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Results Ligation of CD28 by natural ligand, but not antibody, induced polarization of LRs at the cell-bead interface, in absence of TCR ligation. This correlated with activation of Vav-1, increased IC calcium and translocation of NFkB p65, but did not result in proliferation or cytokine production. Using DNA microarrays, we detected induction of a subset of genes, including the Egr1 family of transcription factors. Engagement of CTLA-4 blocked CD86Ig induction of LR polarization and new transcription.

Ligation of CD28 Alone by its Natural Ligand, CD86, Induces Lipid Raft Polarization in Human CD4 T-cells