CD86 and rheumatoid arthritis: To investigate which CTLA4 ligand (CD80 or CD86) was involved in the abatacept-induced downregulation of CD64/FcγRI on monocytes, peripheral blood monocytes from 5 patients with RA were cultured with abatacept in the presence or absence of anti-CD80 mAb, anti-CD86 mAb, a combination of anti-CD80 plus anti-CD86 mAbs, or isotype-control mAb (Fig. 3).