CD52/GPI- T-Cells Are Enriched for Alloreactive Specificity and Predict Acute Graft-Versus-Host-Disease After Stem Cell Transplantation.

[1]  S. Mirarab,et al.  Sequence Analysis , 2020, Encyclopedia of Bioinformatics and Computational Biology.

[2]  G. Tonon,et al.  Immune signature drives leukemia escape and relapse after hematopoietic cell transplantation , 2019, Nature Medicine.

[3]  W. Tse,et al.  Targeting T Cell Malignancies Using CD4CAR T-Cells and Implementing a Natural Safety Switch , 2019, Stem Cell Reviews and Reports.

[4]  J. Falkenburg,et al.  CD4 Donor Lymphocyte Infusion Can Cause Conversion of Chimerism Without GVHD by Inducing Immune Responses Targeting Minor Histocompatibility Antigens in HLA Class II , 2018, Front. Immunol..

[5]  E. Holler,et al.  EBMT—NIH—CIBMTR Task Force position statement on standardized terminology & guidance for graft-versus-host disease assessment , 2018, Bone Marrow Transplantation.

[6]  C. Craddock,et al.  Unique features and clinical importance of acute alloreactive immune responses , 2018, JCI insight.

[7]  H. Veelken,et al.  High Mutation Frequency of the PIGA Gene in T Cells Results in Reconstitution of GPI Anchor−/CD52− T Cells That Can Give Early Immune Protection after Alemtuzumab-Based T Cell–Depleted Allogeneic Stem Cell Transplantation , 2018, The Journal of Immunology.

[8]  Adrian J. Thrasher,et al.  Molecular remission of infant B-ALL after infusion of universal TALEN gene-edited CAR T cells , 2017, Science Translational Medicine.

[9]  P. Moss,et al.  Cytomegalovirus Infection Leads to Development of High Frequencies of Cytotoxic Virus-Specific CD4+ T Cells Targeted to Vascular Endothelium , 2016, PLoS pathogens.

[10]  Pablo Tamayo,et al.  Compendium of Immune Signatures Identifies Conserved and Species-Specific Biology in Response to Inflammation. , 2016, Immunity.

[11]  J. Mesirov,et al.  The Molecular Signatures Database Hallmark Gene Set Collection , 2015 .

[12]  W. Huber,et al.  Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2 , 2014, Genome Biology.

[13]  Paul Theodor Pyl,et al.  HTSeq—a Python framework to work with high-throughput sequencing data , 2014, bioRxiv.

[14]  Robert A. Edwards,et al.  Quality control and preprocessing of metagenomic datasets , 2011, Bioinform..

[15]  A. Pettitt,et al.  Impact of in vivo alemtuzumab dose before reduced intensity conditioning and HLA-identical sibling stem cell transplantation: pharmacokinetics, GVHD, and immune reconstitution. , 2010, Blood.

[16]  C. Huber,et al.  Donor CD4 T cells convert mixed to full donor T-cell chimerism and replenish the CD52-positive T-cell pool after alemtuzumab-based T-cell-depleted allo-transplantation , 2010, Bone Marrow Transplantation.

[17]  Peter J. Woolf,et al.  GAGE: generally applicable gene set enrichment for pathway analysis , 2009, BMC Bioinformatics.

[18]  H. Kolb Graft-versus-leukemia effects of transplantation and donor lymphocytes. , 2008, Blood.

[19]  C. Huber,et al.  Reconstitution of CD52-Negative CD4 T Cells after Alemtuzumab-Based T Cell Depleted Allogeneic Hematopoietic Stem Cell Transplantation , 2008 .

[20]  F. Aversa,et al.  Competing risk analysis using R: an easy guide for clinicians , 2007, Bone Marrow Transplantation.

[21]  J. Cornish,et al.  Early emergence of PNH-like T cells after allogeneic stem cell transplants utilising CAMPATH-1H for T cell depletion , 2005, Bone Marrow Transplantation.

[22]  S. Mackinnon,et al.  Pharmacokinetics of alemtuzumab used for in vivo and in vitro T-cell depletion in allogeneic transplantations: relevance for early adoptive immunotherapy and infectious complications. , 2003, Blood.

[23]  H. Schrezenmeier,et al.  The spectrum of PIG-A gene mutations in aplastic anemia/paroxysmal nocturnal hemoglobinuria (AA/PNH): a high incidence of multiple mutations and evidence of a mutational hot spot. , 2003, Blood.

[24]  Richards,et al.  The PNH phenotype cells that emerge in most patients after CAMPATH‐1H therapy are present prior to treatment , 1999, British journal of haematology.

[25]  Robert Gray,et al.  A Proportional Hazards Model for the Subdistribution of a Competing Risk , 1999 .

[26]  Mark C. Field,et al.  Antibody selection against CD52 produces a paroxysmal nocturnal haemoglobinuria phenotype in human lymphocytes by a novel mechanism. , 1997, The Biochemical journal.

[27]  E. Halapi,et al.  Clonal CD8+ and CD52– T cells are induced in responding B cell lymphoma patients treated with Campath‐1H* (anti‐CD52) , 1997, European journal of haematology.

[28]  W. Rowan,et al.  Emergence of CD52-, glycosylphosphatidylinositol-anchor-deficient lymphocytes in rheumatoid arthritis patients following Campath-1H treatment. , 1996, International immunology.

[29]  H. Heimpel,et al.  Emergence of CD52-, phosphatidylinositolglycan-anchor-deficient T lymphocytes after in vivo application of Campath-1H for refractory B-cell non-Hodgkin lymphoma. , 1995, Blood.

[30]  K. Takatsuki,et al.  Persistence of affected T lymphocytes in long-term clinical remission in paroxysmal nocturnal hemoglobinuria. , 1994, Blood.

[31]  J. Loutit,et al.  “SECONDARY DISEASE” OF RADIATION CHIMERAS: A SYNDROME DUE TO LYMPHOID APLASIA , 1962, Annals of the New York Academy of Sciences.

[32]  C. E. SHANNON,et al.  A mathematical theory of communication , 1948, MOCO.

[33]  G. Hale CD52 (CAMPATH1). , 2001, Journal of biological regulators and homeostatic agents.

[34]  R. Gray A Class of $K$-Sample Tests for Comparing the Cumulative Incidence of a Competing Risk , 1988 .

[35]  A. Chao Nonparametric estimation of the number of classes in a population , 1984 .

[36]  R. Billingham The biology of graft-versus-host reactions. , 1966, Harvey lectures.