NKRP1A molecule is involved in transendothelial migration of CD4+ human T lymphocytes

Among human CD4⁺ T lymphocytes, 5-20% express the C-type lectin molecule NKRP1A. Interestingly, CD4⁺ NKRP1A⁺ T lymphocytes express high levels of β1 and β2 integrins, thus representing a T lymphocyte subset that can possibly adhere and migrate through vascular endothelium. Indeed, resting CD4⁺ NKRP1A⁺ lymphocytes, differently from the CD4⁺ NKRP1A^- subset, migrated across endothelial cell monolayers in a Transwell chamber system. This transendothelial migration was strongly reduced after pre-treatment with an anti-NKRP1A monoclonal antibody (mAb). In addition, the NKRP1A negative Jurkatt CD4⁺ T-cell line that had been stably transfected with NKRP1A cDNA, migrated more rapidly and efficiently than untransfected Jurkatt cells. Finally, mAb-mediated cross-linking of NKRP1A molecule in CD4⁺ T lymphocytes induced the upregulation of the LFA1 Mg²⁺ binding site as well as β1 and β2 integrin chains. Altogether, these findings indicate that NKRP1A molecule is involved in transendothelial migration of resting CD4⁺ T lymphocytes.