Recent research on podocytes has proposed B7-1 as an important player in podocyte biology and as a potential new therapeutic target. B7-1 was upregulated in injured podocytes and described as a
biomarker to identify patients who may benefit from
abatacept, a B7-1 blocker. However, after this initial enthusiasm, several reports have not confirmed the efficiency of
abatacept at inducing
proteinuria remission in patients. In order to resolve these discrepancies, we explored the role of B7-1 in the injured podocyte. Both primary cultured and immortalized podocytes were exposed to
lipopolysaccharides, but this failed to induce B7-1 expression at the
mRNA and protein levels. Importantly, TLR-4 engagement confirmed
lipopolysaccharide efficacy. We then evaluated B7-1 expression in several mouse models of podocyte injury including treatment with
lipopolysaccharide or
Adriamycin, a lupus prone model (NZB/W F1) and subtotal
nephrectomy. Using 3 commercially available anti-B7-1
antibodies and appropriate controls, we could not find B7-1 expression in podocytes, whereas some infiltrating cells were positive. Thus, our findings do not support a role for B7-1 in podocyte biology. Hence, further studies are mandatory before treating proteinuric patients with B7-1 blockers.