complement factor D
Serum Biomarkers of Allergic Contact Dermatitis: A Pilot Study.
Vilnius, Lithuania. In Int Arch Allergy Immunol, Feb 2016
RESULTS: Serum levels of adiponectin, chemokine (C-C motif) ligand 5 (CCL5), C-reactive protein (CRP), chitinase 3-like 1 (CHI3L1), complement factor D (CFD), endoglin, lipocalin-2, osteopontin, retinol-binding protein 4 (RBP4), and platelet factor 4 (PF4) were significantly higher, whereas levels of trefoil factor 3 (TFF3) were significantly lower, in ACD patients than in healthy controls.
Age-related macular degeneration: a complementopathy?
Maastricht, Netherlands. In Ophthalmic Res, 2014
Abundant evidence includes: the identification of drusen components as activators of complement, immunohistochemical data showing the presence of many species of the complement system in the retinal pigment epithelium-Bruch's membrane-choroidocapillary region of AMD eyes, a strong association of AMD with certain genetic complement protein variants, raised complement levels in blood from AMD patients and the preliminary successful treatments of geographic atrophy with complement factor D (FD) inhibitors.
The role of the complement system in age-related macular degeneration.
London, United Kingdom. In Dtsch Arztebl Int, 2014
Several clinical trials designed to interfere specifically with these pathomechanisms have yielded rather disappointing results, although a phase II study of the monoclonal antibody lampalizumab showed that blocking complement factor D lessened the progression of geographic atrophy.
Sorbents in the treatment of renal failure.
United States. In Minerva Urol Nefrol, 2004
Removal of LMWP such as beta2-microglobulin, leptin, complement factor D, angiogenin, and cytokines such as IL-1, IL-6, IL-10, IL-18 and TNFalpha, have been established in animal models of sepsis, and in ESRD patients using sorbents in conjunction with high flux dialysis.
Hemodialysis membranes: interleukins, biocompatibility, and middle molecules.
Vienna, Austria. In J Am Soc Nephrol, 2002
Polymorphonuclear leukocyte degranulation occurring during extracorporeal circulation does not depend on complement activation but rather on intracellular calcium and the presence or absence of the degranulation inhibitory proteins angiogenin and complement factor D. Clinical signs and symptoms of end-stage renal disease patients are at least in part related to the accumulation of middle molecules such as beta(2)-microglobulin, parathyroid hormone, advanced glycation end products, advanced lipoxidation end products, advanced oxidation protein products (formed as a result of oxidative stress, carbonyl stress, or both), granulocyte inhibitory proteins, or leptin.