OBJECTIVES Paroxysmal nocturnal hemoglobinemia (PNH) is a rare but serious condition characterized by complement-mediated red blood cell (RBC) hemolysis and episodic thrombotic attack. It results from decay accelerating factor (CD55), and protectin (CD59), becoming attached to RBC and other cell surfaces. Absence of these protective proteins leaves such cells vulnerable to self attack at the C3...

In the regenerating amphibian limb, positional information has traditionally been considered in terms of short-range cell-cell interactions, not long-range diffusion gradients. A molecule discovered in a differential screen of regenerating limbs turns out to be precisely such a cell surface component, the newt ortholog of mouse CD59.

Complement proteins and complement activation products with effector functions include complement opsonins (C1q, MBL, and C3d), anaphylatoxins (C3a and C5a), and the membrane attack complex (MAC). The complement system also comprises a variety of cellbound and soluble complement regulatory proteins that act on different activation pathways or at different steps in the cascade, and which prevent...

BACKGROUND The presence of paroxysmal nocturnal hemoglobinuria clones in the setting of aplastic anemia or myelodysplastic syndrome has been shown to have prognostic and therapeutic implications. However, the status of paroxysmal nocturnal hemoglobinuria clones in various categories of myelodysplastic syndrome and in other bone marrow disorders is not well-studied. DESIGN AND METHODS By using...

Mesenchymal stem cells (MSC) preferentially migrate to damaged tissues and, due to their immunomodulatory and trophic properties, contribute to tissue repair. Although MSC express molecules, such as membrane cofactor protein (CD46), complement decay-accelerating factor (CD55), and protectin (CD59), which confer protection from complement-mediated lysis, MSC are recruited and activated by anaphy...

BACKGROUND The association of complement with the progression of acute T cell mediated rejection (ATCMR) is not well understood. We investigated the production of complement components and the expression of complement regulatory proteins (Cregs) in acute T-cell mediated rejection using rat and human renal allografts. METHODS We prepared rat allograft and syngeneic graft models of renal transp...

CONTEXT Human CD59, an inhibitor of the membrane attack complex of complement, is inactivated by glycation. Glycation inactivation of CD59 enhances complement-mediated injury in target organs of diabetes complications. OBJECTIVE We hypothesized that circulating soluble glycated CD59 (GCD59) represents a novel biomarker of blood glucose handling and aimed to conduct human study protocols to te...