LOCALIZATION OF THE COMPLEMENT MEMBRANE ATTACK COMPLEX INHIBITOR (CD59) IN HUMAN CONJUNCTIVA AND LACRIMAL GLAND

Recent studies have established that complement is present in the eye and participates in ocular defense. The mechanisms by which ocular tis sues are protected from bystander injury arising from local activation of the cascade, however, have not been characterized. Decay accelerat ing factor (DAF or CD55) and the membrane inhibitor of reactive lysis (MIRL or CD59) are cell surface regulatory proteins that protect blood cells from uptake of autologous C3b and polymerization of autologous C9 on their surfaces. In previous studies, we found that DAF is expres sed in high levels on corneal, conjunctival, and lacrimal gland acinar surfaces. In this study we assayed ocular and lacrimal gland tissues for CD59. Immunohistochemical analyses demonstrated large amounts of t he protein the same locations. The presence of CD59 in these sites is consistent with the proposal that CD59 functions together with DAF in protecting ocular tissues from autologous complement-mediated injury.