extend the spectrum of BCMA expression to human pDCs.

205 study provide further support for the use of BCMA-targeting CAR T cells for myeloma, and reiterate th

206 BCMA activates the JNK pathway conferring on BCMA the specific ability to activate this Ag presentati

207 ghlight the importance of N-glycosylation on BCMA in the regulation of ligand binding and functions o

208 an bind more than one BAFF-R-Fc but only one BCMA-Fc.

209 eptors can trigger NF-kappaB signaling, only BCMA activates the JNK pathway conferring on BCMA the sp

210 ains of APRIL/BAFF receptors found that only BCMA, but not transmembrane activator and calcium-modula

211 essing a mutant BR3 gene, but not in TACI or BCMA null B cells.

212 ell line assays specific for BAFFR, TACI, or BCMA.

213 0-fold selectivity for binding to BAFFR over BCMA.

214 r enrollment, with every patient receiving P-BCMA-ALLO1 infusion, and resulting in a 100% intent-to-t

215 hs (range, 0.7-31.1), 40 patients with prior BCMA-targeted therapy had received subcutaneous 1.5 mg/k

216 Here we show that B cell maturation protein (BCMA), a member of the TNF receptor family that is expre

217 Antibodies to the receptors BAFF-R, BCMA, and TACI were used to define expression of the ind

218 tor (BAFF) binds the three receptors BAFF-R, BCMA, and TACI, predominantly expressed on mature B cell

219 y shown that the TNFR family member receptor BCMA (B cell maturation Ag) is a critical survival recep

220 , BLyS and APRIL, and a homologous receptor, BCMA, that similarly binds both ligands.

221 ) family member APRIL binds to the receptors BCMA on B cells and TACI on B and T cells.

222 s express APRIL and BAFF and their receptors BCMA and BAFFR, but not TACI; APRIL/BCMA is enhanced in

223 expressed one or more of 3 known receptors (BCMA, TACI, and BAFF-R) for BLyS; however, the pattern o

224 cell survival and binds to three receptors (BCMA, TACI, and the recently described BAFF-R).

225 NF) ligand TALL-1 and its cognate receptors, BCMA, TACI and BAFF-R, were recently identified as membe

226 Fc fusion decoy receptors, BCMA-Fc and BAFF-R-Fc, are therapeutic candidates for bl

227 as been reported to bind to three receptors, BCMA (B cell maturation protein), TACI (transmembrane ac

228 F is known to interact with three receptors, BCMA, TACI and BAFF-R, that have distant similarities wi

229 nd with different affinity to two receptors, BCMA and TACI, and induce cell survival and/or prolifera

230 BAFF is already known to bind two receptors, BCMA and TACI, we have identified a third receptor for B

231 this work (CAR-BCMA) specifically recognized BCMA-expressing cells.

232 Soluble BCMA and TACI specifically prevent binding of APRIL and

233 AR T-cell recognition and releases a soluble BCMA (sBCMA) fragment capable of inhibiting CAR T-cell f

234 n pDCs was accompanied by release of soluble BCMA (sBCMA); inhibition of gamma-secretase enhanced sur

235 ficacy and postinfusion reduction of soluble BCMA.

236 No pre-specified BCMA expression level was required.

237 Antibody responses to cell-surface BCMA may contribute directly to tumor rejection in vivo.

238 r samples to GSIs markedly increased surface BCMA levels in a dose-dependent fashion, concurrently de

239 mation by MM cells while sparing surrounding BCMA-negative normal cells.

240 meric antigen receptor T cell therapy (CAR-T-BCMA), for which two clinical trials have recently been

241 producing BAFF and APRIL, which engage TACI, BCMA, and BAFF-R receptors on the B cells.

242 xamined B cells from mice deficient in TACI, BCMA, and BAFF-R.

243 reterm neonatal B cells expressed less TACI, BCMA, and BAFF-R compared with adult B cells and had sig

244 Inhibition of TACI, BCMA, and BAFF-R expression on CLL cells; abrogation of

245 he binding of BLyS to its 3 receptors, TACI, BCMA, and BLyS receptor 3/BAFF-R.

246 BAFF binds three receptors, TACI, BCMA, and BR3, with signaling through BR3 being essentia

247 entiation factor with three receptors, TACI, BCMA, and BR3.

248 BLyS binds to 3 TNF-R receptors, TACI, BCMA, BAFF-R, to regulate B-cell survival, differentiati

249 It binds three receptors: TACI, BCMA, and BR3.

250 with the TNF family receptors (TNFRs) TACI, BCMA, and BAFF-R are crucial to TI antibody responses, w

251 uration antigen), while APRIL binds to TACI, BCMA, and proteoglycans.

252 BiFab-BCMA lysed target BCMA-positive cell lines up to 20-fold more potently tha

253 A dual-targeted BCMA-CD24-CAR-T exhibits improved efficacy compared to m

254 single-chain variable fragment CAR targeting BCMA alone resulted in outgrowth of a BCMA-negative tumo

255 Allogeneic TurboCAR T cells targeting BCMA showed no evidence of aberrant proliferation yet di

256 ric antigen receptor (CAR) T cells targeting BCMA.

257 i-MM therapy, and T-cell therapies targeting BCMA are emerging as the most potent single agents for M

258 Further, therapeutic trials targeting BCMA in patients with multiple myeloma should consider p

259 B-cell maturation antigen-targeting (BCMA)-bispecific T-cell engagers teclistamab and elranat

260 valuate B cell maturation antigen-targeting (BCMA-targeting) CAR T cells in patients with refractory

261 found that BAFF-R-Fc is more effective than BCMA-Fc for blocking BAFF binding to its receptors.

262 w BAFF-R-Fc is 10-fold more efficacious than BCMA-Fc for blocking BAFF-induced B cell proliferation i

263 nd can function through receptors other than BCMA.

264 lso highly regulated and we demonstrate that BCMA expression is only acquired in MB cells and in a ma

265 These results demonstrate that BCMA is a target of donor B-cell immunity in patients wi

266 We demonstrate that BCMA/CS1 bispecific CAR-T cells exhibit superior CAR exp

267 ted human immune cell subsets, we found that BCMA was transcribed in plasmacytoid dendritic cells (pD

268 These data indicate that BCMA is a receptor for TALL-1 and BCMA activates NF-kapp

269 This study unexpectedly reveals that BCMA works to control B cell homeostasis and self-tolera

270 ver, we have used these ligands to show that BCMA and TACI have a distinct role in APRIL-induced B ce

271 We here show that BCMA is universally expressed on the MM cell surface and

272 al effects are driven by duplications in the BCMA (branched-chain methionine allocation) loci control

273 Taken together, the BCMA/CS1 bispecific CAR presents a promising treatment a

274 imilar to the BAFF knockout mouse, while the BCMA knockout mouse has no discernible B cell phenotype.

275 hway in CLL cells, whereas signaling through BCMA/TACI induced activation of the canonical NF-kappaB

276 After engagement of TLR7/8 or TLR9, BCMA was detected also on the cell surface of pDCs.

277 rkers CD319 (SLAMF7/CS1) and CD269 (TNFRSF17/BCMA) are considerably more robust than CD138 and enable

278 the functional significance of antibodies to BCMA in vivo.

279 Binding of BAFF to BCMA-Fc, a bivalent fusion protein consisting of the ext

280 APRIL functions via binding to BCMA (B cell maturation antigen) and TACI (transmembrane

281 ntrast to previous reports, APRIL binding to BCMA decreases cell proliferation by inducing G(2)/M cel

282 elected sequences inhibited APRIL binding to BCMA with IC(50) values of 0.49-27 microM.

283 L shows the opposite selectivity, binding to BCMA with K(D) approximately 16 nM while showing no dete

284 related TNF family ligand that also binds to BCMA and TACI, but not BAFF-R.

285 [9], a close relative of BLyS, also bound to BCMA and TACI.

286 vertebrates, in this study we identified two BCMA-like genes in lampreys, BCMAL1 and BCMAL2, which we

287 Discriminating regulatory roles for the two BCMA-like molecules are suggested by their differential

288 or binding to APRIL was similar to wild-type BCMA.

289 he high selectivity of BAFF for BAFFR versus BCMA is thus partly obscured in these multivalent assays

290 how that the effect of APRIL is mediated via BCMA, which does not activate the classical NF-kappaB pa

291 ating that APRIL and/or TALL-I signaling via BCMA and/or TACI are required for generation of humoral

292 Whereas BCMA is restricted to B cells, TACI is also expressed on

293 fic and redundant: BAFFR binds BAFF, whereas BCMA and TACI bind to either BAFF or APRIL.

294 itory role for this receptor [11, 12], while BCMA null mice have no discernable phenotype [13].

295 ds BAFF with K(D) approximately 16 nM, while BCMA binds with K(D) approximately 1.6 microM, indicatin

296 s at earlier maturation stages compared with BCMA-positive plasma cell phenotypes.

297 21, and one participant did not proceed with BCMA CAR T-cell infusion.

298 ntigen loss occurs more frequently than with BCMA.

299 hat ligation of A20 B cells transfected with BCMA induces the expression of CD40, CD80/B7-1, CD86/B7-

300 lasma cells can be rescued by treatment with BCMA ligands, such as a proliferation-inducing ligand (A