Anti-human very late antigen-alpha4 (CD49d) monoclonal antibody (BU49) cross-reacts with the canine B-cell leukemia cell line GL-1, resulting in the induction of homotypic cell aggregation.

We have found that the anti-human very late antigen-alpha4 (VLA-alpha4) (CD49d) monoclonal antibody (mAb) BU49 cross-reacts with the canine B-cell leukemia cell line GL-1. Interestingly, the BU49 mAb specifically induced the homotypic cell aggregation of GL-1 cells accompanied by morphological changes. Homotypic cell aggregates induced by BU49 mAb were blocked by the presence of a protein kinase C inhibitor, a protein kinase A inhibitor, an actin filament formation inhibitor, and an EDTA. On the other hand, a protein tyrosine kinase inhibitor, a DNA-synthesis inhibitor, and an anti-canine CD45 mAb did not affect the GL-1 homotypic cell aggregation induced by BU49 mAb. The BU49 mAb immunoprecipitated at a molecular weight of about 150kDa in the GL-1 cells, similar to the results in the human monocyte-like cell line U937. Taken together, our results provide the first evidence that human CD49d recognized by BU49 mAb has unique immunological functions against canine cells.