InVivoMAb anti-mouse T15 VH and T15 VL regions of IgM

Clone Catalog # Category
AB1-2 (HB33) BE0072 InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-mouse T15 VH and T15 VL regions of IgM

The AB1-2 monoclonal antibody reacts with mouse IgM of the T15 idiotype. The AB1-2 antibody was raised against purified immunoglobulins from the MOPC 460, MOPC 5558 and HOPC 8 myelomas.

InVivoMAb anti-mouse T15 VH and T15 VL regions of IgM Specifications

Isotype

Mouse IgG1, κ

Recommended Isotype Control(s) InVivoMAb mouse IgG1 isotype control, unknown specificity(BE0083)
Recommended InVivoPure Dilution Buffer InVivoPure pH 7.0 Dilution Buffer(IP0070)
Immunogen

Purified antibodies from MOPC 460, MOPC 5558, and HOPC 8 myelomas

Reported Applications

ELISA

Endotoxin
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
Purity
  • >95%
  • Determined by SDS-PAGE
Formulation
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
Sterility

0.2 μM filtered

Production

Purified from tissue culture supernatant in an animal free facility

Purification

Protein G

Storage

The antibody solution should be stored undiluted at 4°C, and protected from prolonged exposure to light. Do not freeze.

RRID

AB_1125545

Molecular Weight

150 kDa

Application References

InVivoMAb anti-mouse T15 VH and T15 VL regions of IgM (Clone: AB1-2 (HB33))

  Zhao, W., et al. (2015). "Macrophage-specific overexpression of interleukin-5 attenuates atherosclerosis in LDL receptor-deficient mice." Gene Ther 22(8): 645-652. PubMed Interleukin-5 (IL-5) increases the secretion of natural T15/EO6 IgM antibodies that inhibit the uptake of oxidized low-density lipoprotein (LDL) by macrophages. This study aimed to determine whether macrophage-specific expression of IL-5 in LDL receptor-deficient mice (Ldlr(-/-)) could improve cholesterol metabolism and reduce atherosclerosis. To induce macrophage-specific IL-5 expression, the pLVCD68-IL5 lentivirus was delivered into Ldlr(-/-) mice via bone marrow transplantation. The recipient mice were fed a Western-type diet for 12 weeks to induce lesion formation. We found that IL-5 was efficiently and specifically overexpressed in macrophages in recipients of pLVCD68-IL5-transduced bone marrow cells (BMC). Plasma titers of T15/EO6 IgM antibodies were significantly elevated by 58% compared with control mice transplanted with pLVCD68 lacking the IL-5 coding sequence. Plaque areas of aortas in IL-5-overexpressing mice were reduced by 43% and associated with a 2.4-fold decrease in lesion size at the aortic roots when compared with mice receiving pLVCD68-transduced BMCs. The study showed that macrophage-specific overexpression of IL-5 inhibited the progression of atherosclerotic lesions. These findings suggest that modulation of IL-5 cytokine expression represents a potential strategy for intervention of familial hypercholesterolemia and other cardiovascular diseases.

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