Immunology Faculty Member - Francis Luscinskas, PhD

Francis Luscinskas, PhD

Harvard Medical School
NRB, Room 752P
77 Avenue Louis Pasteur
Boston, MA 2115
Tel: 617-525-4337
Fax: 617-525-4333
Email: fluscinskas@rics.bwh.harvard.edu



The research projects in my laboratory study innate and adaptive immune cell interactions with one another during antigen (Ag) priming of T cells, and the mechanisms underlying innate and adaptive immune cell adhesion to and transmigration across vascular endothelium employing in vivo murine and in vitro human cell models. Our focus is to understand the role of CD47 and its ligands, SIRPα and SIRPγ and LFA-1 and VLA-4 integrins in innate and endothelial cell interactions. Our projects employ in vivo models of inflammation and cancer. Inflammation models include Ag-dependent leukocyte activation and recruitment, DC priming of T cells, Experimental Autoimmune Encephalomyelitis (both MOG induced EAE and Relapsing-EAE) and atherosclerosis in collaboration with Andrew Lichtman‘s laboratory at BWH and a dermal air pouch). Our work in cancer biology focuses on the role of CD47 as a therapeutic for hematological cancer in collaboration with the Weinstock lab at Dana-Farber Cancer Institute.

Our laboratory consists of 2 Research Fellows and two senior Research Scientists who use a combination of immunological, biochemical and molecular biological strategies in our in vivo and in vitro models. We have developed a valuable in vitro model that allows direct microscopic examination of live leukocyte - endothelial and T cell- DC interactions under static or defined laminar fluid shear stress conditions. We are supported by NIH awards.

Key Words: CD47; SIRP; endothelium; T cell; monocytes; adhesion; inflammation.

Last Update: 6/15/2018



Last Update: 6/18/2018



Publications

For a complete listing of publications click here.

 


 

Allport, J. R., H. Ding, W. A. Muller, and F. W. Luscinskas. 2000. Monocytes induce reversible focal changes in VE-cadherin complex during transendothelial migration under flow. J.Cell Biol.203-216.

Grabie, N., M. W. Delfs, Y. C. Lim, J. R. Westrich, F. W. Luscinskas, and A. H. Lichtman. 2002. Beta-galactoside alpha2,3-sialyltransferase-I gene expression during Th2 but not Th1 differentiation: implications for core2-glycan formation on cell surface proteins. Eur.J.Immunol 32:2766-2772.

Ancuta, P., R. Rao, A. Moses, A. Mehle, S. K. Shaw, F. W. Luscinskas, and D. Gabuzda. 2003. Fractalkine preferentially mediates arrest and migration of CD16+ monocytes. J.Exp.Med. 197:1701-1707.

Gerszten, R. E., E. Garcia-Zepeda, Y.-C. Lim, M. Yoshida, H. Ding, M. A. Gimbrone Jr., A. D. Luster, F. W. Luscinskas, and A. Rosenzweig. 1999. MCP-1 and IL-8 trigger firm adhesion of monocytes to vascular endothelium under flow conditions. Nature 398:718-723.

Shaw, S. K., P. S. Bamba, B. N. Perkins, and F. W. Luscinskas. 2001. Real-time imaging of vascular endothelial-cadherin during leukocyte transmigration across endothelium. J.Immunol. 167:2323-2330.

Brown JD, Lin CY, Duan Q, Griffin G, Federation A, Paranal RM, Bair S, Newton G, Lichtman A, Kung A, Yang T, Wang H, Luscinskas FW, Croce K, Bradner JE, Plutzky J. NF-κB directs dynamic super enhancer formation in inflammation and atherogenesis. Mol Cell. 2014 Oct 23;56(2):219-231. PMCID: PMC4224636

Zahr A, Alcaide P, Yang J, Jones A, Gregory M, Patel-Hett SR, Luscinskas FW, Saint-Geniez M, Ksander B, D’Amore PA, Argüeso P. Endomucin prevents leukocyte-endothelial cell adhesion and has a critical role under resting and inflammatory conditions. Nat Commun. 2016 Feb 2;7:10363. PMCID: PMC4740757

Janssen E, Hedayat M, Leick M, Tohme M, Kumari S, Ramesh N, Massaad M, Ullas S, Azcuti V, Goodnow C, Randall K, Qaio Q, Wu H, Al-Herz W, Cox D, Hartwig J, Irvine D, FW Luscinskas, and Geha RS. A DOCK8-WIP-WASP complex links the TCR to the actin cytoskeleton. J Clin Invest. 2016 Oct 3;126 (10):3837-3851. PMCID: PMC5096816

Azcutia V, Bassil R, Herter J, Newton G, Mayadas T, Khoury SJ, Parkos CA, Elyaman E, and Luscinskas FW. Defects in CD4+ T cell LFA-1 integrin dependent adhesion and proliferation protect CD47-/- mice in EAE. J. Leuk. Biol. Epub ahead of print December 13, 2016. doi:10.1189/jlb.3A1215-546RR. PMCIS not yet available.

Miyabe Y, Miyabe C, Murooka TT, Kim EY, Newton GA, Kim ND, Haribabu B, Luscinskas FW, Mempel TR, and Luster AD. Complement C5a Receptor is the Key Initiator of Neutrophil Adhesion Igniting Immune Complex-induced Arthritis. In press, Science Immunology. Dec 10, 2016. PMCID: PMC5436313

Folco E, Mawson T, Vromman A, Bernardes-Souza B, Franck G, Persson O, Nakamura M, Newton G, Luscinskas FW, and Libby P. Neutrophil Extracellular Traps Induce Endothelial Cell Activation and Tissue Factor Production through Interleukin-1α and Cathepsin G. In press ATVB. June 2018.

Engelbertsen D, Autio A, Verwilligen RAF, Depuydt MAC, Newton G, Rattik S, Levinsohn E, Saggu G, Jarolim P, Lichtman AH, Luscinskas FW. Increased lymphocyte activation and atherosclerosis in CD47-deficient mice. Submitted, Science Reports



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