S80 Abstracts

historical study details could obviate the needless repetition ofstudies, reduce the number of animals used, expedite modelimplementation projects, refine current animal models andbuild on existing work. The net result would be a significantimprovement in information sharing, much more efficient useof limited research resources and ultimately a decreased timeto identify, develop and market new therapeutics.

doi:10.1016/j.clim.2009.03.233

T.101. Treatment of HIV-Infected Patients with GcProtein-Derived Macrophage Activating Factor(GcMAF) and Its Coned Derivative (GcMAFc)Eradicates HIV-InfectionNobuto Yamamoto1, Masumi Ueda1, Kazuya Hashinaka1,Theodore Sery1, Charles Benson2. 1Socrates Institute forTherapeutic Immunology, Philadelphia, PA; 2University ofPennsylvania, Philadelphia, PA

Serum Gc protein (known as vitamin D-binding protein) isthe precursor for the principal macrophage activating factor(MAF). The MAF precursor activity of serum Gc protein of HIV-infected patients was lost or reduced because Gc protein isdeglycosylated by serum α-N-acetylgalactosaminidase (Naga-lase) secreted from HIV-infected cells. Since Nagalase is theintrinsic component of gp120, serum Nagalase was alreadycomplexed with anti-HIV immunoglobulin G (IgG) in patientblood stream. The IgG-bound virions were infectious andretained Nagalase activity, leading to immunosuppression.Stepwise treatment of purified serum Gc protein or its clonedGc protein with immobilized β-galactosidase and sialidasegenerated the most potent MAF (termed GcMAF or GcMAFc,respectively) ever discovered,which produces no side effect inhumans. Macrophages activated by intramuscular administra-tion of GcMAF or GcMAFc (100 ng/patient) developed a largeamount of Fc-receptors as well as enormous variation ofreceptors that phagocytize IgG bound and unboundHIV virions.Cells harboring HIV provirus were unstable and spontaneouslyreleased the virions at a high rate. After less than 18 weeklyintramuscular administrations of 100 ng GcMAF or GcMAFc totwenty-four nonanemic patients, they exhibited healthycontrol level of Nagalase activity, indicating eradication ofHIV-infection. Since GcMAFc has a potentmitogenic activity onmyeloid progenitor cells (MPC), intravenous administration ofGcMAFc allowed rapid interaction of GcMAFc with MPC in bonemarrow and the systemic cell counts of the activatedmacrophages increased to 220-fold in 2 days. Weekly intrave-nous administration of 100 ng GcMAFc to HIV-infected patientseradicated HIV-infection in 8-13 weeks.

doi:10.1016/j.clim.2009.03.234

T.102. Treatment with TNFα Inhibitors inRheumatoid Arthritis Rescues CD28 Expression inCD4+Cells but does not Affect ProliferativeResponses to Anti-CD3±Anti-CD28Roberto Paganelli1, Marika D'Urbano2, Paola Volpe2,Eleonora Celletti1. 1University “G. d'Annunzio”, Chieti,

Italy; 2Center for Sciences of Aging, Fondazione UdA,Chieti, Italy

In rheumatoid arthritis (RA) CD4+CD28null cells areexpanded, related to high levels of TNFα. We evaluatedthe changes in CD28 expression and in vitro Tcell response toCD28 costimulation in 21 patients (13 F and 8 M) affected byinflammatory rheumatic diseases in which TNFα blockade isindicated (9 had RA, 7 psoriatic arthritis and 5 ankylosingspondilitis). All were newly diagnosed and not previouslytreated. 10 received TNFα inhibitors for at least 1 year,including infliximab (Remicade; 5 mg/kg e.v. every 8 weeks)and etanercept (Enbrel; 25 mg twice weekly s.c.). Expressionof CD28 on CD3+, CD4+and CD8+ lymphocytes was deter-mined by flow cytometry on whole blood, using triplefluorescence analysis on a FACSCalibur (Beckton-Dickinson,San Josè, CA). Mononuclear cells loaded with CFSE (Sigma, StLouis, MO) were cultured for 5 days with/out anti-CD3 andantiCD3+anti-CD28 (Immunotech). Determination of celldivisions through CFSE dilution was obtained by the Flow-Jo software (Tree Star, Inc Ashland, OR). Statistical evalua-tion was performed with SigmaPlot ver.9 (Systat GmbH,Germany). A significant increase of CD28+cells within CD4+lymphocytes was observed in RA patients treated with TNFαinhibitors, but not in other seronegative arthritides. Unsti-mulated lymphoproliferation was increased in untreatedpatients. CD3-induced lymphoproliferation was similar in allpatients, with lower responses in seronegative arthritis aftertreatment. Anti-CD28 increased cell division in only half ofthe patients; this was unrelated to the number of CD28+Tcells. Spontaneous proliferation decreased after treatmentwith TNFα inhibitors, whereas T cell stimulation, as CD28triggering, seem to be unrelated to CD28 molecule expres-sion prior to culture, and unaffected by treatment with TNFαinhibitors.

doi:10.1016/j.clim.2009.03.235

T.103. Pulse Cyclophosphamide Therapy canPrevent Neuromyelitis Optica Relapses in SystemicLupus Erythematosus Associated CasesAnna Polgár1, Csilla Rózsa2, Judit Matolcsi2, Gyula Poór1,Emese Kiss1. 1National Institute of Rheumatology andPhysiotherapy, Budapest, Hungary; 2Jahn Ferenc TeachingHospital, Budapest, Hungary

Neuromyelitis optica (NMO, Devic's disease) is an uncom-mon demyelinating neuro-immunological disease, withrelapsing course, causing early disability. It's characterisedby optic neuritis, transverse myelitis and 2 from thefollowing criteria: myelitis involving more than 3 segments;brain MRI, non-diagnostic for multiple sclerosis; presence ofanti-aquaporin-4 antibody. NMO can be associated withsystemic autoimmune diseases, but there are only fewpublications about individual cases. In a systemic lupuserythematosus (SLE) associated case NMO revealed yearsbefore other SLE manifestations. There are no specificrecommendations for the treatment of NMO, especially notfor the SLE overlapping cases. High dose corticosteroidmedication followed by long time immunosuppression seems