描述：
B-cell activating factor (BAFF), also known as BlyS, TALL-1, TNAK, and zTNF4, is a TNF ligand
superfamily member and has been designated TNFSF13B. It is produced by macrophages,
dendritic cells, and T lymphocytes. BAFF promotes the survival of B-cells and is essential for
B cell maturation. BAFF binds to three TNF receptor superfamily members: B-cell maturation
antigen (BCMA/TNFRSF17), transmembrane activator and calciummodulator and cyclophilin
ligand interactor (TACI/TNFRSF13B) and BAFF receptor (BAFF- R/BR3/TNFRSF 13C). These
receptors are type III transmembrane proteins that lack a signal peptide. Whereas TACI and
BCMA bind BAFF and another TNF superfamily ligand, APRIL(a proliferationinducing ligand),
BAFF-R selectively binds BAFF. Mouse BAFF-R cDNA encodes a 175 amino acid residue (aa)
transmembrane protein with a 71 aa extracellular domain, a 21 aa transmembrane domain,
and a 83 aa cytoplasmic region. A second isoform of BAFF-R that has a 72 aa cytoplamic region
can also be produced by alternative splicing. The BAFF-R extracellular domain lacks the TNF
receptor canonical cysteinerich domain (CRD) and contains only a partial CRD with four
cysteine residues. Human and mouse BAFF-R share 56% aa sequence identity. BAFF-R is highly
expressed in spleen, lymph node and resting B cells. It is also expressed at lower levels in
activated B cells, in resting CD4+ T cells, in thymus and peripheral blood leukocytes. BAFF
knockout mice lack mature B cells and has profound defects in antibody mediated immune
responses. Similarly, A/WySnJ mice that are defective in BAFF-R intracellular signaling also lack
mature B cells, suggesting that BAFF R is the critical receptor for BAFF during B lymphopoiesis.
In contrast, BCMAor TACIdeficient mice have no major defect in B-cell development. While
the function of BCMA is not defined, TACI has been shown to control B-cell homeostasis and
Tcellindependent immune responses.
原厂资料：
B-cell activating factor (BAFF), also known as BlyS, TALL-1, TNAK, and zTNF4, is a TNF ligand
superfamily member and has been designated TNFSF13B. It is produced by macrophages,
dendritic cells, and T lymphocytes. BAFF promotes the survival of B-cells and is essential for
B cell maturation. BAFF binds to three TNF receptor superfamily members: B-cell maturation
antigen (BCMA/TNFRSF17), transmembrane activator and calciummodulator and cyclophilin
ligand interactor (TACI/TNFRSF13B) and BAFF receptor (BAFF- R/BR3/TNFRSF 13C). These
receptors are type III transmembrane proteins that lack a signal peptide. Whereas TACI and
BCMA bind BAFF and another TNF superfamily ligand, APRIL(a proliferationinducing ligand),
BAFF-R selectively binds BAFF. Mouse BAFF-R cDNA encodes a 175 amino acid residue (aa)
transmembrane protein with a 71 aa extracellular domain, a 21 aa transmembrane domain,
and a 83 aa cytoplasmic region. A second isoform of BAFF-R that has a 72 aa cytoplamic region
can also be produced by alternative splicing. The BAFF-R extracellular domain lacks the TNF
receptor canonical cysteinerich domain (CRD) and contains only a partial CRD with four
cysteine residues. Human and mouse BAFF-R share 56% aa sequence identity. BAFF-R is highly
expressed in spleen, lymph node and resting B cells. It is also expressed at lower levels in
activated B cells, in resting CD4+ T cells, in thymus and peripheral blood leukocytes. BAFF
knockout mice lack mature B cells and has profound defects in antibody mediated immune
responses. Similarly, A/WySnJ mice that are defective in BAFF-R intracellular signaling also lack
mature B cells, suggesting that BAFF R is the critical receptor for BAFF during B lymphopoiesis.
In contrast, BCMAor TACIdeficient mice have no major defect in B-cell development. While
the function of BCMA is not defined, TACI has been shown to control B-cell homeostasis and
Tcellindependent immune responses.
京公网安备11010802025653 版权所有：北京逸优科技有限公司
