Animal-Free BAFF/TNFSF13B Protein, Mouse (His)

B-cell Activating Factor (BAFF), belongs to tumor necrosis factor family, also known as B lymphocyte stimulator (BLyS), dendritic cell-derived TNF-like molecule, and TNF- and APOL-related leukocyte expressed ligand 1 (TALL-1). BAFF is the surpotor of autoreactive B cells, mainly expressed in myeloid cell lines. The expression level of BAFF is important with immunity, while excessive BAFF signaling can lead to autoimmunity. For example, BAFF is commonly overexpressed in Systemic Lupus Erythematosus (SLE). Furthermore, BAFF seems to be involved in adipogenesis, atherosclerosis, neuro-inflammatory processes and ischemia reperfusion (I/R) injury^[1]. DeltaBAFF is a conserved alternate splice isoform of BAFF, with a lack of 57 nt encoding the A-A1 loop. DeltaBAFF is co-expressed with BAFF in many mouse and human myeloid cells. DeltaBAFF in mouse is inefficiently released by proteolysis on plasma membrane, and binds to BAFF in heteromultimers to diminish BAFF bioactivity and release. Mouse BAFF protein has two glycosylated domains and one transmembrane domain (48-68 a.a.), and can be cleaved into membrane-type peptide fragments and soluble peptide fragments. Moreover, the protein sequences between human and mice are different with similarity of 68.23%^[2]. BAFF also involves in cancer immunity. BAFF upregulates multiple B cell costimulatory molecules; augments IL-12a expression and enhances B cell antigen-presentation to CD4⁺ Th cells in vitro. it also modulates T cell function through increased T cell activation and TH1 polarization, enhanced expression of the proinflammatory leukocyte trafficking chemokine CCR6, and promotion of a memory phenotype, leading to enhanced antitumor immunity. BAFF has distinct immunoregulatory functions, promoting the expansion of CD4+Foxp3+ Tregs in the spleen and tumor microenvironment (TME)^[3].

BAFF (5 μg/mL; 72 h) activated B cells demonstrate enhanced antigen-presentation (APC) to CD4+ Th cells in isolated CD4⁺ and CD8⁺ T cells^[3].
BAFF (5 μg/mL; 48 h) upregulates multiple B cell costimulatory molecules (CD21, CD23, CD4, CD5, CD8, CD86, ICOS-L, MHCII, and PD-L1) and induces a Be-1 phenotype in B cells^[3].

BAFF (mouse; 0.5 mg/kg; i.p.; daily for 7 d) upregulates B cell CD4 and PD-L1 expression in a syngeneic mouse model of melanoma, also increases T cell activation but also induces an increase in Treg frequency^[3].