InVivoMAb anti-mouse BTLA (CD272)

Catalog #BE0210
Clone:
8F4
Reactivities:
Mouse

$150.00 - $3,920.00

In stock
Only %1 left

Product Details

The 8F4 monoclonal antibody reacts with mouse B- and T-lymphocyte attenuator (BTLA) also known as CD272. BTLA is an Ig superfamily member which is expressed on B cells, T cells, macrophages, dendritic cells, NK cells, and NKT cells. Like PD-1 and CTLA-4, BTLA interacts with a B7 homolog, B7-H4. However, unlike PD-1 and CTLA-4, BTLA displays T cell inhibition via interaction with tumor necrosis family receptors, not just the B7 family of cell surface receptors. BTLA is a ligand for herpes virus entry mediator (HVEM). BTLA-HVEM complexes have been shown to negatively regulate T cell immune responses. The 8F4 antibody reacts with BALb/c and C57BL/6 mouse BLTA.

Specifications

Isotype Mouse IgG1, κ
Recommended Isotype Control(s) InVivoMAb mouse IgG1 isotype control, unknown specificity
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Immunogen C57BL/6 mouse BTLA Ig domain
Reported Applications Flow cytometry
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <2EU/mg (<0.002EU/μg)
Determined by LAL gel clotting assay
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 μM filtered
Production Purified from tissue culture supernatant in an animal free facility
Purification Protein G
RRID AB_10948994
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
Flow Cytometry
Shao, L., et al. (2015). "Aberrant germinal center formation, follicular T-helper cells, and germinal center B-cells were involved in chronic graft-versus-host disease" Ann Hematol 94(9): 1493-1504. PubMed

Chronic graft-versus-host disease (cGVHD) is an important complication after allogeneic hematopoietic stem cell transplantation (HSCT). To define the roles of T-cells and B-cells in cGVHD, a murine minor histocompatibility complex-mismatched HSCT model was used. Depletion of donor splenocyte CD4(+) T-cells and B220(+) B-cells alleviated cGVHD. Allogeneic recipients had significantly increased splenic germinal centers (GCs), with significant increases in follicular T-helper (Tfh) cells and GC B-cells. There were increased expressions in Tfh cells of inducible T-cell co-stimulator (ICOS), interleukin (IL)-4 and IL-17, and in GC B-cells of B-cell activating factor receptor and ICOS ligand. Depletion of donor splenocyte CD4(+) T-cells abrogated aberrant GC formation and suppressed Tfh cells and GC B-cells. Interestingly, depletion of donor splenocyte B200(+) B-cells also suppressed Tfh cells in addition to GC B-cells. These results suggested that in cGVHD, both Tfh and GC B-cells were involved, and their developments were mutually dependent. The mammalian target of rapamycin (mTOR) inhibitor everolimus was effective in suppressing cGVHD, Tfh cells, and GC B-cells, either as a prophylaxis or when cGVHD had established. These results implied that therapeutic targeting of both T-cells and B-cells in cGVHD might be effective. Signaling via mTOR may be another useful target in cGVHD.

Flow Cytometry
Vaeth, M., et al. (2014). "Follicular regulatory T cells control humoral autoimmunity via NFAT2-regulated CXCR5 expression" J Exp Med 211(3): 545-561. PubMed

Maturation of high-affinity B lymphocytes is precisely controlled during the germinal center reaction. This is dependent on CD4(+)CXCR5(+) follicular helper T cells (TFH) and inhibited by CD4(+)CXCR5(+)Foxp3(+) follicular regulatory T cells (TFR). Because NFAT2 was found to be highly expressed and activated in follicular T cells, we addressed its function herein. Unexpectedly, ablation of NFAT2 in T cells caused an augmented GC reaction upon immunization. Consistently, however, TFR cells were clearly reduced in the follicular T cell population due to impaired homing to B cell follicles. This was TFR-intrinsic because only in these cells NFAT2 was essential to up-regulate CXCR5. The physiological relevance for humoral (auto-)immunity was corroborated by exacerbated lupuslike disease in the presence of NFAT2-deficient TFR cells.