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1 TACI binds the cytokines BAFF and APRIL, and previous st
2 TACI binds two ligands, APRIL and BAFF, with high affini
3 TACI is a member of the tumor necrosis factor receptor s
4 TACI is likely to influence Mvarphi phenotype by mediati
5 TACI lacks a TIR domain, yet triggered CSR via the DNA-e
6 TACI proteolysis involved shedding by a disintegrin and
7 TACI's role is controversial based on defects in TI anti
8 TACI(+) transitional cells from BAFF-transgenic mice are
9 TACI(-/-) mice develop fatal autoimmune glomerulonephrit
10 TACI-driven proliferation, isotype switching, and antibo
11 TACI-Fc (atacicept), a soluble fusion protein containing
12 TACI-Ig treatment normalized serum levels of IgM that ar
13 TACI-induced CSR was impaired in mice and humans lacking
20 normal individuals harbor the C140R or A181E TACI variants and have no outward signs of CVID, and it
21 ygosity for A144E in mice resulted in absent TACI expression in B cells, indicating that the mutant p
23 t loss of a TNFRSF13B allele does not affect TACI expression, activation responses, or establishment
24 We found that B1b cells express BAFFR and TACI and that the surface expression of both receptors i
26 known as BLyS, with its receptors BAFFR and TACI on B cells is critical for B cell homeostasis and f
28 ave used these ligands to show that BCMA and TACI have a distinct role in APRIL-induced B cell stimul
31 ifferent affinity to two receptors, BCMA and TACI, and induce cell survival and/or proliferation, whe
33 ceptors B-cell maturation antigen (BCMA) and TACI with high affinity; both of these receptors have al
34 ntibodies to the receptors BAFF-R, BCMA, and TACI were used to define expression of the individual BL
37 cannot generate CTLs in B-cell-deficient and TACI-deficient mice, strongly supporting a need for B-ce
42 ACI expression and whether an agonistic anti-TACI antibody could induce activation-induced cytidine d
44 )F(1) mice, AdTACI induced neutralizing anti-TACI antibodies and failed to reduce the numbers of B ce
45 eceptors that recognize both BAFF and APRIL, TACI (transmembrane-activator-1 and calcium-modulator- a
46 mall-interfering RNAs targeting BAFF, APRIL, TACI, and BCMA inhibited HRS cell accumulation in vitro
47 studies are the first to characterize APRIL-TACI-specific signaling and suggest a role for this liga
49 an important role in CLL and that the APRIL-TACI interaction might be a selective novel therapeutic
53 ution to BAFF-mediated humoral autoimmunity, TACI(+) transitional B cells from BAFF-transgenic mice s
54 mice demonstrates that BAFF-BCMA and/or BAFF-TACI interactions contribute to SLE, and that a profound
56 lete ACAR-mediated tumor clearance of BCMA(+)TACI(-) and BCMA(-)TACI(+) cells, and a single-chain var
57 tumor clearance of BCMA(+)TACI(-) and BCMA(-)TACI(+) cells, and a single-chain variable fragment CAR
59 ssed one or more of 3 known receptors (BCMA, TACI, and BAFF-R) for BLyS; however, the pattern of expr
60 gand TALL-1 and its cognate receptors, BCMA, TACI and BAFF-R, were recently identified as members of
61 in CLL cells, whereas signaling through BCMA/TACI induced activation of the canonical NF-kappaB pathw
62 cts at a remote time from activation because TACI is not necessary for activation and proliferation o
63 gly, some individuals with mutations in both TACI alleles do not present with CVID, suggesting that T
68 Interruption of BAFF and APRIL signaling by TACI-Ig decoy receptor, which binds to and neutralizes B
70 or 9 triggering normally up-regulates B-cell TACI expression, this was defective for all subjects wit
76 f a TNFRSF13B allele did result in decreased TACI expression on memory B cells, resulting in impaired
78 on and its human counterpart, A181E, disrupt TACI signaling and impair TACI-dependent B-cell function
82 erentiation earlier during clonal expansion, TACI may decrease the chances of autoantibody production
84 sors, HRS cells lacked BAFF-R, but expressed TACI and BCMA, a phenotype similar to that of plasmacyto
85 om individuals with TACI mutations expressed TACI but did not produce IgG and IgA in response to the
90 e data indicate a disparity in the roles for TACI and BAFFR in primary T cell-independent antibody re
92 ated Mcl-1, suggesting that a BAFF/APRIL --> TACI --> COX-2 --> PGE2--> Mcl-1 pathway reduces activat
95 gely distinct sets of surface-IgM(+)CD138(hi)TACI(+)CXCR4(+)CD1d(int)Tim1(int) plasma cells expressin
98 f the JCI, Romberg and colleagues report how TACI mutations impact B cell activation, removal of auto
103 on with reduced TACI expression and impaired TACI function, APRIL or BAFF did not activate the classi
109 gonist, CpG led to a significant increase in TACI expression and restored TACI-mediated functions.
110 of subjects with CVID who have mutations in TACI but normal immune globulin levels still have detect
113 st that TACI A181E heterozygosity results in TACI haploinsufficiency with increased susceptibility to
115 immunodeficiency-associated gene variants in TACI, BAFFR, ICOS, CD21, LRBA, and CD27 as genetically d
116 oration of the role of genetic variations in TACI in CVID populations has improved our understanding
117 rough MyD88-dependent mechanisms to increase TACI expression, they differ in terms of their downstrea
118 ther Toll-like receptor 9 agonists increased TACI expression and whether an agonistic anti-TACI antib
119 ontrols a B cell-intrinsic, TIR-independent, TACI-dependent pathway for immunoglobulin diversificatio
120 tor by physically interacting and inhibiting TACI and BCMA, members of the tumor necrosis factor (TNF
123 transmembrane activator and CAML interactor (TACI) influences wild-type TACI function is unclear; dif
124 transmembrane activator and CAML interactor (TACI) mutation C104R, which abolishes ligand binding, fa
125 transmembrane activator and CAML interactor (TACI) result in common variable immune deficiency, a syn
126 Transmembrane activator and CAML interactor (TACI) signals are critical for BAFF-mediated autoimmunit
127 transmembrane activator and CAML interactor (TACI), and CD23 activation markers after TLR9 stimulatio
129 lating cyclophilin ligand (CAML) interactor (TACI) and B-cell maturation antigen (BCMA), has been sho
130 or and cyclophilin ligand (CAML) interactor (TACI) and B-lymphocyte stimulator (BLyS) provide an earl
131 transmembrane activator and CAML-interactor (TACI), and BAFF receptor-3 (BR3)) for APRIL and the clos
132 modulator and cyclophilin ligand interactor (TACI) and B cell maturation Ag (BCMA), which bind both B
133 modulator and cyclophilin ligand interactor (TACI) and B cell maturation Ag, the early role was attri
134 -modulator and cytophilin ligand interactor (TACI) and B cell maturation antigen (BCMA), on B cells.
135 um-modulating cyclophilin ligand interactor (TACI) are found in 8% to 10% of subjects with common var
136 um-modulating cyclophilin ligand interactor (TACI) controls differentiation of long-lived plasma cell
138 d cyclophilin [corrected] ligand interactor (TACI) is a TNFR family member molecule with a pivotal ro
139 tor and calcium modulator ligand interactor (TACI) is important for T-independent antibody responses.
140 modulator and cyclophilin ligand interactor (TACI) mutations in the pathogenesis of CVID was further
141 modulator and cyclophilin ligand interactor (TACI) often display dysfunctional antibody production.
143 modulator and cyclophilin ligand interactor (TACI), a member of the TNFR family, required for TI-2 Ab
144 modulator and cyclophilin ligand interactor (TACI), a receptor for BLyS and APRIL, mounted an initial
145 ctivator and cylclophilin ligand interactor (TACI), and also interacts independently with heparan sul
147 modulator and cyclophilin ligand interactor (TACI), contribute to common variable immunodeficiency an
148 modulator and cyclophilin ligand interactor (TACI), is a key molecule for plasma cell maintenance and
149 odulating and cyclophilin ligand interactor (TACI)-Ig fusion protein (which neutralizes both BAFF and
152 modulator and cyclophilin ligand-interactor (TACI), which also bind a proliferation-inducing ligand (
153 -cell-conditional mTOR deficiency interrupts TACI signaling via NF-kappaB and cooperation with TLRs,
154 s BLyS and expressed primarily intracellular TACI, and cell surface TACI levels increased following m
158 Preterm neonatal B cells expressed less TACI, BCMA, and BAFF-R compared with adult B cells and h
160 lls and pre-B cells transduced with the long TACI isoform retained surface CD19 and immunoglobulin G,
162 tumor necrosis factor receptor family member TACI (transmembrane activator and calcium-modulator and
163 necrosis factor receptor superfamily member TACI are associated with CVID and autoimmune manifestati
164 PRIL shares two TNF receptor family members, TACI and BCMA, with another TNF homolog, BLyS/BAFF.
165 Here, we report that compared with WT mouse, TACI KO Muvarphis expressed lower levels of Toll-like re
166 rate that C104R and the corresponding murine TACI mutant, C76R, which also does not bind ligand, domi
169 immunization of newborn BALB/c mice but not TACI knockout mice with CpG ODN containing (4-hydroxy-3-
170 d that reconstitution with wild-type but not TACI-knockout B cells restored normal CTL responses supp
171 and their receptors BCMA and BAFFR, but not TACI; APRIL/BCMA is enhanced in HCC, compared with norma
172 i phenotype revealed that, in the absence of TACI, Muvarphis adapt the alternatively activated (M2) p
174 is effect, we administered a short course of TACI-Ig with and without six doses of CTLA4-Ig to 18- to
176 Fc) that express the extracellular domain of TACI (amino acid [aa] 1-126) restored CTL priming in B-c
177 Here we found that the cytoplasmic domain of TACI encompasses a conserved motif that bound MyD88, an
178 n, truncation of the MyD88-binding domain of TACI, or B-cell-conditional mTOR deficiency interrupts T
179 d in the context of the inhibitory effect of TACI-Ig on B cell maturation at the transitional stage.
181 the surface and intracellular expression of TACI protein in EBV-transformed B cells of patients and
183 investigate the effect on B-cell function of TACI A181E heterozygosity in reportedly healthy subjects
185 These studies highlight the importance of TACI signaling for the maintenance of ASCs and protectio
186 t-term IgG secretion occurs independently of TACI as DNA double-strand breaks associated with isotype
189 /-) mice, expressed half the normal level of TACI on their B cells and exhibited similar defects in a
191 es using gene KO mice indicated that loss of TACI affected only T-cell-independent antibody responses
193 tory effects correlated with the presence of TACI+ T cells in aggregate and diffuse synovitis and the
194 findings suggest that the high prevalence of TACI deficiency in humans might reflect enhanced host de
195 ucleotides (CpG ODN) led to up-regulation of TACI expression on newly formed, follicular, and margina
198 ct of its murine equivalent, mTACI A144E, on TACI signaling in transfected cells and on TACI function
200 n of inducible costimulator (ICOS) ligand on TACI-deficient B cells, given that ablation of one copy
201 ansgenic mice expressing the A144E mutant on TACI(-/-) background had low serum IgA levels and signif
202 ine the consequence of the A181E mutation on TACI function, we studied the effect of its murine equiv
203 ich killed targets expressing either BCMA or TACI (P < .01 and P < .05, respectively, cf. control, ef
204 that signaling through BR3, but not BCMA or TACI, activated the alternative nuclear factor of kappa
205 ell generation in mice deficient for BCMA or TACI, respectively, suggested that the interaction of BA
207 ional B cell defects such as BTK, BAFF-R, or TACI deficiency, were found to have higher BAFF levels t
210 oreover, low doses of a TACI fusion protein (TACI-Fc) that express the extracellular domain of TACI (
211 receptors, BCMA (B cell maturation protein), TACI (transmembrane activator and CAML [calcium-modulato
212 -like antibody responses by linking proximal TACI signaling events with distal immunometabolic transc
215 ediated down-regulation of the BLyS receptor TACI (transmembrane activator and calcium modulator and
216 in signaling from the cell surface receptor TACI in lymphocytes, although its role and mechanism of
222 ectively, these results suggest that reduced TACI expression is responsible for the unresponsiveness
224 icular and marginal zone B cells up-regulate TACI in response to TLR9 stimulation, only marginal zone
228 tive products, but instead reveals selective TACI haploinsufficiency at later stages of B-cell develo
229 oglobulin G, cells transduced with the short TACI isoform completely lost these B-cell characteristic
233 tion of endogenous BAFF and APRIL by soluble TACI and BCMA decoy receptors attenuates the survival of
234 neutralization of BAFF and APRIL by soluble TACI and BCMA decoy receptors could be useful to dampen
239 imarily intracellular TACI, and cell surface TACI levels increased following monocyte activation.
241 gnificantly lower in A181E-heterozygous than TACI-sufficient Swedish blood donors never immunized wit
242 cells remained in the cell cycle longer than TACI-proficient QM cells and had impaired plasma cell di
247 eir receptors in newborn mice and found that TACI expression on B lymphocytes was dramatically reduce
253 ype 3 serotype pneumococcus, indicating that TACI is required for T cell-independent antibody respons
254 thus resolving the longstanding paradox that TACI may have both B cell-inhibitory and -stimulatory fu
259 e antigen, it has previously been shown that TACI is critical for T cell-independent antibody respons
262 ted B cells, APRIL does not, suggesting that TACI but not BLyS receptor 3 may share survival promotin
263 formation in Taci(-/-) mice, suggesting that TACI is more important for the survival of plasma cells
264 es do not present with CVID, suggesting that TACI mutations influence CVID pathogenesis via dominant
265 by an activated, cycling phenotype, and the TACI(+) cell subset is specifically enriched for autorea
268 d not produce IgG and IgA in response to the TACI ligand APRIL, probably reflecting impaired isotype
270 ing a need for B-cell-DC cooperation through TACI-BLyS during CTL first encounter with antigens in vi
273 APRIL with the TNF family receptors (TNFRs) TACI, BCMA, and BAFF-R are crucial to TI antibody respon
275 ting of one APRIL and two BAFF (ABB) bind to TACI and BCMA and weakly to BAFFR in accordance with the
284 CAML interactor (TACI) influences wild-type TACI function is unclear; different models suggest eithe
285 the B cell developmental subsets undergoing TACI-dependent activation in settings of excess BAFF rem
286 ation by delivering nonredundant signals via TACI and BCMA receptors through both autocrine and parac
288 rtcomings of host response in newborns where TACI expression is reduced and in combined variable immu
290 that together reveal the mechanism by which TACI engages high affinity ligand binding through a sing
291 inant BAFF and anti-IgM in an assay in which TACI-Fc fusion protein inhibits B-cell proliferation.
292 tward signs of CVID, and it is not clear why TACI deficiency in this group does not cause disease.
294 G (1.6-fold) NP-specific ASCs, compared with TACI-positive QM mice in response to immunization with N
295 roenvironment and that, upon engagement with TACI, APRIL mediates activation of the phosphatidylinosi
299 did not interfere with ligand binding by WT TACI, suggesting that they may act by disrupting ligand-
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