progression after 100% donor (2); death from infection priorto 100% donor chimerism (1); conversion to 100% donor afterstopping immunosuppression (2); and, achievement of pro-longed mixed chimerism, transfusion-free MDS for 14 monthsand then transformation to AML (1). These findings confirm ahigh engraftment rate in recipients of truly NMAT. Recipientsof MRD and MUD transplants in this moderately sized cohortexperienced similar engraftment/donor chimerism patterns.

doi:10.1016/j.clim.2006.04.434

Su.8. Engraftment and Clearance of ParoxysmalNocturnal Hemoglobinuria (PNH) Cells AfterNonmyelablative Unrelated Transplant in aHighly-Transfused Patient.Robert Nelson,1 Michael Robertson,1 Jennifer Schwartz,1

Gail Vance,2 Kelly Ward,1 John Griep,3 Magdalena Czader,3

Rafat Abonour.1 1Internal Medicine, Division ofHematology/Oncology, Hematology Malignancy Program andStem Cell Transplantation, Indianapolis, IN; 2Department ofMedical and Molecular Genetics, Indiana University Schoolof Medicine, Indianapolis, IN; 3Departments of Pathologyand Laboratory Medicine, Indiana University School ofMedicine, Indianapolis, IN.

A 37-year-old was diagnosed with aplastic anemia at theage of 19 and was treated at various times with erythropoi-etin, prednisone, and danacrine. She received over 300transfusions over 17 years. Pre-transplant evaluationrevealed loss of glycosylphosphatidylinositol-anchored anti-gens CD55 and CD59 consistent with PNH. She was allosensi-tized to blood group antigens E, c, K, Cw. Alveolar lavagedone to evaluate chronic had bilateral ground glass infi-trates showed only hemosiderin-laden macrophages. Shereceived 2.2 � 106 CD34+ and 2.0 � 108 CD3+ cells/kg of10/10 HLA- and ABO-matched unrelated donor PBMCsfollowing immunosuppressive dosages of cyclophosphamideand fludarabine. Cyclosporine (CSA) and mycophenolatemofetil were used for GVHD prophylaxis. She experiencedno mucositis, engraftment syndrome day +8 that resolvedwith moderate-dose steroids, sustained engraftment by day+12 and posterior reversible encephalopathy syndrome,which resolved temporally with switching CSA to tacrolimus.Flow cytometric analysis of CD55 and CD59 showed noevidence of PNH by day +25 and she was discharged on Day+26. Peripheral blood cell chimerism was 100% donor on day+30. With 100% PBMC donor cell chimerism at day +106,bone marrow morphology revealed trilineage hematopoie-sis, mild erythroid and mast cell hyperplasia. Immunorecon-stitution thus far reveals the following on Day +106: SerumIgG, 463 mg/dL; WBC, 4,400; ALC, 880/mm 3; CD2, 92%;CD3, 80%; CD4, 29%; CD8, 50%; CD16, 16%, Cd19, 1%. She iscurrently day +126, transfusion-independent without GVHD.This report documents sustained early engraftment andelimination of the malignant clone in a highly allo-sensitizedadult across unrelated minor histocompatability barrierswithout radiation- or ATG-containing conditioning.

doi:10.1016/j.clim.2006.04.435

Su.9. Graft-Versus-Host Disease (GVHD) AfterNonmyeloablative Transplantation.Robert Nelson,1 Michael Robertson,1 Jennifer Schwartz,1

Steven Billings,2 Rafat Abonour.1 1Internal Medicine,Division of Hematology/Oncology, Hematology MalignancyProgram and Stem Cell Transplantation, Indiana UniversitySchool of Medicine, Indianapolis, IN; 2Departments ofPathology and Laboratory Medicine and Dermatology,Indiana University School of Medicine, Indianapolis, IN.

Forty-nine consecutive patients with hematological ma-lignancies (median age, 55 years) received HLA-matchedPBMCs following immunosuppressive dosages of cyclophos-phamide and fludarabine. GVHD prophylaxis included cyclo-sporine +/�mycophenolate mofetil (MMF). Patients werefollowed until death or at least 7 months (range, 25—1675days;median 413 days). Overall rates of aGVHD and grade 3 or4 aGVHD were 65.3% (32/49) and 28.6% (14/49); no patientsexperienced antecedent mucositis and rates were equivelentfor MRD (n = 26) and MUD (n = 23) recipients. Median time toonset was 34 days. ‘‘Late onset’’ acute GVHDwas diagnosed in10 patients at a mean of 109.8 days, 8 of whom hadconcomitant histological features of chronic lichenoid GVHD(see Figure). Overall rates chronic GVHD (cGVHD) were 69.8%(57.2% extensive), diagnosed at a median of day +168; 50%(13/26) in the MRD and 69% (11/16) MUD groups, respectively(p = 0.344). Extensive cGVHD was associated with thepresence of grade 3 or 4 aGVHD Fourteen of 24 (58%) ofsurvivors are livingwith extensive cGVHD, 11 (78.5%) ofwhomare tolerating reductions in immunosuppressive therapy. Two(14.3%) are requiring pulmonary specialty care for symptom-atic bronchiolitis obliterans; no patients have experiencedprogressive sclerotic dermal disease, malabsorption orchronic liver disease. Clinical features GVHD that differ fromthat typically observed after conventional transplantationinclude time of onset and no requirement for mucositis as aninitiator. We observed no difference in GVHD incidence inthose who did and did not receive MMF. cGVHD may resolve insome patients, suggesting tolerance occurs over time in someolder patients, even with unrelated donors.

doi:10.1016/j.clim.2006.04.436

Diabetes and Other Autoimmune EndocrineDiseases

Su.10. Rapid Restoration of Anti-IsletAutoimmunity Following Transplantation of Isletswith Native Insulin Sequence Versus Insulin GeneKnockout Islets with Mutated B16:A Insulin.Maki Nakayama, Joshua Beilke, Jean Jasinski, Dongmei Miao,Masakazu Kobayashi, Liping Yu, Roberto Gianani, Edwin Liu,Ron Gill, George Eisenbarth. Barbara Davis Center forChildhood Diabetes, Univ. of Colorado Health Sciences Center,Aurora, CO.

Recently we found that NODmice lacking native proinsulingenes but with a mutated (B16:Alanine) proinsulin transgeneare protected from the development of insulin antoantibo-

AbstractsS162