Dr. Donald R. Branch received his Bachelor’s degrees in Chemistry and Cell & Molecular Biology from San Francisco State University. He is certified in clinical medical technology as well as clinical toxicology. He obtained his Specialist in Blood Banking from the American Society of Clinical Pathologists after completing an internship at St. Luke’s Hospital in San Francisco. He obtained his PhD in Immunology from the University of Alberta under the mentorship of Dr. Larry J. Guilbert and did postdoctoral training in signal transduction under Dr. Gordon B. Mills in the Department of Immunology at the University of Toronto.
Dr. Branch is currently Professor appointed in both Medicine (Division of Hematology) and Laboratory Medicine and Pathobiology at the University of Toronto. He is also an Affiliated Scientist in the Division of Advanced Diagnostics, Infection and Immunity Group, Toronto General Hospital Research Institute (TGHRI) and a Staff Scientist in Hematology/Oncology at the University Health Network (UHN).
Dr. Branch’s research is currently focused on immunotherapy and interaction of phagocytes with antibody-opsonized cells. His projects relate to the mechanism of action and replacement of intravenous immunoglobulin (IVIG). His research into the mechanism of action of high-dose IVIG, used therapeutically to ameliorate autoimmune/inflammatory diseases, has challenged current models and revealed a potential universal mechanism of action involving IVIG-induced production of interleukin-11 (IL-11).
Dr. Branch has published more than 150 original research papers and has received awards of distinction from the American Society of Hematology, American Association of Blood Banks and the Canadian Society for Transfusion Medicine. Dr. Branch currently works as a Scientist in the Centre for Innovation for the Canadian Blood Services in Toronto.
Dr. Branch’s research focuses mainly in the area of immunotherapy and transfusion medicine: A major area of his research is related to the mechanism of action and replacement of high-dose intravenous immunoglobulin (IVIG) used in patients having autoimmune/inflammatory diseases.
In this work, Dr. Branch utilizes both in vitro and in vivo methods. He uses an in vitro assay of monocyte, M1 and M2 macrophage phagocytosis to investigate interactions of antibody-opsonized red blood cells and ability of possible IVIG replacements to inhibit phagocytosis compared to IVIG. Using mouse models of immune thrombocytopenia (ITP) and rheumatoid arthritis (RA) he examines the mechanism of amelioration of these conditions by IVIG and potential replacements. His research into the mechanism of IVIG amelioration of ITP has challenged current models and revealed a potential universal mechanism of action involving IVIG-induced production of interleukin-11 (IL-11).
Dr. Branch is actively involved in drug discovery for a small molecule replacement for IVIG as well as collaborating with a company to examine efficacy of fully recombinant Fc multimers. In this work he has discovered a class of pyrazole compounds that are effective at inhibiting phagocytosis in vitro and at least one candidate molecule that shows efficacy in an animal model of immune thrombocytopenia (ITP).
In addition, Dr. Branch has found that fully recombinant Fc hexamers are 10-100-fold more efficacious than IVIG for inhibiting phagocytosis in vitro and 10-fold more efficacious than IVIG to ameliorate ITP or RA.
Dr. Branch also collaborates with the 5 Toronto-based hospitals to examine the potential clinical significance of antibodies to red blood cell in a transfusion setting using an assay called the monocyte monolayer assay (MMA) which he pioneered in the 1980s. This assay is used to aid the hospitals in the selection of donor blood for transfusion in certain patients
The laboratory is a certified Level 2 facility and is located at 67 College St. within the Canadian Blood Services building. The lab environment is exceptional. We have approximately 1000 square feet of research and office space. We have a fully equipped laboratory with all necessary equipment for biomedical research including three double -80C freezers and four -20C freezers, plus two cold (4C) cabinets, a walk in 4C cold room, a PCR room, a radioisotope work room certified by CNSC as an intermediate level radiation laboratory, four biological containment cabinets, low and high-speed centrifuges, water baths and four double CO2 incubators.
We collaborate with and share equipment with Principal Investigators within the Toronto General Research Institute (TGRI) located on the 4th floor of the Canadian Blood Services building. Thus, we have access to two FACS machines, a phosphorimager, lightcycler real-time PCR, film dark room and developer, fluorescent microscope, cell disrupters, ultra-centrifuges, liquid nitrogen storage, another walk in cold room, as well as a library with most relevant current journals and extra computers. We have use of the UHN small animal facility located on the 6th floor of the Canadian Blood Services building.
Spirig R, Campbell IK, Koernig S, Chen CB, Lewis BJB, Butcher R, Muir I, Taylor S, Chia J, Leong D, Simmonds J, Scotney P, Schmidt P, Fabri L, Hofmann A, Jordi M, Spycher MO, Cattepoel S, Brasseit J, Panousis C, Rowe T, BRANCH DR, Baz Morelli A, Kaesermann F, Zuercher AW. rIgG1 Fc hexamer inhibits antibody-mediated autoimmune disease via effects on complement and FcγRs. J Immunol 2018; [Epub ahead of print].
Qadri SM, Donkor DA, Nazy I, BRANCH DR, Sheffield WP. Bacterial neuraminidase-mediated erythrocyte desialyation provokes cell surface aminophospholipid exposure. Eur J Haematol 2018;[Epub ahead of print].
BRANCH DR, Hellberg A, Bruggeman CW, Storry JR, Sakac D, Blacquiere M, Tong TN, Burke-Murphy E, Binnington B, Parmar N, Riden LS, Willie K, Armali C, Aziz J, Lieberman L, Laroche V, Callum J, Lin Y, Shehata N, Pavenski K, Lau W, Hannach B, Kuijpers TW, Olsson ML, Cserti-Gazdewich C, Pendergrast J. ABO zygosity, but not secretor or Fc receptor status, is a significant risk factor for IVIG-associated hemolysis. Blood 2018;131(7):830-835.
Schneider C, Wicki S, Graeter S, Timcheva TM, Keller CW, Quast I, Leontyev D, Djoumerska-Alexieva IF, Kaesermann F, Jakob SM, Dimitrova PA, BRANCH DR, Cummings RD, Lunemann JD, Kaufmann T, Simon HU, von Gunten S. IVIG regulates the survival of human but not mouse neutrophils. Sci Rep 2017;7(1):1296.
Da Silveira Cavalcante L, BRANCH DR, Duong TT, Yeung RSM, Acker JP, Holovati JL. The immune-stimulation capacity of liposome-treated red blood cells. J Liposome Res 2017; Mar 9:1-9.
Le Sage V, Cinti A, McCarthy S, Amorim R, Rao S, Daino GL, Tramontano E, BRANCH DR, Mouland AJ, Virology 2017;502:73-83.
BRANCH DR, Westhoff CM. Shining a light on AHG “blind” spot(s). Transfusion 2016;56:2913-2915.
Liu J, Santhanakrishnan M, Natarajan P, Gibb DR, Eisenbarth SC, Tormey CA, Siddon AJ, Stowell SR, BRANCH DR, Hendrickson JE. Antigen modulation as a potential mechanism of anti-KEL immunoprophylaxis in mice. Blood 2016;128(26):3159-3168.
Tong TN, Burke-Murphy E, Sakac D, Pendergrast J, Cserti-Gazdewich C, Laroche V, BRANCH DR. Optimal conditions for the performance of a monocyte monolayer assay. Transfusion 2016;56(11):2680-2690.
Neschadim A, Kotra LP, BRANCH DR. Small molecule phagocytosis inhibitors of immune cytopenias. Autoimmun Rev 2016;15(8):843-847.
Kozlowski HN, Lai ET, Havugimana PC, White C, Emili A, Sakac D, Binnington B, Neschadim A, McCarthy SD, BRANCH DR. Extracellular histones identified in crocodile blood inhibit in-vitro HIV-1 infection. AIDS 2016;30(13):2043-2052.
Tong TN, Cserti-Gazdewich CM, BRANCH DR. Value of MMA crossmatch? Transfus Med 2016;26(4):301-302.
Neschadim A, BRANCH DR. Mouse models for immune-mediated platelet destruction or immune thrombocytopenia (ITP). Curr Protoc Immunol 2016;113:15.30.1-15.30.13.
McCarthy SD, Sakac D, Neschadim A, BRANCH DR. c-SRC protein tyrosine kinase regulates early HIV-1 infection post-entry. AIDS 2016;30(6):849-858.
McCarthy SD, Majchrzak-Kita B, Racine T, Kozlowski HN, Baker DP, Hoenen T, Kobinger GP, Fish EN, BRANCH DR. A rapid screening assay identifies monotherapy with interferon-β and combination therapies with nucleoside analogs as effective inhibitors of Ebola virus. PLoS Negl Trop Dis 2016;10(1):e000436