Howard B. Fleit, Ph.D., Associate Professor.
Howard B. Fleit, Ph.D.
Associate Professor
Vice Chair for Education
Stony Brook University School of Medicine
Stony Brook University
Stony Brook, NY 11794-8691
Tel: 631-444-3020
Fax: 631-444-3424
Email: hfleit@notes.cc.sunysb.edu
Education:
| 1973 | B.A., Biology, State University of New York at Buffalo, Buffalo, New York |
| 1974 | M.S., Natural Sciences, State University of New York at Buffalo, Roswell Park Memorial Institute Division, Buffalo, New York |
| 1980 |
Ph.D. Cell Biology-Basic Medical Sciences, New York University, New York, New York |
Postdoctoral Training:
| 1980-1983 | The Rockefeller University, Department of Cellular Physiology and Immunology, New York, NY |
Awards and Honors:
| 1981-1983 | American Cancer Society Fellowship |
| 1986 | Catacosinos Young Investigator Award |
| 1986 | Sinsheimer Foundation Scholar Award |
| 2008 |
Aesculapius Award for Teaching |
Teaching Activities: Ahmad, Magdy, Howard B. Fleit, Marc G. Golightly, and Edmund F. La Gamma. Dexamethasone therapy interferes with the development of the neutrophil oxidative burst in vitro in very low birth weight infants. American Journal of Perinatology 24: 223-225, 2007 Ahmad, Magdy, Howard B. Fleit, Marc G. Golightly, and Edmund F. La Gamma. In vivo effect of rh-granulocyte colony stimulating factor on phagocytic function and oxidative burst in septic neutropenic neonates. Biology of the Neonate. 86: 48-54, 2004. Cooper, Nichola, Nancy M. Heddle, Masja de Haas, Marion E. Reed, Martin L. Lesser, Howard B. Fleit, Michael B.R. Woloski, and James B. Bussel. Modulation of cytokine and platelet responses by FcgRIIa and FcgRIIIa polymorphisms following infusion of IV anti-D in adults with immune thrombocytopenia purpura; Comparison to IVIG. British Journal of Haematology 124:511-518, 2004. Howard B. Fleit and Bernard P. Lane. FcgR receptor mediated phagocytosis by human neutrophil cytoplasts. Inflammation, 23: 253-262, 1999. Kocher, Markus, Jeffrey C. Edberg, Howard B. Fleit, and Robert P. Kimberly. Anti-neutrophil cytoplasmic antibodies preferentially engage FcgRIIIb on human neutrophils. J. Immunol. 161:6909-6914, 1998. Payne, Nathaniel R. and Howard B. Fleit. Extremely low birth weight infants have lower FcgRIII (CD16) plasma levels and their PMN produce less FcgRIII compared to adults. Biol. Neonate 69: 235-242, 1996. Ghazizadeh, Soosan, and Howard B. Fleit. Tyrosine phosphorylation provides an obligatory early signal for FcgRII-mediated endocytosis in the monocytic cell line THP-1. J. Immunol. 152: 30-41, 1994.
Course director for HBP 531 General Pathology, first year School of Medicine: (schedule TBA)
Course director for HBP 533 Immunology (schedule here)
Howard Fleit is an immunologist whose research focuses on cellular components of the innate immune system. Phagocytic cells, such as macrophages and neutrophils, are members of the innate immune system and have receptors (Fcg receptors) on their plasma membranes that bind antibody molecules and thereby bridge the adaptive immune response to cells of the innate immune system. Fleit utilizes biochemical and cell biological techniques to study how different classes of these receptors transduce a signal in the phagocytes to trigger them to release toxic oxygen intermediates, such as superoxide, which can destroy antibody-coated bacteria.
Selected Recent Publications:
Ghazizadeh, Soosan, Joseph B. Bolen, and Howard B. Fleit. Tyrosine phosphorylation and association of Syk with FcgRII in monocytic THP-1 cells. Biochemical Journal. 305: 669-674, 1995.
Ghazizadeh, Soosan, Joseph B. Bolen, and Howard B. Fleit. Physical and functional association of src-related protein tyrosine kinases with FcgRII in monocytic THP-1 cells. J. Biol. Chem. 269: 8878-8884, 1994.
Last updated by andrea.schmidt on October 16, 2009