BAFF

Official Full Name

TNF superfamily member 13b

Organism

Homo sapiens

Gene ID

10673

Background

The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This cytokine is a ligand for receptors TNFRSF13B/TACI, TNFRSF17/BCMA, and TNFRSF13C/BAFFR. This cytokine is expressed in B cell lineage cells, and acts as a potent B cell activator. It has been also shown to play an important role in the proliferation and differentiation of B cells. Alternatively spliced transcript variants encoding distinct isoforms have been identified. [provided by RefSeq, Mar 2011]

Synonyms

TNFSF13B; DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNLG7A; TNFSF20

Cat.No.	Product Name	Price
CSC-DC000241	Panoply™ Human ADAM29 Knockdown Stable Cell Line	Inquiry
CSC-DC016376	Panoply™ Human TNFSF13B Knockdown Stable Cell Line	Inquiry
CSC-SC000241	Panoply™ Human ADAM29 Over-expressing Stable Cell Line	Inquiry
CSC-SC016376	Panoply™ Human TNFSF13B Over-expressing Stable Cell Line	Inquiry
CSC-RT2210	Human TNFSF13B Knockout Cell Line-A549	Inquiry
CLOE-1768	Human TNFSF13B(Fc) HEK293 Cell Lysate	Inquiry
CLOE-1770	Human TNFSF13B HEK293 Cell Lysate	Inquiry

Cat.No.	Product Name	Price
AD00644Z	Human Adam29 adenoviral particles	Inquiry
AD16686Z	Human TNFSF13B adenoviral particles	Inquiry
LV28343L	human TNFSF13B (NM_006573) lentivirus particles	Inquiry
LV28344L	human TNFSF13B (NM_001145645) lentivirus particles	Inquiry

Cat.No.	Product Name	Price
SHH231574	shRNA set against Human Adam29 (NM_014269.4)	Inquiry
SHH231578	shRNA set against Mouse Adam29 (NM_175939.3)	Inquiry
SHH432140	shRNA set against Mouse TNFSF13B (NM_033622.1)	Inquiry
SHH432144	shRNA set against Rat TNFSF13B (NM_001109112.1)	Inquiry
SHL085486	shRNA set against Mouse Tnfsf13b(NM_033622.1)	Inquiry
SHW004843	shRNA set against Chicken TNFSF13B (NM_204327)	Inquiry
SHW012213	shRNA set against Danio rerio TNFSF13B (NM_001113590)	Inquiry

Cat.No.	Product Name	Price
RP00640	Biotinylated Human TNFSF13B (N-Avi-Fc)	Inquiry
RP00651	Recombinant Rhesus Macaque TNFSF13B (N-Fc)	Inquiry

Cat.No.	Product Name	Price
MiUTR3H-06420	TNFSF13B miRNA 3'UTR clone	Inquiry
MiUTR1M-12009	TNFSF13B miRNA 3'UTR clone	Inquiry
CDFR008658	Rat Tnfsf13b cDNA Clone(NM_001109112.1)	Inquiry
CDFH000316	Human ADAM29 cDNA Clone(NM_001130704.1)	Inquiry
CDFH000315	Human ADAM29 cDNA Clone(NM_001130705.1)	Inquiry
CDFH000314	Human ADAM29 cDNA Clone(NM_001130703.1)	Inquiry
MiUTR3H-06419	TNFSF13B miRNA 3'UTR clone	Inquiry
CDCS408535	Human TNFSF13B ORF Clone (BC020674)	Inquiry
CDCR375735	Rat Tnfsf13b ORF Clone(NM_001109112.1)	Inquiry
CDCR349615	Human ADAM29 ORF Clone(NM_001130705.1)	Inquiry
CDCR273311	Mouse Adam29 ORF Clone(NM_175939.3)	Inquiry
CDCR024510	Human ADAM29 ORF clone (NM_001130703.1)	Inquiry
CDCL182806	Mouse BAFF ORF clone(NM_033622.1)	Inquiry
CDCB188042	Rabbit ADAM29 ORF clone (XM_008249950.1)	Inquiry
CDCB180262	Rabbit TNFSF13B ORF clone (NM_001099964.2)	Inquiry
CDCB173688	Danio rerio TNFSF13B ORF Clone (NM_001113590)	Inquiry
CDCB166318	Chicken TNFSF13B ORF Clone (NM_204327)	Inquiry
CDCR349613	Human ADAM29 ORF Clone(NM_001130704.1)	Inquiry
CDCB156564	Cynomolgus TNFSF13B ORF clone	Inquiry

Detailed Information

B-cell activating factor (BAFF), a member of the family of TNF-like cytokines, supports the survival and differentiation of B cells. In myeloid cells, BAFF is expressed in a membrane-bound form on the cell surface (mBAFF) and can then be released as a soluble form after cleavage by furin protease. BAFF is an active ligand as a homotrimer, which is the main form of BAFF found in the circulation, however, unlike other TNF family cytokines, a 60-mer form of BAFF was obtained at physiological pH, which is also capable of binding to its receptor. Although this form has been described in a mouse model, it is still unclear whether it can be detected in humans.

The role of BAFF in promoting survival and selection of autoreactive B cells

BAFF binds to three receptors, BAFF-R, TACI transmembrane activator and calcium modulator host interactor (TACI) and B cell maturation antigen (BCMA), which are expressed by B cells at different times during the development of the individual. In humans, BAFF-R is widely expressed by all B cells except for bone marrow plasma cells. TACI is expressed by CD27+ memory B cells, by plasma cells, and by certain subsets of naive and activated B cells. BCMA is expressed by tonsillar memory B cells, GC B cells and plasma cells. BAFF-R is specific for BAFF, whereas TACI and BCMA also bind APRIL (a protein of the TNF superfamily recognized by the cell surface receptor TACI). BAFF-R signaling activates the alternative NF-κB pathway, and Akt mTOR and Pim2, and also weakly stimulates the classic NF-κB pathway, enhancing B cell survival, growth and metabolic fitness. TACI and BCMA signal through the classical NF-κB pathway and through other pathways to counteract apoptosis and promote class switching. BAFF does not work in central B cell selection in BM because immature B cells have very low BAFF-R expression.

After their exit from the BM, B cells that encounter self-antigens in the periphery face a stringent tolerance checkpoint at the transitional stage. Strong BCR signaling allows cells to be deleted or unresponsive during early transitional stages, but improves the survival of late transitional and mature follicular B cells; at the same time, these cells also compete for survival signals transmitted by BAFF and BAFF-R interactions. BCR and BAFF-R mediated signals work in multiple ways. First, BCR crosslinking in naive cells triggers the expression of BAFF-R via the PI3K signaling pathway. Second, the alternative NF-κB pathway activated by BAFF-R requires the substrate p100, which is transcribed after BCR-mediated activation of the classical NF-kB pathway. BAFF-R is involved in up-regulating CD19 expression by regulating the transcription factor PAX5, thus enhancing BCR signaling and presumably increasing p100 production. Finally, BCR and BAFF-R inhibit the apoptotic pathway by altering the expression of different pro-survival and pro-apoptotic proteins. The effect of BAFF on the survival of naive B cells may be as early as the immature start of the T1 transition, as the amount of BCR expressed regulates the expression of BAFF-R in these cells.

These studies in sum show that supraphysiologic BAFF excess does not alter negative selection that occurs before or at the T1 stage but rescues autoreactive cells that are anergized after the T1 stage and promotes their maturation into follicular and or marginal zone cells. Conversely, BAFF inhibition preferentially depletes anergic autoreactive transitional B cells compared with non-autoreactive cells and self-reactive B cells with higher affinity receptors are more readily eliminated than ones with lower affinity BCRs. Importantly, if competition is provided by non-self-reactive B cells, BAFF excess has a much smaller effect on B cell selection.

Fig. 1. Effects of BAFF/APRIL on various immune cells in SLE. (Liu et al. Experimental cell Research. 2011).

References:

Liu Z, Davidson A. BAFF and selection of autoreactive B cells. Trends in immunology. 2011;32(8):388-394.
Fabien B. Vincent, Damien Saulep-Easton, William A. Figgett, Kirsten A. Fairfax, Fabienne Mackay. The BAFF/APRIL system: Emerging functions beyond B cell biology and autoimmunity. Cytokine & Growth Factor Reviews. 2013.
Zheng Liu, Anne Davidson. BAFF inhibition: A new class of drugs for the treatment of autoimmunity. Experimental cell Research. 2011.
Xu H, He X, Xu R. B Cell Activating Factor, Renal Allograft Antibody-Mediated Rejection, and Long-Term Outcome. Journal of Immunology Research. 2018; 2018:5251801.
Musumeci G, Castrogiovanni P, Trovato FM, et al. Biomarkers of Chondrocyte Apoptosis and Autophagy in Osteoarthritis. Malemud CJ, ed. International Journal of Molecular Sciences. 2015;16(9):20560-20575.

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